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1.
Chinese Journal of Biotechnology ; (12): 3005-3019, 2021.
Article in Chinese | WPRIM | ID: wpr-921402

ABSTRACT

Formins are widely distributed in eukaryotes such as fungi, plants and animals. They play crucial roles in regulating the polymerization of actin, coordinating the synergistic interactions between actin and microtubules, and determining cell growth and morphology. Unlike formins from fungi and animals, plant formins have been evolved into two plant-specific types. Generally, type Ⅱ formins are believed to regulate the polarized growth of cells, and type Ⅰ formins may regulate the cell expansion and division processes. Recent studies on the function of plant formins suggest it is inappropriate to classify the function of formins purely based on their structures. This review summarizes the domain organization of formins and their corresponding functions, as well as the underpinning mechanisms. Furthermore, the unsolved or unexplored issues along with future perspectives on plant formins are proposed and discussed.


Subject(s)
Actins , Formins , Microfilament Proteins , Plant Cells , Plant Development , Plants
2.
Article in Chinese | WPRIM | ID: wpr-879601

ABSTRACT

OBJECTIVE@#To explore the genetic basis for a Chinese pedigree affected with non-syndromic hearing loss (NSHL).@*METHODS@#Commercialized gene chip was applied to detect common mutations associated with congenital deafness. Whole exome sequencing was carried out for patients for whom gene chip yielded a negative result. Candidate variants were verified by Sanger sequencing.@*RESULTS@#Two patients from the pedigree were discovered to carry compound heterozygous variants of the TRIOBP gene, namely c.3299C>A and c.5185-2A>G. Their parents had normal hearing and were both heterozygous carriers of the above variants. Both variants had co-segregated with the disease phenotype in the pedigree and were unreported previously.@*CONCLUSION@#Pathogenic variants of the TRIOBP gene comprise an important factor for NSHL. The novel c.5185-2A>G and c.3299C>A variants discovered in this study have enriched the mutational spectrum of the TRIOBP gene and enabled molecular diagnosis and genetic counseling for the family.


Subject(s)
Deafness/genetics , Hearing Loss, Sensorineural/genetics , Heterozygote , Humans , Microfilament Proteins/genetics , Mutation , Pedigree , Whole Exome Sequencing
3.
Article in Chinese | WPRIM | ID: wpr-776775

ABSTRACT

OBJECTIVE@#To explore phenotypic and mutational characteristics of a pedigree affected with autosomal dominant Charcot-Marie-Tooth disease (CMT) and nephropathy.@*METHODS@#Clinical data of the proband and his family members was collected. Electrophysiology, renal biopsy and next-generation sequencing were carried out for the proband.@*RESULTS@#The proband presented with distal lower limb weakness and proteinuria in childhood. His mother and brother had similar symptoms. Electrophysiological test of the proband revealed demyelination and axonal changes in both motor and sensory nerves. Renal biopsy suggested focal segmental glomerulosclerosis. Genetic testing revealed a heterozygous c.341G>A (p.G114D) mutation in exon 2 of the INF2 gene.@*CONCLUSION@#The phenotypic feature of the pedigree is autosomal dominant intermediate CMT and focal segmental glomerulosclerosis, which may be attributed to the c.341G>A mutation of the INF2 gene.


Subject(s)
Charcot-Marie-Tooth Disease , Genetics , Child , Female , Glomerulosclerosis, Focal Segmental , Genetics , Heterozygote , Humans , Male , Microfilament Proteins , Genetics , Mutation , Pedigree
4.
Article in Chinese | WPRIM | ID: wpr-772067

ABSTRACT

OBJECTIVE@#To investigate the expression of calponin-1 (CNN1) in systemic sclerosis (SSc) and its pathogenic role in fibrosis.@*METHODS@#Skin biopsy samples were collected from 19 patients with SSc and 21 healthy subjects. Real-time PCR was used to detect the expression of and mRNAs in the samples, and the protein expression of CNN1 was detected using immunohistochemistry. In cultured primary human dermal fibroblasts, expression was knocked down RNA interference, and the mRNA expression levels of and the fibrosis-related genes , , , , and were detected using real-time PCR; the proliferation of the cells was assessed using a real-time cell proliferation detection system.@*RESULTS@#Compared with that in samples from normal subjects, the expression of mRNA was significantly increased in the skin tissue of patients with SSc ( < 0.05) with a positive correlation with α-SMA (=0.7219, < 0.0001); the protein expression of CNN1 was also significantly increased in the skin tissue of patients with SSc. In cultured primary skin fibroblasts, the expression of CNN1 mRNA was positively correlated with and mRNA expressions (=0.6547, < 0.05; =0.6438, < 0.05). knockdown in the fibroblasts significantly inhibited the cell proliferation, obviously lowered the expressions of fibrosis-related genes, and reduced the protein expression of collagen.@*CONCLUSIONS@#The expression of is increased in the skin tissues of patients with SSc, and knockdown can reduce the activity of dermal fibroblasts, suggesting the close correlation of CNN1 with fibrosis in SSc.


Subject(s)
Calcium-Binding Proteins , Cells, Cultured , Fibroblasts , Fibrosis , Humans , Microfilament Proteins , Scleroderma, Systemic , Skin
5.
Article in English | WPRIM | ID: wpr-739670

ABSTRACT

BACKGROUND: The natural compound curcumin was known to inhibit migration and invasion of glioblastoma (GBM) cells. Fascin, a kind of actin-binding proteins, is correlated with migration and invasion of GBM cells. The purpose of this study was to investigate anti-migration and anti-invasion effects of curcumin via suppression of fascin expression in GBM cells. METHODS: U87 cell line was used as an experimental model of GBM. Fascin was quantified by Western blot analysis. And, the signal transducer and activator of transcription 3 (STAT3), known to play an important role in migration and invasion of tumor cells, were analyzed by sandwich-ELISA. Migration and invasion capacities were assessed by attachment, migration and invasion assays. Cellular morphology was demonstrated by immunofluorescence. RESULTS: At various concentrations of curcumin and exposure times, fascin expression decreased. After temporarily exposure to 10 µM/L curcumin during 6 hours as less invasive concentration and time, fascin expression temporarily decreased at 12 hours (18.4%, p=0.024), and since then recovered. And, the change of phosphrylated STAT3 level also reflected the temporarily decreased pattern of fascin expression at 12 hours (19.7%, p=0.010). Attachment, migration, and invasion capacities consistently decreased at 6, 12, and 24 hours. And, immunofluorescence showed the change of shape and the reduction of filopodia formation in cells. CONCLUSION: Curcumin is likely to suppress the fascin expression in GBM cells, and this might be a possible mechanism for anti-migration and anti-invasion effects of Curcumin via inhibition of STAT3 phosphorylation.


Subject(s)
Blotting, Western , Cell Line , Curcumin , Emigration and Immigration , Fluorescent Antibody Technique , Glioblastoma , Microfilament Proteins , Models, Theoretical , Phosphorylation , Pseudopodia , STAT3 Transcription Factor
6.
Rev. bras. cir. cardiovasc ; 33(3): 211-216, May-June 2018. tab, graf
Article in English | LILACS | ID: biblio-958403

ABSTRACT

Abstract Objective: The present study aimed the functional recovery evaluation after long term of cardiac arrest induced by Custodiol (crystalloid-based) versus del Nido (blood-based) solutions, both added lidocaine and pinacidil as cardioplegic agents. Experiments were performed in isolated rat heart perfusion models. Methods: Male rat heart perfusions, according to Langendorff technique, were induced to cause 3 hours of cardiac arrest with a single dose. The hearts were assigned to one of the following three groups: (I) control; (II) Custodiol-LP; and (III) del Nido-LP. They were evaluated after ischemia throughout 90 minutes of reperfusion. Left ventricular contractility function was reported as percentage of recovery, expressed by developed pressure, maximum dP/dt, minimum dP/dt, and rate pressure product variables. In addition, coronary resistance and myocardial injury marker by alpha-fodrin degradation were also evaluated. Results: At 90 minutes of reperfusion, both solutions had superior left ventricular contractile recovery function than the control group. Del Nido-LP was superior to Custodiol-LP in maximum dP/dt (46%±8 vs. 67%±7, P<0.05) and minimum dP/dt (31%±4 vs. 51%±9, P<0.05) variables. Coronary resistance was lower in del Nido-LP group than in Custodiol-LP (395%±50 vs. 307%±13, P<0.05), as well as alpha-fodrin degradation, with lower levels in del Nido-LP group (P<0.05). Conclusion: Del Nido-LP cardioplegia showed higher functional recovery after 3 hours of ischemia. The analysis of alpha-fodrin degradation showed del Nido-LP solution provided greater protection against myocardial ischemia and reperfusion (IR) in this experimental model.


Subject(s)
Animals , Male , Cardioplegic Solutions/pharmacology , Myocardial Reperfusion/methods , Potassium Compounds/pharmacology , Pinacidil/pharmacology , Heart Arrest, Induced/methods , Lidocaine/pharmacology , Time Factors , Vascular Resistance/physiology , Cardioplegic Solutions/chemistry , Carrier Proteins/analysis , Blotting, Western , Rats, Wistar , Coronary Vessels/physiopathology , Glucose/pharmacology , Glucose/chemistry , Heart/drug effects , Mannitol/pharmacology , Mannitol/chemistry , Microfilament Proteins/analysis
7.
Article in Chinese | WPRIM | ID: wpr-775829

ABSTRACT

OBJECTIVE@#To study the effect of Wdr1 deletion in germ cells on ovarian function of mice.@*METHODS@#Oocyte-specific gene knockout mouse model was constructed by crossing Wdr1female mice with Cre recombinase transgenic male mice which was driven by a germ cell-specific promoter. Wdr1; Ddx4-Cre mice and control mice were sacrificed at 14 days, 28 days and 4 months after birth, whose ovaries were subjected to photography, paraffin sectioning and Hematoxylin-Eosin (HE) staining. The ovarian volume and follicular numbers were recorded at various time points.@*RESULTS@#The ovarian volume of Wdr1 ; Ddx4-Cre mice was slightly lower than that of the controls at 14 days. HE staining showed that primordial follicles, primary follicles and secondary follicles were slightly reduced compared with the control mice at 14 days. The ovarian volume of Wdr1 ; Ddx4-Cre mice was significantly lower than that of the control mice at 28 days and 4 months. HE staining showed that all developmental follicles were significantly reduced compared with the control mice.@*CONCLUSION@#Wdr1 gene deletion in germ cells can influence early ovarian function of mice and lead to premature ovarian failure.


Subject(s)
Animals , Female , Germ Cells , Male , Mice , Mice, Knockout , Mice, Transgenic , Microfilament Proteins , Genetics , Oocytes , Ovarian Follicle
8.
Neuroscience Bulletin ; (6): 912-920, 2018.
Article in English | WPRIM | ID: wpr-775500

ABSTRACT

Astrocytes are closely associated with Alzheimer's disease (AD). However, their precise roles in AD pathogenesis remain controversial. One of the reasons behind the different results reported by different groups might be that astrocytes were targeted at different stages of disease progression. In this study, by crossing hAPP (human amyloid precursor protein)-J20 mice with a line of GFAP-TK mice, we found that astrocytes were activated specifically at an early stage of AD before the occurrence of amyloid plaques, while microglia were not affected by this crossing. Activation of astrocytes at the age of 3-5 months did not affect the proteolytic processing of hAPP and amyloid plaque loads in the brains of hAPP-J20 mice. Our data suggest that early activation of astrocytes does not affect the deposition of amyloid β in an animal model of AD.


Subject(s)
Aldehyde Dehydrogenase , Metabolism , Alzheimer Disease , Genetics , Metabolism , Pathology , Amyloid beta-Peptides , Metabolism , Amyloid beta-Protein Precursor , Genetics , Metabolism , Animals , Astrocytes , Metabolism , Brain , Pathology , Calcium-Binding Proteins , Metabolism , Cell Proliferation , Disease Models, Animal , Gene Expression Regulation , Genetics , Glial Fibrillary Acidic Protein , Glutamine , Metabolism , Green Fluorescent Proteins , Genetics , Metabolism , Humans , Ki-67 Antigen , Metabolism , Mice , Mice, Transgenic , Microfilament Proteins , Metabolism , Mutation , Genetics , Nerve Tissue Proteins , Metabolism
9.
Neuroscience Bulletin ; (6): 1058-1066, 2018.
Article in English | WPRIM | ID: wpr-775472

ABSTRACT

While inflammatory bowel disease (IBD) might be a risk factor in the development of brain dysfunctions, the underlying mechanisms are largely unknown. Here, mice were treated with 5% dextran sodium sulfate (DSS) in drinking water and sacrificed on day 7. The serum level of IL-6 increased, accompanied by elevation of the IL-6 and TNF-α levels in cortical tissue. However, the endotoxin concentration in plasma and brain of mice with DSS-induced colitis showed a rising trend, but with no significant difference. We also found significant activation of microglial cells and reduction in occludin and claudin-5 expression in the brain tissue after DSS-induced colitis. These results suggested that DSS-induced colitis increases systemic inflammation which then results in cortical inflammation via up-regulation of serum cytokines. Here, we provide new information on the impact of colitis on the outcomes of cortical inflammation.


Subject(s)
Animals , Calcium-Binding Proteins , Metabolism , Caspase 3 , Metabolism , Cerebral Cortex , Pathology , Claudin-5 , Metabolism , Colitis , Pathology , Cytokines , Genetics , Metabolism , Dextran Sulfate , Toxicity , Disease Models, Animal , Encephalitis , Gene Expression Regulation , Mice , Microfilament Proteins , Metabolism , Occludin , Metabolism , Polysaccharides , Blood , Toxicity , Time Factors
10.
Article in Chinese | WPRIM | ID: wpr-771460

ABSTRACT

OBJECTIVE@#To study the effect of knocking down fascin on cervical cancer cell proliferation and tumorigenicity in nude mice.@*METHODS@#Cervical cancer CaSki cells were infected with a lentiviral vector carrying fascin siRNA or with a negative control lentivirus, and fascin mRNA and protein expressions in the cells were detected using qRT-PCR and Western blotting. MTT assay was used to determine the proliferation of CaSki cells with fascin knockdown. CaSki cells transfected with fascin siRNA or the control lentiviral vector and non-transfected CaSki cells were inoculated subcutaneously in nude mice, and the volume and weight of the transplanted tumor were measured; Western blotting was used to detect the expressions of proliferating cell nuclear antigen (PCNA), survivin, cyclin dependent kinase 4 (CDK4) and p21 proteins in the tumor xenograft.@*RESULTS@#Infection with the lentiviral vector carrying fascin siRNA, but not the negative control vector, caused significant reductions in the expression levels of fascin mRNA and protein in CaSki cells ( < 0.05). Fascin knockdown resulted in significantly reduced proliferation of CaSki cells ( < 0.05). The nude mice inoculated with CaSki cells with fascin knockdown showed reduced tumor volume and weight, lowered levels of PCNA, survivin and CDK4, and increased expression of p21 protein in the tumor xenograft compared with the control mice. The negative control lentivirus did not affect the proliferation or tumorigenicity of CaSki cells in nude mice or the expression levels of PCNA, survivin, CDK4 or p21 proteins in the xenografts.@*CONCLUSIONS@#Knocking down fascin can inhibit the growth and tumorigenicity of cervical cancer cells in nude mice.


Subject(s)
Animals , Apoptosis , Carrier Proteins , Genetics , Metabolism , Cell Line, Tumor , Cell Proliferation , Cyclin-Dependent Kinase 4 , Metabolism , Cyclin-Dependent Kinase Inhibitor p21 , Metabolism , Female , Gene Knockdown Techniques , Genetic Vectors , Humans , Mice , Mice, Nude , Microfilament Proteins , Genetics , Metabolism , Proliferating Cell Nuclear Antigen , Metabolism , RNA, Messenger , Metabolism , RNA, Small Interfering , Survivin , Metabolism , Transfection , Tumor Burden , Uterine Cervical Neoplasms , Pathology
11.
Article in Chinese | WPRIM | ID: wpr-813167

ABSTRACT

To explore the mechanism for the role of autophagy in endometriosis, and to provide a theoretical basis for prevention and treatment of endometriosis.
 Methods: The endometrial CRL-7566 cells were treated with ATG5 siRNA, autophagic activator rapamycin and autophagic inhibitor 3-MA, respectively. The cell proliferation and invasion were detected by clonal formation, cell growth curve and MTT assay. The clinical specimens of endometriosis were collected from 20 cases. The expression of autophagy marker LC3II and autophagy substrate protein P62 were detected.
 Results: Rapamycin inhibited the proliferation and clonal formation of CRL-7566 cells, while autophagy inhibitor 3-MA and ATG5 siRNA showed opposite effect. Moreover, rapamycin inhibited filopodia growth in endometriosis, whereas overexpression of filopodia-relevant protein fascin-1 inhibited the decrease in invasiveness caused by rapamycin. In clinical samples, we also found a significant decrease of LC3II while an increase in P62 compared with the control group.
 Conclusion: Autophagy inhibition may contribute to an increase in endometrial cell proliferation and invasiveness. Autophagy activation could be a potential strategy for endometriosis therapy.


Subject(s)
Autophagy , Genetics , Carrier Proteins , Genetics , Metabolism , Cell Line , Cell Proliferation , Endometriosis , Endometrium , Cell Biology , Female , Gene Expression Regulation , Humans , Microfilament Proteins , Genetics , Metabolism , Microtubule-Associated Proteins , Genetics , RNA-Binding Proteins , Genetics , Sirolimus , Pharmacology
12.
Article in Korean | WPRIM | ID: wpr-718852

ABSTRACT

The cytoskeleton consists of 3 filamentous components: intermediate filaments, microtubules, and actin filaments. Actin filaments continuously assemble and disassemble far out of equilibrium to adapt cells in response to external stimuli. Actin filaments organization and dynamic are controlled by a multitude of actin-binding proteins including actin-bundling proteins. L-plastin, expressed abundantly in lymphocytes and monocytes, is an actin-bundling protein that roles in immune defense and in metastatic invasion of cancer cells. The actin-bundling activity of L-plastin is regulated not only by intracellular calcium concentration, but by phosphorylation of Ser5. The actin-bundling activity of L-pastin decreases by increased calcium concentration but is promoted by phosphorylation of Ser5. The morphology changes and motility of cells requires continuous remodeling of actin filaments which demands the sensitive nature of L-plastin to Ca2+-signal, phosphorylation of Ser5, and probably additional regulation. This review briefly describes the structure and regulation of L-plastin, and roles for L-plastin in cancer invasion and in macrophages.


Subject(s)
Actin Cytoskeleton , Calcium , Cytoskeleton , Intermediate Filaments , Lymphocytes , Macrophages , Microfilament Proteins , Microtubules , Monocytes , Phosphorylation
13.
Article in Chinese | WPRIM | ID: wpr-773805

ABSTRACT

OBJECTIVE@#To investigate the effect of rosuvastatin on homocysteine (Hcy) induced mousevascular smooth muscle cells(VSMCs) dedifferentiation and endoplasmic reticulum stress(ERS).@*METHODS@#VSMCs were co-cultured with Hcy and different concentration of rosuvastatin (0.1, 1.0 and 10 μmol/L). Cytoskeleton remodeling, VSMCs phenotype markers (smooth muscle actin-α, calponin and osteopontin) and ERS marker mRNAs (Herpud1, XBP1s and GRP78) were detected at predicted time. Tunicamycin was used to induce, respectively 4-phenylbutyrate(4-PBA) inhibition, ERS in VSMCs and cellular migration, proliferation and expression of phenotype proteins were analyzed. Mammalian target of rapamycin(mTOR)-P70S6 kinase (P70S6K) signaling agonist phosphatidic acid and inhibitor rapamycin were used in Rsv treated VSMCs. And then mTOR signaling and ERS associated mRNAs were detected.@*RESULTS@#Compared with Hcy group, Hcy+ Rsv group (1.0 and 10 μmol/L) showed enhanced α-SMA and calponin expression (<0.01), suppressed ERS mRNA levels (<0.01) and promoted polarity of cytoskeleton. Compared with Hcy group, Hcy+Rsv group and Hcy+4-PBA group showed suppressed proliferation, migration and enhanced contractile protein expression (<0.01); while tunicamycin could reverse the effect of Rsv on Hcy treated cells. Furthermore, alleviated mTOR-P70S6K phosphorylation and ERS (<0.01)were observed in Hcy+Rsv group and Hcy+rapamycin group, compared with Hcy group; while phosphatidic acid inhibited the effect of Rsv on mTOR signaling activation and ERS mRNA levels (<0.01).@*CONCLUSIONS@#Rosuvastatin could inhibit Hcy induced VSMCs dedifferentiation suppressing ERS, which might be regulated by mTOR-P70S6K signaling.


Subject(s)
Actins , Metabolism , Animals , Calcium-Binding Proteins , Metabolism , Cell Dedifferentiation , Cells, Cultured , Endoplasmic Reticulum Stress , Heat-Shock Proteins , Metabolism , Homocysteine , Membrane Proteins , Metabolism , Mice , Microfilament Proteins , Metabolism , Muscle, Smooth, Vascular , Cell Biology , Myocytes, Smooth Muscle , Cell Biology , Ribosomal Protein S6 Kinases, 70-kDa , Metabolism , Rosuvastatin Calcium , Pharmacology , TOR Serine-Threonine Kinases , Metabolism , X-Box Binding Protein 1 , Metabolism
14.
Chinese Medical Journal ; (24): 2320-2331, 2018.
Article in English | WPRIM | ID: wpr-690219

ABSTRACT

<p><b>Background</b>XB130 is a recently discovered adaptor protein that is highly expressed in many malignant tumors, but few studies have investigated its role in hepatocellular carcinoma (HCC). Therefore, this study explored the relationship between this protein and liver cancer and investigated its molecular mechanism of action.</p><p><b>Methods</b>The expression of XB130 between HCC tissues and adjacent nontumor tissues was compared by real-time polymerase chain reaction, immunochemistry, and Western blotting. XB130 silencing was performed using small hairpin RNA. The effect of silencing XB130 was examined using Cell Counting Kit-8, colony assay, wound healing assay, and cell cycle analysis.</p><p><b>Results</b>We found that XB130 was highly expressed in HCC tissues (cancer tissues vs. adjacent tissues: 0.23 ± 0.02 vs. 0.17 ± 0.02, P < 0.05) and liver cancer cell lines, particularly MHCC97H and HepG2 (MHCC97H and HepG2 vs. normal liver cell line LO-2: 2.35 ± 0.26 and 2.04 ± 0.04 vs. 1.00 ± 0.04, respectively, all P < 0.05). The Cell Counting Kit-8 assay, colony formation assay, and xenograft model in nude mice showed that silencing XB130 inhibited cell proliferative ability both in vivo and in vitro, with flow cytometry demonstrating that the cells were arrested in the G0/G1 phase in HepG2 (HepG2 XB130-silenced group [shA] vs. HepG2 scramble group [NA]: 74.32 ± 5.86% vs. 60.21 ± 3.07%, P < 0.05) and that the number of G2/M phase cells was decreased (HepG2 shA vs. HepG2 NA: 8.06 ± 2.41% vs. 18.36 ± 4.42%, P < 0.05). Furthermore, the cell invasion and migration abilities were impaired, and the levels of the epithelial-mesenchymal transition-related indicators vimentin and N-cadherin were decreased, although the level of E-cadherin was increased after silencing XB130. Western blotting showed that the levels of phosphorylated phosphoinositide 3-kinase (PI3K) and phospho-protein kinase B (p-Akt) also increased, although the level of phosphorylated phosphatase and tensin homolog increased, indicating that XB130 activated the PI3K/Akt pathway. Furthermore, we found that a reduction in XB130 increased liver cancer cell sensitivity to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis.</p><p><b>Conclusions</b>Our findings suggest that XB130 might be used as a predictor of liver cancer as well as one of the targets for its treatment.</p>


Subject(s)
Adaptor Proteins, Signal Transducing , Genetics , Metabolism , Animals , Apoptosis , Carcinoma, Hepatocellular , Metabolism , Pathology , Cell Movement , Cell Proliferation , Gene Knockdown Techniques , Liver Neoplasms , Metabolism , Pathology , Mice , Mice, Nude , Microfilament Proteins , Genetics , Metabolism , Neoplasm Invasiveness , Phosphatidylinositol 3-Kinases , Signal Transduction
16.
Braz. j. med. biol. res ; 49(3): e4861, Mar. 2016. tab, graf
Article in English | LILACS | ID: lil-771938

ABSTRACT

The present study screened potential genes related to lung adenocarcinoma, with the aim of further understanding disease pathogenesis. The GSE2514 dataset including 20 lung adenocarcinoma and 19 adjacent normal tissue samples from 10 patients with lung adenocarcinoma aged 45-73 years was downloaded from Gene Expression Omnibus. Differentially expressed genes (DEGs) between the two groups were screened using the t-test. Potential gene functions were predicted using functional and pathway enrichment analysis, and protein-protein interaction (PPI) networks obtained from the STRING database were constructed with Cytoscape. Module analysis of PPI networks was performed through MCODE in Cytoscape. In total, 535 upregulated and 465 downregulated DEGs were identified. These included ATP5D, UQCRC2, UQCR11 and genes encoding nicotinamide adenine dinucleotide (NADH), which are mainly associated with mitochondrial ATP synthesis coupled electron transport, and which were enriched in the oxidative phosphorylation pathway. Other DEGs were associated with DNA replication (PRIM1, MCM3, and RNASEH2A), cell surface receptor-linked signal transduction and the enzyme-linked receptor protein signaling pathway (MAPK1, STAT3, RAF1, and JAK1), and regulation of the cytoskeleton and phosphatidylinositol signaling system (PIP5K1B, PIP5K1C, and PIP4K2B). Our findings suggest that DEGs encoding subunits of NADH, PRIM1, MCM3, MAPK1, STAT3, RAF1, and JAK1 might be associated with the development of lung adenocarcinoma.


Subject(s)
Humans , Male , Female , Middle Aged , Aged , Adenocarcinoma/genetics , Gene Expression Profiling/methods , Lung Neoplasms/genetics , Microfilament Proteins/genetics , Down-Regulation/genetics , Gene Regulatory Networks , Mitogen-Activated Protein Kinase 1/genetics , NAD/genetics , Protein Interaction Maps/genetics , Proto-Oncogene Proteins c-raf/genetics , Up-Regulation/genetics
17.
Article in Chinese | WPRIM | ID: wpr-289880

ABSTRACT

<p><b>OBJECTIVE</b>To study on the expression patterns of proteins associated with cell junctions in the developing mouse testes.</p><p><b>METHOD</b>The expression levels of reproductive related cell lines spermatogonia cell line GC1 spg, spermatocyte cell line GC2 spg, leydig cell line TM3, and sertoli cell line TM4, primary sertoli cells, and 1-6-week mouse testes were analyzed using Western blot.</p><p><b>RESULTS</b>The sertoli cell junction-associated membrane proteins adhesion molecule A, Occludin and Claudin, and the sertoli-germ cell junction-associated membrane proteins junctional adhesion molecule C, Nectin-3, and E-cadherin were stage-specific in the seminiferous tubules in the mouse testes. The adaptor proteins associated with cell juctions zonula occludens-1, zonula occludens-2, Afadin, Β-catenin, and CD2-associated protein were not stage-specific in the seminiferous tubules in the mouse testes.</p><p><b>CONCLUSIONS</b>In the seminiferous tubules in the mouse testes, the membrane proteins associated with cell junctions are stage-specific. However, the expressions of adaptor proteins associated with cell junctions do not obviously change.</p>


Subject(s)
Adaptor Proteins, Signal Transducing , Metabolism , Animals , Cdh1 Proteins , Metabolism , Cell Adhesion Molecules , Metabolism , Cell Line , Cytoskeletal Proteins , Metabolism , Humans , Intercellular Junctions , Metabolism , Male , Membrane Proteins , Metabolism , Mice , Microfilament Proteins , Metabolism , Nectins , Seminiferous Tubules , Cell Biology , Metabolism , Sertoli Cells , Cell Biology , Testis , Cell Biology , Zonula Occludens-1 Protein , Metabolism , Zonula Occludens-2 Protein , Metabolism , beta Catenin , Metabolism
18.
Chinese Journal of Biotechnology ; (12): 1204-1211, 2016.
Article in Chinese | WPRIM | ID: wpr-310547

ABSTRACT

The purpose of this study is to reveal the role of Girdin in regulating the aggregation of actin filaments by studying the relationship between PKB/Akt and Girdin. First we used Scansite software (http://scansite.mit.edu) to predict relevant target sites of PKB/Akt on mouse Girdin. To gain insight into the role of phosphorylation of Girdin by PKB/Akt, we assessed the location of phosphorylated Girdin in fertilized eggs by staining with anti-P-Girdin 1 417 Ab. We detected a distinct increase in the fluorescence signal of F-actin and P-Girdin 1 417 after microinjection of Akt WT and myr-Akt. The addition of myr-Akt induced phosphorylation of Girdin in mouse fertilized eggs. In addition, siRNA-mediated Akt-knockdown blocked phosphorylation of Girdin. The distribution of actin filaments was obviously scattered. These results strongly suggest that PKB/Akt could directly phosphorylate Girdin on Ser1 417 and promote its function in mouse fertilized eggs.


Subject(s)
Actins , Physiology , Animals , Mice , Microfilament Proteins , Physiology , Phosphorylation , Proto-Oncogene Proteins c-akt , Physiology , RNA, Small Interfering , Vesicular Transport Proteins , Physiology , Zygote
19.
Chinese Journal of Pediatrics ; (12): 218-221, 2016.
Article in Chinese | WPRIM | ID: wpr-298273

ABSTRACT

<p><b>OBJECTIVE</b>To explore the clinical and gene mutation characteristics of children with peroneal myoatrophy FGD4 mutations.</p><p><b>METHOD</b>The clinical data of a patient with peroneal myoatrophy with novel FGD4 gene mutations were collected, the related literature was searched from China National Knowledge Infrastructure, Wanfang Data Knowledge Service Platform, National Center for Biotechnology Information and PubMed (up to December 2014) by using search terms"muscular disorders, atrophic"peripheral nervous system diseases"genes". The clinical features and treatment of the patients with FGD4 gene mutations were studied.</p><p><b>RESULT</b>The patient was a 10-years-old boy, he was presented to our clinic due to lower extremity weakness for 3 years, worsening for one year with normal family history and birth history. When he was 6 years old, his feet turned inward as he walked, at 7 years of age, his toes pointed toward the ground, the heel could not touch the ground, the right foot was more serious. During the recent year his symptoms were worsened, manifested as clubfoot, foot drop, arched feet, crane legs, difficult in squatting, walking with swaying gait, easy to fall. He was brought to a number of domestic general hospitals' neurology clinic, he was clearly diagnosed as peroneal myoatrophy, but failed to make typing. Electromyography (EMG) showed neurogenic damage (peripheral neuropathy - motor and sensory fibers are involved). Target gene sequencing showed that the child had FGD4 genes compound heterozygous mutation: c. 338A> G and c. 1730G> A, where the former was inherited from his father, the latter inherited from his mother, it was a new mutation unreported previously. Literature search retrieved six reports (all in English literature) with FGD4 10 cases with mutations, which were expressed as peroneal myoatrophy, but were homozygous mutation.</p><p><b>CONCLUSION</b>This study found the FGD4 4th and the 14th exons' c. 338A> G and c. 1730G> A heterozygous mutations, and this mutations may lead to peroneal myoatrophy.</p>


Subject(s)
Atrophy , Child , China , Exons , Heterozygote , Humans , Male , Microfilament Proteins , Muscular Diseases , Mutation
20.
Article in Chinese | WPRIM | ID: wpr-328253

ABSTRACT

<p><b>OBJECTIVE</b>To observe the effect of Wenyang Huoxue Lishui Recipe (WHLR) containing serum on the expression of cathepsin L (CatL) in puromycin aminonucleoside-induced injury of mouse glomerular podocytes.</p><p><b>METHODS</b>Mouse podocyte cells (MPCs) in vitro cultured were divided into the normal control group, the model group, the dexamethasone (DEX) group, 10% WHLR containing serum group, 20% WHLR containing serum group, the vehicle serum control group. MPCs in the normal control group were cultured at 37 degrees C culture solution for 24 h. 45 mg/L puromycin was acted on MPCs in the model group for 24 h. On the basis of puromycin intervention, 1 limol/L DEX was co-incubated in MPCs of the DEX group for 24 h; 10% or 20% WHLR containing serum was co-incubated in MPCs of the 10% WHLR containing serum group and 20% WHLR containing serum group for 24 h. The vehicle serum control group was also set up by incubating with WHLR containing serum alone for 24 h. The expression of CatL and its substrate Synaptopodin in podocytes were detected by cell immunofluorescence staining. FITC-conjugated phalloidin was used to stain F-actin. A cortical F-actin score index (CFS index) was designed to quantify the degree of cytoskeletal reorganization in cultured podocytes.</p><p><b>RESULTS</b>Compared with the normal control group, the expression of synaptopodin significantly decreased and the expression of CatL significantly-increased in the model group. F-actin arranged in disorder, gradually forming pericellular F-actin ring. CFS index was obviously elevated (P < 0.01). Compared with the model group, the epression of synaptopodin increased, the expression of CatL decreased, and CFS index also decreased in the DEX group, 10% WHLR containing serum group, and 20% WHLR containing serum group (P < 0.05, P < 0.01). Compared with the DEX group, the expression of synaptopodin decreased in 10% WHLR containing serum group, CFS index also decreased in 20% WHLR containing serum group (P < 0.05).</p><p><b>CONCLUSIONS</b>WHLR could up-regulate the expression of synaptopodin, down-regulate the expression of CatL, and alleviate cytoskeletal reorganization of F-actin. It was helpful to stabilize the cytoskeleton of F-actin and improve the merging of podocytes.</p>


Subject(s)
Actins , Metabolism , Animals , Cathepsin L , Metabolism , Cells, Cultured , Down-Regulation , Drugs, Chinese Herbal , Pharmacology , Kidney Glomerulus , Cell Biology , Mice , Microfilament Proteins , Metabolism , Podocytes , Pathology , Puromycin Aminonucleoside , Up-Regulation
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