Effects of miR-130b-5p targeting E26 transformation specific-1 on proliferation,migration and invasion of prostatic cancer cells and its mechanism / 中国生物制品学杂志

@#Objective To investigate the effects of miR-130b-5p targeting E26 transformation specific-1(ETS1)on proliferation,migration and invasion of prostatic cancer(PCa)cells and its mechanism. Methods The mRNA transcription level of miR-130b-5p gene in PCa tissues,adjacent tissues,(LNCap,PC-3,DU-145)and normal prostate cells(RPWE-1)PCa cells was measured by qRT-PCR,and the expression of ETS1 protein in PCa cells was detected by Western blot. Bioinformatics,fluorescein experiment,qRT-PCR and Western blot were used to predict and verify the targeting relationship between miR-130b-5p and ETS1. PC-3 cells were divided into control group(without any treatment),mimic group(transfected with miR-130b-5p mimic)and mimic + ETS1 group(transfected with miR-130b-5p mimic + pcDNA-ETS1). The cells were detected for the proliferation and viability by clone formation assay and CCK-8 respectively,measured for the migration and invasion by scratch test and Transwell chamber assay,and detected for the expression of invasion-related proteins and PI3K/AKT/mTOR pathway-related proteins by Western blot. Results The transcription level of miR-130b-5p mRNA in PCa tissues was significantly lower than that in adjacent tissues(t = 12. 450,P < 0. 001);Compared with RPWE-1 cells,the transcription level of miR-130b-5p mRNA in LNCap,PC-3 and DU-145 cells decreased significantly(t = 4. 463,7. 103 and 5. 741,P = 0. 001 2,< 0. 001 and < 0. 001,respectively),while the expression level of ETS1protein increased significantly(t = 4. 850,9. 325 and 7. 723,P = 0. 008,< 0. 001 and = 0. 002,respectively). miR-130-5p targeted and negatively regulated the expression of ETS1. Compared with the control group,the cloning rate,viability and scratch healing rate of cells in mimic group decreased significantly(t = 11. 370,10. 640 and 15. 660,respectively,each P < 0. 001),the number of invasive cells decreased significantly(t = 10. 160,P < 0. 001),the expression levels of matrix metalloproteinase-2(MMP-2),MMP-9 and vimentin decreased significantly(t = 15. 120,9. 992 and 12. 600,P < 0. 001,< 0. 001 and = 0. 002,respectively),while the expression level of E-cadherin increased significantly(t = 6. 928,P < 0. 001),and the phosphorylation levels of phosphatidylinositol-3 kinase(PI3K),protein kinase B(AKT)and mammalian target of rapamycin(mTOR)decreased significantly(t = 7. 746,8. 041 and 11. 510,P = 0. 002,0. 002,and < 0. 001,respectively);Compared with mimic group,the cell cloning rate,viability,scratch healing rate significantly increased in mimic + ETS1 group(t = 6. 988,6. 642 and 6. 660,respectively,each P < 0. 001),the number of invasive cells significantly increased(t = 4. 082,P = 0. 002),the expression levels of MMP-2,MMP-9 and vimentin proteins were significantly up-regulated(t = 10. 410,6. 754 and 8. 521,P = 0. 002,0. 003 and 0. 002,respectively),however,the expression level of E-cadherin was significantly down-regulated(t = 4. 648,P < 0. 01),and the phosphorylation levels of PI3K,AKT and mTOR were significantly up-regulated(t = 4. 850,4. 323 and 10. 840,P = 0. 008,0. 008 and < 0. 001,respectively)Conclusion miR-130b-5p targets ETS1 to inhibit the proliferation,migration and invasion of PC-3 cells,which may be through the regulation of PI3K/AKT/mTOR signaling pathway.

The Long Non-coding RNA ILF3-AS1 Inhibited Proliferation of Cervical Cancer Cells Through the MiR-130a-3p/PTEN Axis / 中国生物化学与分子生物学报

ILF3 antisense RNA 1 (ILF3-AS1), the antisense RNA of interleukin enhancer binding factor 3 (ILF3), is a lncRNA located on chromosome 19p13. 2. ILF3-AS1 played a key role in the occurrence and development of a variety of tumors, but its role in cervical cancer had not been explored yet. Therefore, we first used TCGA and GTEx database to conduct bioinformatics analysis. The results suggested that ILF3-AS1 was down-regulated in cervical cancer tissues (P < 0. 001) and was associated with a good prognosis (P = 0. 045). The qRT-PCR experiment showed that expression of ILF3-AS1 in cervical cancer tissues and SiHa, HeLa, CaSki cervical cancer cell lines was lower than that in control groups. Subsequently, overexpressing of ILF3-AS1 can significantly inhibit the cancer cell viability and stimulate apoptosis (P<0. 001). Analysis using the Star Base v3. 0 database suggested that ILF3-AS1 can target miR-130a-3p; while miR-130a-3p may target PTEN. The qRT-PCR test showed that the expression of miR-130a-3p in cervical cancer was significantly higher than that in normal cervical tissues (P < 0. 01). The results of the luciferase reporter assay showed that ILF3-AS1 can specifically bind to miR-130a-3p (P<0. 01). After overexpression of ILF3-AS1 in HeLa cells, the expression of miR-130a-3p was significantly down-regulated (P < 0. 01). Co-transfection with pcDNA3. 1-ILF3-AS1 and miR-130a-3p mimics, the inhibitory effect of LF3-AS1 on cell proliferation can partially be reversed (P<0. 001). After HeLa cells overexpressed ILF3-AS1, the expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN) mRNA (P < 0. 001) and proteins (P < 0. 001) significantly increased; when miR-130a-3p mimics was simultaneously used in HeLa cell, the increased expression of PTEN mRNA (P <0. 001) and proteins (P < 0. 001) was notably inhibited. In summary, ILF3-AS1 inhibited the proliferation of cervical cancer cells by sponging miR-130a-3p to regulate the expression of PTEN.

microRNA-130b downregulation potentiates chondrogenic differentiation of bone marrow mesenchymal stem cells by targeting SOX9

Osteoarthritis (OA) is a chronic health condition. MicroRNAs (miRs) are critical in chondrocyte apoptosis in OA. We aimed to investigate the mechanism of miR-130b in OA progression. Bone marrow mesenchymal stem cells (BMSCs) and chondrocytes were first extracted. Chondrogenic differentiation of BMSCs was carried out and verified. Chondrocytes were stimulated with interleukin (IL)-1β to imitate OA condition in vitro. The effect of miR-130b on the viability, inflammation, apoptosis, and extracellular matrix of OA chondrocytes was studied. The target gene of miR-130b was predicted and verified. Rescue experiments were performed to further study the underlying downstream mechanism of miR-130b in OA. miR-130b first increased and drastically reduced during chondrogenic differentiation of BMSCs and in OA chondrocytes, respectively, while IL-1β stimulation resulted in increased miR-130b expression in chondrocytes. miR-130b inhibitor promoted chondrogenic differentiation of BMSCs and chondrocyte growth and inhibited the levels of inflammatory factors. miR-130b targeted SOX9. Overexpression of SOX9 facilitated BMSC chondrogenic differentiation and chondrocyte growth, while siRNA-SOX9 contributed to the opposite trends. Silencing of SOX9 significantly attenuated the pro-chondrogenic effects of miR-130b inhibitor on BMSCs. Overall, miR-130b inhibitor induced chondrogenic differentiation of BMSCs and chondrocyte growth by targeting SOX9.

microRNA-130b downregulation potentiates chondrogenic differentiation of bone marrow mesenchymal stem cells by targeting SOX9

Osteoarthritis (OA) is a chronic health condition. MicroRNAs (miRs) are critical in chondrocyte apoptosis in OA. We aimed to investigate the mechanism of miR-130b in OA progression. Bone marrow mesenchymal stem cells (BMSCs) and chondrocytes were first extracted. Chondrogenic differentiation of BMSCs was carried out and verified. Chondrocytes were stimulated with interleukin (IL)-1β to imitate OA condition in vitro. The effect of miR-130b on the viability, inflammation, apoptosis, and extracellular matrix of OA chondrocytes was studied. The target gene of miR-130b was predicted and verified. Rescue experiments were performed to further study the underlying downstream mechanism of miR-130b in OA. miR-130b first increased and drastically reduced during chondrogenic differentiation of BMSCs and in OA chondrocytes, respectively, while IL-1β stimulation resulted in increased miR-130b expression in chondrocytes. miR-130b inhibitor promoted chondrogenic differentiation of BMSCs and chondrocyte growth and inhibited the levels of inflammatory factors. miR-130b targeted SOX9. Overexpression of SOX9 facilitated BMSC chondrogenic differentiation and chondrocyte growth, while siRNA-SOX9 contributed to the opposite trends. Silencing of SOX9 significantly attenuated the pro-chondrogenic effects of miR-130b inhibitor on BMSCs. Overall, miR-130b inhibitor induced chondrogenic differentiation of BMSCs and chondrocyte growth by targeting SOX9.

Overexpression of miR-130a-3p attenuates cardiomyocyte hypertrophy / 生物医学工程学杂志

This study aimed to explore the role of miR-130a-3p in cardiomyocyte hypertrophy and its underlying mechanisms. Pressure-overload induced myocardial hypertrophy mice model was constructed by thoracic aortic constriction (TAC). , norepinephrine (NE) was used to stimulate neonatal rat cardiomyocytes (NRCMs) and H9c2 rat cardiomyocytes to induce hypertrophic phenotypes. The expression of miR-130a-3p was detected in mice hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. The mimics and inhibitors of miR-130a-3p were transfected into H9c2 cells to observe the role of miR-130a-3p on the hypertrophic phenotype change of cardiomyocytes separately. Furthermore, whether miR-130a-3p regulated hypertrophic related signaling pathways was explored. The results showed that the expression of miR-130a-3p was significantly decreased in hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. After transfection of miR-130a-3p mimics, the expression of hypertrophic marker genes, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC), and the cell surface area were notably down-regulated compared with the control group (mimics N.C. + NE group). But after transfection of miR-130a-3p inhibitor, the expression of ANP, BNP and β-MHC in H9c2 cells increased significantly, and the cell area increased further. By Western blot, it was found that the protein phosphorylation level of Akt and mTOR were down-regulated after over-expression of miR-130a-3p. These results suggest that miR-130a-3p mimics may alleviate the degree of cardiomyocyte hypertrophy, meanwhile its inhibitor can further aggravate cardiomyocyte hypertrophy. Over-expression of miR-130a-3p may attenuate cardiomyocytes hypertrophy by affecting the Akt pathway.

Computational Prediction of miR130a Target Genes in Cancer

@#Introduction: Cancer is one of the main causes of mortality globally and the incidence has been rising over the years. Studies have shown that miRNAs have the potential as cancer biomarkers. The miR-130a has been reported to be upregulated in several types of cancer, which indicate the important roles of miR-130a in cancer development and metastasis. The aim of this study is to identify potential target genes and to predict the regulatory function of miR130a-3p and 5p in cancer. Methods: Three bioinformatics platforms namely miRWalk, the Database for annotations, visualization and integrated discovery (DAVID) Gene Functional Classification Tool and miRanda-miRSVR analysis tools were used to identify possible interaction between miR-130a and its target. Protein-protein interaction (PPI) network for the predicted target genes was then constructed. Results: The analyses have identified nine predicted target genes for miR-130a-3p (RAPGEF4, SOS2, NRP1, RPS6KB1, MET, IL15, ACVR1, RYR2 and ITPR1), and ten for miR-130a-5p (BCL11A, SPOPL, NLK, PPARGC1A, POU4F2, CPEB4, ST18, RSBN1L, ELF5 and ARID4B), that might play an important role in the development of cancer. Findings from this report suggest that miR-130a may involves in controlling cancer related genes; MET, ACVR1 and BCL11A. miR-130a-3p may regulates MET which involves in apoptosis and metastasis, and ACVR1 which involves in metastasis and angiogenesis. miR-130a-5p may regulates BCL11A which involves in apoptosis, proliferation and tumorigenesis. Conclusion: This study has highlighted the molecular interaction of miR-130a with associated genes and pathways, suggesting therapeutic potential of miR130a as personalised targeted therapy for cancer.

miR-130a-3p inhibits invasion of breast cancer MCF-7 cells through HGF/MET pathway / 中国肿瘤生物治疗杂志

@# Objective: To explore the molecular mechanism of miR-130a-3p regulating epithelial mesenchymal transition (EMT) to affect the invasion and metastasis of breast cancer cells through HGF/MET pathway. Methods: A total of 22 pairs of cancer tissues and adjacent normal tissues from breast cancer patients, who were admitted to Affiliated Hospital of Chengde Medical College from January 2018 to October 2018, were collected for this study; in addition, breast cancer cell lines (MCF-7, MDA-MB-231 and MDA-MB453) and normal breast epithelial cells MCF10A were obtained from the Institute of Basic Sciences, Chengde Medical College. And then, the expression of miR-130a-3p in tissues and cell lines were detected by qRT-PCR. The experiment cells were divided into control group, miR-130a-3p mimics group, miR-130a-3p inhibitor group, PHA665752 (a small-molecule MET inhibitor) transfection group and PHA665752+miR-130a-3p inhibitor co-transfection group. CCK-8 assay and Transwell assay were performed to detect the proliferation, invasion and migration of MCF-7 cells, respectively. The expressions of EMT and HGF/MET signaling pathway related proteins in MCF-7 cells were detected by WB. In addition, the targeted relationship between miR-130a-3p and MET was verified by Dual luciferase reporter gene assay. Results: miR-130a-3p was down-regulated in breast cancer tissues and cell lines. Over-expression of miR130a-3p could suppress the proliferation, invasion, migration and EMT of MCF-7 cells, while knockdown of miR-130a-3p had the opposite results. The results of Dual luciferase reporter gene assay indicated that miR-130a-3p targetedly down-regulated the expression of MET, and miR-130a-3p negatively regulated the expression of HGF/MET signaling pathway. Further experiments confirmed that miR-130a-3p inhibited the proliferation, invasion, migration and EMT of MCF-7 cells by blocking HGF/MET signaling pathway. Conclusion: miR-130a-3p suppresses the EMT of MCF-7 cells via blocking HGF/MET signaling pathway, thereby repressing the invasion and metastasis of MCF-7 cells.

Knockdown of LncRNA H19 Relieves LPS-Induced Damage by Modulating miR-130a in Osteoarthritis

PURPOSE: Osteoarthritis (OA) is a commonly occurring illness without a definitive cure, at present. Long non-coding RNAs (lncRNAs) have been widely confirmed to be involved in the modulation of OA progression. This study aimed to investigate the role and mechanism of lncRNA H19 in OA. MATERIALS AND METHODS: Abundances of H19 and microRNA-130a (miR-130a) in lipopolysaccharide (LPS)-treated C28/I2 cells were measured by reverse-transcription quantitative PCR (RT-qPCR). CCK-8 and flow cytometry analyses were carried out to assess cell viability and apoptosis. Starbase online software was used to predict the putative binding sites between H19 and miR-130a. Luciferase reporter, RNA pull down, and RT-qPCR were performed to analyze the true interaction between H19 and miR-130a. RESULTS: A notably dose-dependent elevation of H19 levels was observed in LPS-treated C28/I2 cells. Knockdown of H19 ameliorated the injury of LPS-induced C28/I2 cells, reflected by induced viability, decreased apoptosis, and reduced inflammatory factor secretions. Moreover, H19 negatively regulated the expression of miR-130a via acting as a molecular sponge for miR-130a. The stimulatory effects of H19 on cell damage were abolished following the restoration of miR-130a. CONCLUSION: LncRNA H19 aggravated the injury of LPS-induced C28/I2 cells by sponging miR-130a, hinting a novel regulatory mechanism and a potential therapeutic target for OA.

Study on the expression and cancer-promoting mechanism of miR-130b in human retinoblastoma / 国际眼科杂志(Guoji Yanke Zazhi)

@#AIM: To study the expression and cancer-promoting mechanism of miR-130b in human retinoblastoma(RB).<p>METHODS: Detected the expression levels of miR-130b in human RB carcinoma tissues, adjacent tissues and human RB cell lines(HXO-Rb44 and Y79)by qRT-PCR; detected the expression levels of PTEN in HXO-Rb44 and Y79 cells by qRT-PCR, Western Blot and immunofluorescence; verified the target relationship between miR-130b and PTEN by dual-luciferase reporter gene test; the co-transfection test was used to investigate the relationship between PTEN and miR-130b on the expression of PI3K/Akt signaling pathway in RB cell line.<p>RESULTS: The expression level of miR-130b in cancer tissue of RB was significantly higher than that of paracancerous tissue(<i>P</i><0.05). Compared with axben-181 cells, the expression level of miR-130b in HXO-Rb44 and Y79 cells was significantly increased(<i>P</i><0.05). Compared with RB cancer tissue, the expression level of PTEN in its paracancerous tissue was significantly increased(<i>P</i><0.05). The expression level of miR-130b was negatively correlated with the expression level of PTEN(<i>P</i><0.001). The mRNA and protein expression levels of PTEN in HXO-Rb44 cells overexpressing miR-130b were significantly reduced, while the mRNA and protein expression levels of PTEN in Y79 cells after miR-130b interference were significantly increased(<i>P</i><0.05). Compared with miR-130b mimics+PTEN-NC group, the luciferase activity of miR-130b mimics+wt-PTEN group was significantly reduced(<i>P</i><0.05).In the HXO-Rb44 cells co-transfected with miR-130b mimics+PTEN-NC, the expression levels of p-Akt 308 and p-Akt 473 protein were significantly increased(<i>P</i><0.05), while the expression levels of PTEN protein were significantly decreased(<i>P</i><0.05). In the HXO-Rb44 cells co-transfected with miR-130b mimics+PTEN, no significant changes were observed in the above three proteins.<p>CONCLUSION: miR-130b is highly expressed in RB tissues and cell lines. PTEN is the target gene of miR-130b, and miR-130b may negatively regulate PTEN to affect the expression of PI3K/Akt signaling pathway and ultimately play a role in promoting cancer.

Circular RNA-ZFR Inhibited Cell Proliferation and Promoted Apoptosis in Gastric Cancer by Sponging miR-130a/miR-107 and Modulating PTEN / Journal of the Korean Cancer Association, 대한암학회지

PURPOSE: This study aimed to probe into the associations among circular RNA ZFR (circ-ZFR), miR-130a/miR-107, and PTEN, and to investigate the regulatory mechanism of circ-ZFR–miR-130a/miR-107–PTEN axis in gastric cancer (GC). MATERIALS AND METHODS: GSE89143 microarray data used in the study were acquired from publicly available Gene Expression Omnibus database to identify differentially expressed circular RNAs inGC tissues. The expressions of circ-ZFR, miR-130a, miR-107, and PTEN were examined by real-time reverse transcription polymerase chain reaction, while PTEN protein expression was measured by western blot. The variation of GC cell proliferation and apoptosis was confirmed by cell counting kit-8 assay and flow cytometry analysis. The targeted relationships among circZFR, miR-130a/miR-107, and PTEN were predicted via bioinformatics analysis and demonstrated by dual-luciferase reporter assay and RNA immunoprecipitation assay. The impact of ZFR on gastric tumor was further verified in xenograft mice model experiment. RESULTS: Circ-ZFR and PTEN were low-expressed whereas miR-107 and miR-130a were highexpressed in GC tissues and cells. There existed targeted relationships and interactions between miR-130a/miR-107 and ZFR/PTEN. Circ-ZFR inhibited GC cell propagation, cell cycle and promoted apoptosis by sponging miR-107/miR-130a, while miR-107/miR-130a promoted GC cell propagation and impeded apoptosis through targeting PTEN. Circ-ZFR inhibited cell proliferation and facilitated apoptosis in GC by sponging miR-130a/miR-107 and modulating PTEN. Circ-ZFR curbed GC tumor growth and affected p53 protein expression in vivo. CONCLUSION: Circ-ZFR restrained GC cell proliferation, induced cell cycle arrest and promoted apoptosis by sponging miR-130a/miR-107 and regulating PTEN.

miR-130b-3p may serve as a marker for human bladder cancer / 基础医学与临床

Objective To further understand potential mechanism of miRNAs in bladder cancer .Mtehods Human microarray was used to analyze the expression of miRNAs in four pair human BC cancer tissues and adjacent normal tissues.Then RT-Qpcr was used to verified that the expression of two most up -regulated miRNAs and target genes for results of miRNA/Mrna microarray.Subsequently, it was deduced that miR-130b-3p could target at PTEN through a bioinformatics approach and dual-luciferase reporter assay.CCK8, EDU, flow cytometry, wound healing, Transwell and cytoskeleton assay were applied to prove that miR-130b could affect proliferation, apoptosis, migration and invasion of BC cells.The effects of PTEN regula-ted by miR-130b-3p on the key target protein expression of PI 3K/AKT and integrin β1/FAK signaling pathway were determined by Western blot.Resulst miR-130b-3p was significantly up-regulated and nega-tively correlated with PTEN expression in clinical bladder cancer specimens as compared with normal urothelial tissue.miR-130b-3p mimics could down-regulate PTEN expression, which leads to the activation of PI3K/AKT and integrinβ1/FAK signaling pathway related to cell proliferation , migration and invasion in bladder cancer EJ cells.When the cells were transfected with miR-130b-3p inhibitors, they could be sur- veyed with rearranging cytoskeleton.Conclusions miR-130b/PTEN may be used as a marker for bladder cancer.

Effects of Shexiang Wulong Pills on the expression levels of miR-146a, miR-130 and miR-223 of peripheral blood in patients with RA / 中成药

AIM To explore the effects of Shexiang Wulong Pills (Moschus Artifactus,Aconiti Radix Cocta,Pheretima,etc.) drug serum on the expression levels of miR-146a,miR-130 and miR-223 in peripheral blood mononuclear cells (PBMCs) of patients with rheumatoid arthritis (RA).METHODS PBMCs were extracted from blood of 30 cases of RA patients,cells were divided into three groups,blank control group,serum-free groupand Shexiang Wulong Pills drug serum group.After 48 hours,total RNA was extracted,then the expression levels of three miRs were detected by RT-PCR.RESULTS Compared with the serum-free group,the expression levels of miR-146a,miR-130 and miR-223 in the Shexiang Wulong Pills drug serum group were significantly decreased (P ＜ 0.01).CONCLUSION Shexiang Wulong Pills can inhibit inflammation in RA patients by down-regulating the expression levels of miR-223,miR-130 and miR-146a in PBMCs.

miR-130b accelerates the neuronal migration in the developing embryonic mice cortex / 基础医学与临床

Objective To study the effects of miR-130b on the neuronal migration in the developing embryonic mice cortex.Methods Pregnancy E15.5 mice were selected and plasmid of miR-130b was injected into the lateral ventricle of the embryonic brain.Two days after eletroporation,murine embryos were collected and cut into frozon coronal slices,then surveyed the neuronal migration under the fluorescence microscope.Results The neuronal migration rates were higher in miR-130b overexpression embryonic cortex,of which 75.1％ eletroporated neurons migrated into MZ,compared with the 22.1％ in control group.On the contrary,only 7.9％ eletroporated neurons stayed in the VZ/ SVZ in the experimental group,compared with the 69.3％ in control group.Conclusions miR-130b accelerates the neuronal migration in the developing embryonic mice cortex,its regulational role is worth studying.

The correlation between urinary albumin excretion rate and the level of serum miR-130b in patients with type 2 diabetes mellitus / 中华内分泌代谢杂志

[Summary] The aim of this study was to detect the levels of serum miR-130b expression in patients with type 2 diabetes mellitus and to analyze their correlation with diabetic renal damage. 243 patients with type 2 diabetes mellitus were divided into three groups according to urinary albumin/creatinine ratio ( UACR ): normoalbuminuria group (UACR300 mg/g, n=54). The levels of serum miR-130b were validated by realtime polymerase chain reaction. Serum transforming growth factor-β1 (TGF-β1) and tumor necrosis factor-α(TNF-α) were determined by enzyme-linked immunosorbent assay ( ELISA) in all patients and 59 healthy volunteers. Compared with control group, the level of serum miR-130b in the type 2 diabetes mellitus group were significantly decreased, gradually with the increases of UACR. The level of serum miR-130b was inversely correlated with blood urea nitrogen ( r=-0. 295, P<0.05), serum creatinine(r=-0. 316, P<0. 05), UACR(r=-0. 463, P<0. 05), but positively related to the estimated glomerular filtration rate(r=0. 367, P<0. 01). The level of serum miR-130b was also negatively correlated to homeostasis model assessment for insulin resistance, triglyceride, low density lipoprotein-cholesterol, TNF-α, and TGF-β1 (r=-0. 257,-0. 345,-0. 242,-0. 562,-0. 622, all P<0. 01). The present study indicates that serum miR-130b might be a potential new biomarker for early diagnosis of diabetic nephropathy. Serum miR-130b might be involved in the pathogenesis of diabetic nephropathy.

MiR-130a regulates neurite outgrowth and dendritic spine density by targeting MeCP2

MicroRNAs (miRNAs) are critical for both development and function of the central nervous system. Significant evidence suggests that abnormal expression of miRNAs is associated with neurodevelopmental disorders. MeCP2 protein is an epigenetic regulator repressing or activating gene transcription by binding to methylated DNA. Both loss-of-function and gain-of-function mutations in the MECP2 gene lead to neurodevelopmental disorders such as Rett syndrome, autism and MECP2 duplication syndrome. In this study, we demonstrate that miR-130a inhibits neurite outgrowth and reduces dendritic spine density as well as dendritic complexity. Bioinformatics analyses, cell cultures and biochemical experiments indicate that miR-130a targets MECP2 and down-regulates MeCP2 protein expression. Furthermore, expression of the wild-type MeCP2, but not a loss-of-function mutant, rescues the miR-130a-induced phenotype. Our study uncovers the MECP2 gene as a previous unknown target for miR-130a, supporting that miR-130a may play a role in neurodevelopment by regulating MeCP2. Together with data from other groups, our work suggests that a feedback regulatory mechanism involving both miR-130a and MeCP2 may serve to ensure their appropriate expression and function in neural development.