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1.
Cell Death Dis ; 15(5): 368, 2024 May 28.
Article in English | MEDLINE | ID: mdl-38806480

ABSTRACT

Transforming growth factor beta (TGFß) signaling plays a critical role in tumorigenesis and metastasis. However, little is known about the biological function of TGFbeta-induced lncRNA in cancer. In this study, we discovered a novel TGFbeta-induced lncRNA, termed TGILR, whose function in cancer remains unknown to date. TGILR expression was directly activated by the canonical TGFbeta/SMAD3 signaling axis, and this activation is highly conserved in cancer. Clinical analysis showed that TGILR overexpression showed a significant correlation with lymph node metastasis and poor survival and was an independent prognostic factor in gastric cancer (GC). Depletion of TGILR caused an obvious inhibitory effect on GC cell proliferation, invasion, and epithelial-mesenchymal transition (EMT) in vitro and in vivo. More importantly, we demonstrated that TGFbeta signaling in GC was overactivated due to cancer-associated fibroblast (CAF) infiltration. Mechanistically, increased level of CAF-secreted TGFbeta activates TGFbeta signaling, leading to TGILR overexpression in GC cells. Meanwhile, TGILR overexpression inhibited the microRNA biogenesis of miR-1306 and miR-33a by interacting with TARBP2 and reducing its protein stability, thereby promoting GC progression via TCF4-mediated EMT signaling. In conclusion, CAF infiltration drives GC metastasis and EMT signaling through activating TGFbeta/TGILR axis. Targeted blocking of CAF-derived TGFbeta should be a promising anticancer strategy in GC.


Subject(s)
Cancer-Associated Fibroblasts , Disease Progression , Epithelial-Mesenchymal Transition , MicroRNAs , Signal Transduction , Stomach Neoplasms , Transforming Growth Factor beta , Stomach Neoplasms/pathology , Stomach Neoplasms/metabolism , Stomach Neoplasms/genetics , Humans , Transforming Growth Factor beta/metabolism , Cancer-Associated Fibroblasts/metabolism , Cancer-Associated Fibroblasts/pathology , Cell Line, Tumor , Animals , MicroRNAs/metabolism , MicroRNAs/genetics , Cell Proliferation , RNA, Long Noncoding/metabolism , RNA, Long Noncoding/genetics , Gene Expression Regulation, Neoplastic , Male , Mice, Nude , Female , Mice , Mice, Inbred BALB C , Smad3 Protein/metabolism
2.
Front Bioeng Biotechnol ; 10: 928041, 2022.
Article in English | MEDLINE | ID: mdl-35992335

ABSTRACT

Endothelial progenitor cells (EPCs) expressing vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) and bone marrow mesenchymal stem cells (BMSCs) expressing endogenous bone morphogenetic protein-2 (BMP-2) play the important role in new bone formation. This study investigated the effects of a porous hydroxyapatite (HA)/chitosan (CS)/polycaprolactone (PCL) composite scaffold-engrafted EPCs and BMSCs on the expression of BMP-2, VEGF, and PDGF in the calvarial defect rabbit model in vivo. It showed that a three-dimensional composite scaffold was successfully constructed by physical interaction with a pore size of 250 µm. The HA/CS/PCL scaffold degraded slowly within 10 weeks and showed non-cytotoxicity. By X-ray, micro-CT examination, and H&E staining, compared with the HA/CS/PCL group, HA/CS/PCL + EPCs, HA/CS/PCL + BMSCs, and HA/CS/PCL + EPCs + BMSCs groups performed a more obvious repair effect, and the dual factor group presented particularly significant improvement on the percentages of bone volume at week 4 and week 8, with evident bone growth. Osteogenesis marker (BMP-2) and vascularization marker (VEGF and PDGF) expression in the dual factor group were much better than those of the HA/CS/PCL control group and single factor groups. Collectively, the HA/CS/PCL composite scaffold-engrafting EPCs and BMSCs is effective to repair calvarial defects by regulating endogenous expression of BMP-2, VEGF, and PDGF. Thus, this study provides important implications for the potential clinical application of biomaterial composite scaffold-engrafted engineering cells.

3.
Front Physiol ; 13: 854606, 2022.
Article in English | MEDLINE | ID: mdl-35514329

ABSTRACT

Objectives: The aim of this study was to investigate the relationship between periodontitis and heart failure using the Third National Health and Nutrition Examination Survey (NHANES III). Methods: Participants who had received a periodontal examination were included and investigated for the occurrence of heart failure. The included participants were divided into no/mild periodontitis and moderate/severe periodontitis groups according to their periodontal status. Weighted prevalence of heart failure was calculated, and weighted logistic regressions models were used to explore the association between periodontitis and heart failure. Possible influencing factors were then explored through subgroup analysis. Results: Compared with that of the no/mild periodontitis group, the incidence of heart failure in participants with moderate/severe periodontitis was 5.72 times higher (95% CI: 3.76-8.72, p < 0.001). After adjusting for gender, age, race, body mass index, poverty income ratio, education, marital status, smoking status, drinking status, hypertension, diabetes, stroke, and asthma, the results showed that the incidence of heart failure in the moderate/severe group was 3.03 times higher (95% CI: 1.29-7.13, p = 0.012). Subgroup analysis showed that criteria, namely, male, 40-60 years old, non-Hispanic white, body mass index >30, poverty income ratio ≥1, not more than 12 years of education, currently drinking, stroke but no diabetes, or asthma supported moderate/severe periodontitis as a risk factor for heart failure (p < 0.05). Conclusion: According to data from this nationally representative sample from the United States, periodontitis is associated with an increased risk of heart failure.

4.
Mol Med Rep ; 17(6): 8221-8227, 2018 Jun.
Article in English | MEDLINE | ID: mdl-29658566

ABSTRACT

The present study aimed to investigate whether bone morphogenetic protein­2 (BMP­2) was involved in the repair of mandibular defects using polyether­ether­ketone biphasic bioceramic (PEEK­BBC) composites in rabbits. PEEK­BBC composites with abundant and interconnected pores were prepared by calcination and characterized by scanning electron microscope. A mandibular defect model in rabbits was established using dental grinder to produce a square hole. A total of 60 rabbits were divided into four groups: Control, sham, surgery, and PEEK. In the PEEK group, the holes were filled with the PEEK­BBC composite stents. In the surgery group, the holes were produced but not filled with the composite stents. In the sham group, only the molar grooves were exposed and grinding was not performed. Animals without any treatment served as the control group. The success rate of model establishment was 100%. At 4, 8, and 16 weeks after the model was established, samples were collected from the molding sites. Bone repair was evaluated by H&E staining and Goldner trichrome staining. Bone structures in both control and sham groups were intact. A small number of osteocytes were observed in the surgery group. However, in the PEEK group, osteocytes were already evidently present in the composites at 4 weeks after surgery. At 8 and 16 weeks, there were large numbers of osteocytes in the pores of the composites. The mRNA and protein expression levels of BMP­2 were determined by reverse transcription­quantitative polymerase chain reaction and western blotting, respectively. The mRNA and protein expression levels of BMP­2 between the control and sham groups were similar and were continuously stable. However, following defect treatment, BMP­2 mRNA and protein expression was upregulated, which was enhanced by the PEEK­BBC composites. In conclusion, PEEK­BBC composites promoted the growth of osteocytes and repaired mandibular defects in rabbits, potentially via the upregulation of BMP­2 expression.


Subject(s)
Bone Morphogenetic Protein 2/genetics , Bone Regeneration/genetics , Gene Expression Regulation , Ketones/pharmacology , Mandible/abnormalities , Polyethylene Glycols/pharmacology , Animals , Benzophenones , Disease Models, Animal , Gene Expression , Ketones/chemistry , Polyethylene Glycols/chemistry , Polymers , Rabbits
5.
Biomed Pharmacother ; 98: 325-332, 2018 Feb.
Article in English | MEDLINE | ID: mdl-29274589

ABSTRACT

This study aimed to investigate the effect of exogenous vascular endothelial growth factor (VEGF) introduced by bioceramic composite materials on jawbone defect. Rabbits were randomly divided into four groups: control, sham, model, and stent. In the model group, holes of jawbone defect were created through surgery. In the stent group, rabbits with jawbone defect were treated with polyether ketone (PEK)/biphasic bioceramic ((PEK-BBC)) composite materials encapsulating VEGF. At 4, 8, and 16 weeks post-operation, HE and Van Gieson staining of jawbones were performed to characterize the repair status of the bone defect. For all time intervals, we found intact bone structures in the control and sham groups and there was no improvement in the bone defect position in the model group. However, in the stent group, we excitingly observed the growth of many osteocytes in the margin of stents at 8 and 16 weeks. RT-PCR, western blot, and immunofluorescence analysis were conducted to investigate the VEGF expression at 4, 8, and 16 weeks post-operation. At 8 weeks, the level of VEGF in the model group was sharply downregulated as compared with the control group (P < .05) and interestingly, the stent group had a much higher level of VEGF than the model group (P < .05). At 16 weeks, the VEGF expression in the model group was further reduced comparing to the control group (P < .05), which was also elevated to a relative high level by the stent treatment (P < .05). As for the sham group, the VEGF level was stable without any difference from the control group at all time intervals. Therefore, exogenous VEGF introduced by bioceramic composite materials promoted the restoration of bone defect in rabbits.


Subject(s)
Biocompatible Materials/pharmacology , Bone Regeneration/drug effects , Bone and Bones/drug effects , Ceramics/pharmacology , Vascular Endothelial Growth Factor A/administration & dosage , Animals , Jaw/drug effects , Ketones/pharmacology , Osteocytes/drug effects , Rabbits , Tissue Engineering/methods
6.
Oncotarget ; 8(30): 48996-49004, 2017 Jul 25.
Article in English | MEDLINE | ID: mdl-28446725

ABSTRACT

BACKGROUND: Associations between interleukin-8 (IL-8) gene polymorphisms and periodontitis susceptibility have been investigated in many published studies, but the conclusions are still inconsistent. Therefore, we performed this systematic review and meta-analysis to review which polymorphisms have been researched and to obtain a precise result of the same polymorphism from different studies. RESULTS: Finally 10 publications involving 1938 patients and 1569 controls were yielded, including 12 polymorphisms. Six studies investigated rs4073 polymorphism; two focused on rs2227306 and rs2227307; two referred to rs2227532 and T-738A; one detected rs2230054, rs1126579 and rs1126580; one inspected A2767T, T11722T2 and C1633T, and one for rs2234671 polymorphism. Of them, IL-8 C1633T and rs1126580 polymorphisms showed positive association while the other ten polymorphisms revealed negative results. MATERIALS AND METHODS: A comprehensive literature search from PubMed, Web of Science, and Chinese National Knowledge Infrastructure was conducted for all potentially relevant studies published before January 2, 2017. Two authors selected the studies and extracted data. The pooled analysis was conducted using the RevMan 5.1 software if a polymorphism was reported by two or more studies. CONCLUSIONS: Based on current evidence, the IL-8 rs4073, A2767T, T11722T2, rs2234671, rs2230054, rs1126579, rs2227306, rs2227307, rs2227532, and T-738A polymorphisms were not associated with periodontitis susceptibility; the IL-8 C1633T and rs1126580 polymorphisms were associated with increased risk of periodontitis.


Subject(s)
Genetic Association Studies , Genetic Predisposition to Disease , Interleukin-8/genetics , Periodontitis/genetics , Polymorphism, Single Nucleotide , Alleles , Genotype , Humans , Odds Ratio
7.
Shanghai Kou Qiang Yi Xue ; 22(4): 407-13, 2013 Aug.
Article in Chinese | MEDLINE | ID: mdl-24100899

ABSTRACT

PURPOSE: To investigate the influence of dental Co-Cr-Mo alloys on biological behaviour of L929 mouse fibroblasts. METHODS: Leaching liquor of medical pure titanium, Co-Cr-Mo alloys, Co-Cr alloys and Ni-Cr alloys was prepared and used to culture the L929 cells for 24 h, 48 h and 72 h, respectively; then the growth of L929 cells was observed under inverted phase contrast microscope, and the cytotoxicity grades of 4 kinds of materials were evaluated by using CCK-8 test. The apoptosis of L929 cells was measured by flow cytometry(FCM) and acridine orange staining was used to observe the L929 cells adhered on the surface of samples under fluorescent microscope. The data was statistically analyzed with SPSS17.0 software package. RESULTS: Under inverted phase contrast microscope, at each time point, L929 cells grew in a good condition except in the Ni-Cr alloys group that minor karyopyknosis was indicating slight celluar cytotoxicity. Optical density (OD), apoptosis rate and cell adhesion number in Co-Cr-Mo alloys group at each time point were significantly less than in medical pure titanium group (P<0.05), and higher than in Co-Cr alloys group (P<0.05) and Ni-Cr alloys group (P<0.05). During observation period, the cytotoxicity grades of medical pure titanium group, Co-Cr-Mo alloys group and Co-Cr alloys group was grade 1, while Ni-Cr alloy group was grade 2, i.e. mild cytotoxicity. CONCLUSIONS: Co-Cr-Mo alloys have no adverse effect on the biological behavior of L929 cells, which may be suitable for dental clinical application with good biocompatibility.


Subject(s)
Dental Alloys , Fibroblasts , Alloys , Animals , Mice , Titanium
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