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ObjectiveAlthough expression of the TEAD1 protein in preadipocytes has been established, its function remains unclear. In this study, we sought to detect transcripts of TEAD1 in chicken and to examine the effects of this protein on the proliferation, migration, apoptosis, and differentiation of immortalized chicken preadipocyte cell lines (ICP1). MethodsThe full-length sequence of the TEAD1 gene was cloned and the two transcripts were subjected to bioinformatics analysis. The subcellsular localization of TEAD1 transcripts was determined based on indirect immunofluorescence. The effects of TEAD1 transcripts overexpression on the proliferation of ICP1 cells were examined by RT-qPCR, CCK-8, and EdU assays; the effects of TEAD1 transcripts on ICP1 cells migration were examined based on the scratch test; and the effects of TEAD1 transcripts overexpression on ICP1 cells apoptosis were analyzed using apoptosis-Hoechst staining and RT-qPCR. The expression of TEAD1 transcripts in different tissues, cells lines, and ICP1 at different periods of differentiation was analyzed by RT-qPCR. The effects of TEAD1 transcripts overexpression on lipid droplet accumulation and adipogenic-related gene expression in ICP1 cells were analyzed based on Oil Red O and BODIPY staining, RT-qPCR, Western blot, and dual-luciferase reporter gene assays. Finally, the content of triglyceride (TG) was measured in TEAD1 overexpressed ICP1 cells. ResultsThe full-length TEAD1 was cloned and two TEAD1 transcripts were identified. The TEAD1-V1 protein was found to be localized primarily in the cell nucleus, whereas the TEAD1-V2 protein is localized in the cell cytoplasm and nucleus. The overexpression of both TEAD1-V1 and TEAD1-V2 significantly inhibited the proliferation of ICP1 cells. Whereas the overexpression of TEAD1-V1 promoted ICP1 cell migration, the overexpression of TEAD1-V2 had no significant effects on ICP1 migration; the overexpression of both TEAD1-V1 and TEAD1-V2 significantly promoted the apoptosis of ICP1 cells. We found that the different transcripts of TEAD1 have similar expression pattern in different tissues and cells lines. During induced preadipocyte differentiation, the expression of these genes initially declined, although subsequently increased. Overexpression of TEAD1-V1 promoted a significant reduction in lipid droplet formation and inhibited C/EBPα expression during the differentiation of ICP1 cells (P<0.05). However, the overexpression of TEAD1-V2 had no significant effect on lipid droplet accumulation or the expression of adipogenic-related proteins (P>0.05). Overexpression of TEAD1-V1 significantly decreased triglyceride content in ICP1 cells (P<0.05), while overexpression of TEAD1-V2 had no effect on triglyceride content in ICP1 cells (P>0.05). ConclusionIn this study, for the first time, identified two TEAD1 transcripts. Overexpressed transcripts TEAD1-V1 and TEAD1-V2 both inhibited the proliferation of chicken preadipocytes and promoted apoptosis of chicken preadipocytes. TEAD1-V1 inhibited the differentiation of preadipocytes and promoted the migration of preadipocytes, while TEAD1-V2 had no effect on the differentiation and migration of preadipocytes.
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@#Objective - To analyze the prevalence and influencing factors of work related musculoskeletal disorders (WMSDs) Methods among painters in the manufacturing industry. A total of 639 painters from one shipbuilding enterprise, one automobile manufacturing enterprise and three wooden furniture manufacturing enterprises in Guangdong Province were selected as the research subjects using typical sampling method. The Chinese version of Musculoskeletal Disorders Questionnaire was Results used to investigate the prevalence of WMSDs in the past one year, and the influencing factors were analyzed. The total prevalence rate of WMSDs among painters in the manufacturing industry was 37.4%. The prevalence of WMSDs in different vs vs P industries from high to low was shipbuilding, automobile and furniture manufacturing (50.0% 38.7% 29.0%, <0.01). The prevalence of WMSDs in different parts of the body from high to low was neck, ankle/foot, shoulder, low back, upper back, knee, vs vs vs vs vs vs vs vs P hand/wrist, hip/leg and elbow (20.7% 19.2% 17.4% 15.8% 14.1% 13.8% 13.5% 9.5% 6.6%, <0.01). Multivariate logistic regression analysis results showed that working in uncomfortable postures was a risk factor for neck, ankle/ P P foot and shoulder WMSDs (all <0.01); long time head turning was a risk factor for neck and shoulder WMSDs (both <0.05); P overweight and obesity, and bending and turning frequently at the same time were risk factors for ankle/foot WMSDs (all <0.05); P adequate rest time was a protective factor for neck and ankle/foot WMSDs (both <0.01); participated in physical exercise more P than once a week was a protective factor of neck and shoulder WMSDs in painters (all <0.05), after excluding the influence of Conclusion confounding factors. The prevalence of WMSDs in manufacturing painters was high, and the main body parts E mail 4813545@qq.com E mail wangzhongxu2003@163.com· · 中国职业医学 年 月第 卷第 期 ， ， ， 482 2022 10 49 5 Chin Occup Med October 2022 Vol.49 No.5 involved were neck, ankle/foot and shoulder. The influencing factors include individual factors, poor ergonomics factors and unreasonable work organization.
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<p><b>OBJECTIVE</b>To study the interaction between insulin-like growth factor binding protein-3 (IGFBP-3) and thyroid hormone receptor α1 (TRα1) and the modulatory effect of IGFBP-3 on transcription of the thyroid hormone responsive gene.</p><p><b>METHODS</b>The interaction between IGFBP-3 and TRα1 was detected with glutathione-S-transferase pull-down method, co-immunoprecipitation, fluorescence resonance energy transfer test. The cellular distribution of these two proteins was observed by confocal laser scanning microscopy. The effect of IGFBP-3 on the growth hormone promoter activity stimulated by triiodothyronine (T3) was determined by dual-luciferase reporter assay.</p><p><b>RESULTS</b>IGFBP-3 interacted with TRα1 both in vivo and in vitro. IGFBP-3 and TRα1 were shown to co-localize in the nucleus of HEK-293 cells. The overexpressed IGFBP-3 inhibited the growth hormone promoter activity stimulated by T3 (P<0.01).</p><p><b>CONCLUSIONS</b>IGFBP-3 interacts with TRα1 and inhibits T3 responsive gene transcription. This finding further confirms the insulin-like growth factor-independent role of IGFBP-3 in the nucleus.</p>