ArticleHypertension research : official journal of the Japanese Society of Hypertension2022
TWIST1 transcriptionally upregulates complement 3 in glomerular mesangial cells from spontaneously hypertensive rats.
Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 3 citations in OpenAlex.
- Construction of a metabolic-immune model for predicting the risk of diabetic nephropathy and study of gut microbiota.Journal of diabetes investigation · 2025Article
- Update on Hypertension Research in 2021.Hypertension research : official journal of the Japanese Society of Hypertension · 2022Review
- Twist-related protein 1 induces epithelial-mesenchymal transition and renal fibrosis through the upregulation of complement 3.PloS one · 2022Article
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6 authors at 1 institution in 1 country.
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Abstract
We have shown that complement 3 (C3) is upregulated in cardiovascular and renal organs, which induces the synthetic phenotype and exaggerates the growth of mesenchymal cells from spontaneously hypertensive rats (SHRs). However, the mechanisms of the upregulation of C3 have remained unclear. In the present study, we investigated the role of TWIST1, a transcription factor that regulates mesodermal embryogenesis, in the upregulation of C3 in glomerular mesangial cells (GMCs) from SHRs and Wistar-Kyoto (WKY) rats. Immunocytochemical staining and western blot analysis showed that the expression of TWIST1 in GMCs from SHRs was higher than that in GMCs from WKY rats in vivo and in vitro. Real-time PCR analysis showed increases in the expression of Twist1 mRNA with attenuated expression of miR-151-3p in GMCs from SHRs compared to that in cells from WKY rats. Chromatin immunoprecipitation assays showed increases in TWIST1 binding to the C3 promoter in GMCs from SHRs compared to that in cells from WKY rats. Transfection of Twist1 cDNA by a lentiviral vector increased the expression of C3 mRNA in GMCs from WKY rats. TWIST1 siRNA significantly decreased the mRNA expression of C3 and osteopontin in GMCs from SHRs. These results indicate that the increases in TWIST1 expression, attenuation of miR-151-3p, and strong binding of TWIST1 upregulate C3 gene expression in GMCs from SHRs. The enhanced TWIST1-C3 system induces the synthetic phenotype of mesenchymal tissue that may be associated with cardiovascular and renal remodeling in hypertension.
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