Wang, Haijing; Feng, Zhuolei; Han, Xue; Xing, Yue; Zhang, Xiaomei published the artcile< Downregulation of acylglycerol kinase suppresses high-glucose-induced endothelial-mesenchymal transition in human retinal microvascular endothelial cells through regulating the LPAR1/TGF-β/Notch signaling pathway>, Recommanded Product: (2S,3R,4S,5S,6R)-6-(Hydroxymethyl)tetrahydro-2H-pyran-2,3,4,5-tetraol, the main research area is acylglycerolkinase glucose endothelialmesenchymal retinal microvascular endothelialcell LPAR1 TGFb Notch; acide lysophosphatidique; acylglycerol kinase; acylglycérol kinase; cellule endothéliale des microvaisseaux rétiniens; endothelial-mesenchymal transition; high glucose; hyperglycémie; lysophosphatidic acid; retinal microvascular endothelial cell; transition de l’endothélium au mésenchyme.
The endothelial-mesenchymal transition (EndMT) participates in the progression of diabetic retinopathy (DR), but cell-intrinsic factors modulating this process remain elusive. In this study, we explored the role of lysophosphatidic acid (LPA) – producing enzyme, acylglycerol kinase (AGK), in the EndMT of human retinal microvascular endothelial cells (HRECs) under high-glucose (HG) conditions. We found that AGK was significantly elevated in HG-treated cells. In addition, AGK knockdown reversed the HG-induced EndMT in HRECs, which was evidenced by the increased endothelial markers (CD31 and VE-cadherin) and decreased mesenchymal markers (FSP1 and β-SMA). Furthermore, downregulation of AGK inhibited the HG-induced activation of transforming growth factor β (TGF-β)/Notch pathways, whereas exogenous TGF-β1 (10 ng/mL) impeded the inhibitory effects of AGK knockdown on HG-induced EndMT in HRECs. Addnl., the silencing of AGK abolished the HG-induced upregulation of LPA and its receptor, LPA receptor 1 (LPAR1), and overexpression of LPAR1 further rescued the AGK knockdown-mediated inhibition of the EndMT process. In conclusion, we demonstrate that downregulation of AGK suppresses HG-induced EndMT in HRECs through regulating the LPAR1/TGF-β/Notch signaling pathway, indicating that AGK might be a potential therapeutic target for the treatment of DR.
Canadian Journal of Physiology and Pharmacology published new progress about Adhesion G protein-coupled receptor E2 Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 492-62-6 belongs to class alcohols-buliding-blocks, and the molecular formula is C6H12O6, Recommanded Product: (2S,3R,4S,5S,6R)-6-(Hydroxymethyl)tetrahydro-2H-pyran-2,3,4,5-tetraol.
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