ArticlePflugers Archiv : European journal of physiology2018
Glucose-regulated protein 78 in lipid rafts elevates vascular smooth muscle cell proliferation of spontaneously hypertensive rats by controlling platelet-derived growth factor receptor signaling.
Article in Pflugers Archiv : European journal of physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 2 citations in OpenAlex.
- Expression and Functional Analysis of lncRNAs Involved in Platelet-Derived Growth Factor-BB-Induced Proliferation of Human Aortic Smooth Muscle Cells.Frontiers in cardiovascular medicine · 2021Article
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7 authors at 2 institutions in 2 countries.
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Abstract
The multifunctional glucose-regulated protein 78 (GRP78) is known to be differentially expressed in the lipid rafts of vascular smooth muscle cells (VSMCs) from spontaneously hypertensive rats (SHRs) and normal Wistar-Kyoto (WKY) rats. However, its role in VSMCs from SHRs remains to be elucidated. This work was conducted to investigate the contribution made by GRP78 in VSMCs. GRP78 expression in VSMC lipid rafts decreased in WKY rats with age, but not in SHRs. Transfection with GRP78-siRNA attenuated not only platelet-derived growth factor (PDGF)-BB-induced VSMC proliferation and aortic sprout outgrowth but also the phosphorylation of PDGF receptor (PDGFR)-β, Akt, and extracellular signal-regulated kinase (Erk) 1/2 in VSMCs in response to PDGF-BB. Moreover, GRP78 knockdown also reduced the PDGF-BB-induced dimerization of PDGFR-β and GRP78 in SHR VSMCs. The phosphorylation of GRP78 and PDGFR-β was elevated in VSMCs treated with PDGF-BB and was completely abolished by AG1296 (a PDGFR inhibitor). Moreover, the binding of PDGFR-β to GRP78 and the co-localization of GRP78 to PDGFR-β in VSMCs were stronger in SHRs than in WKY rat controls. This study demonstrates that the PDGF-BB-induced proliferation of SHR VSMCs is mediated by the expressional upregulation of GRP78 on VSMC lipid rafts in SHRs, probably via the regulation of PDGFR-β-GRP78 binding and their cross-activation. These observations indicate that GRP78 may play important roles in the pathological progression of SHR VSMCs.
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