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Angiotensin II stimulates glucose transport activity in cultured vascular smooth muscle cells

The glucose transport system in cultured rat vascular smooth muscle cells has been examined by measuring the uptake of 2-deoxyglucose. Angiotensin II (Ang II) stimulated 2-deoxyglucose uptake in cells made quiescent by removing serum from the culture medium in a dose- and time-dependent manner that...

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Bibliographic Details
Published in:The Journal of biological chemistry 1992-10, Vol.267 (29), p.20740-20745
Main Authors: Low, B C, Ross, I K, Grigor, M R
Format: Article
Language:English
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Summary:The glucose transport system in cultured rat vascular smooth muscle cells has been examined by measuring the uptake of 2-deoxyglucose. Angiotensin II (Ang II) stimulated 2-deoxyglucose uptake in cells made quiescent by removing serum from the culture medium in a dose- and time-dependent manner that was shown to be receptor-mediated. Epidermal growth factor (EGF), fetal calf serum, thrombin, and arginine vasopressin also stimulated glucose transport. Cycloheximide did not affect the immediate-early (30 min) activation by either Ang II or EGF, but abolished any further increase. This suggested that, whereas the initial activation of glucose transport was independent of protein synthesis, the sustained increase required the synthesis of new glucose transporters. This was supported by 4-fold and 2-fold accumulations of GLUT-1 mRNA 4 h after exposure to Ang II and EGF, respectively. The induction of GLUT-1 mRNA was preceded by rapid and transient expression of c-fos and c-jun protooncogenes. In nuclear run-on assays, nuclei from Ang II-treated cells showed increased synthesis of GLUT-1 mRNA at 30 min and 1 h after hormone treatment. In contrast, in cells exposed to actinomycin D, pretreatment with Ang II had no effect on the turnover rates of GLUT-1 mRNa. These results are consistent with Ang II acting to stimulate the rate of transcription of the GLUT-1 gene leading to increased production of GLUT-1 protein and glucose transport.
ISSN:0021-9258
1083-351X
DOI:10.1016/S0021-9258(19)36748-1