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-methyl-D-glucopyranoside uptake in renal proximal tubule cells
1 Department of Veterinary Physiology, College of Veterinary Medicine, Hormone Research Center, Chonnam National University, Gwangju, Korea, Democratic People's Rep
2 College of Veterinary Medicine, Chonbuk National University, Jeonju, Korea, Democratic People's Rep
* To whom correspondence should be addressed. E-mail: hjhan{at}chonnam.ac.kr.
Angiotensin II (ANG II) and Na+/glucose cotransporter have been reported to be associated with the onset of diverse renal diseases. However, the effect of ANG II on Na+/glucose cotransporter activity was not elucidated. The effect of ANG II on 14C-
-methyl-D-glucopyranoside (-MG) uptake and its related signal pathways were examined in the primary cultured rabbit renal proximal tubule cells (PTCs). ANG II (>2 hr; > 10-9 M) inhibited -MG uptake in time- and concentration- dependent manner
and decreased protein level of Na+/glucose cotransporters, whose expression was abrogated by both actinomycin D and cycloheximide exposure. ANG II-induced
inhibition of -MG uptake was blocked by losartan, an angiotensin II type 1 (AT1) receptor blocker, but not by PD 123319, an angiotensin II type 2 (AT2) receptor blocker. ANG II-induced inhibition of -MG uptake was blocked by genistein, herbimycin A [tyrosine kinase (TK) inhibitors], mepacrine and AACOCF3 (phospholipase A2
inhibitors), suggesting the role of TK phosphorylation and arachidonic acid. Indeed, ANG II increased arachidonic acid (AA) release, which was blocked by losartan or TK
inhibitors. The effects of ANG II on AA release and -MG uptake also were abolished by staurosporine and bisindolylmaleimide I (protein kinase C inhibitors) or PD 98059 (p44/42 MAPK inhibitor), but not SB 203580 (p38 MAPK inhibitor), respectively. Indeed, ANG II increased p44/42 MAPK activity. ANG II-induced activation of p44/42
MAPK was blocked by staurosporine. In conclusion, ANG II inhibited -MG uptake via PKC-MAPK-cPLA2 signal cascade through AT1 receptor in the PTCs.
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