NDLI: Intracellular ANG II directly induces in vitro transcription of TGF-beta1, MCP-1, and NHE-3 mRNAs in isolated rat renal cortical nuclei via activation of nuclear AT1a receptors.

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Intracellular ANG II directly induces in vitro transcription of TGF-beta1, MCP-1, and NHE-3 mRNAs in isolated rat renal cortical nuclei via activation of nuclear AT1a receptors.

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Intracellular ANG II directly induces in vitro transcription of TGF-beta1, MCP-1, and NHE-3 mRNAs in isolated rat renal cortical nuclei via activation of nuclear AT1a receptors.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Li, Xiao C. Zhuo, Jia L.
Description	Country affiliation: United States Author Affiliation: Li XC ( Division of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Hospital, Detroit, MI 48202, USA.)
Abstract	The present study tested the hypothesis that intracellular ANG II directly induces transcriptional effects by stimulating AT(1a) receptors in the nucleus of rat renal cortical cells. Intact nuclei were freshly isolated from the rat renal cortex, and transcriptional responses to ANG II were studied using in vitro RNA transcription assays and semiquantitative RT-PCR. High-power phase-contrast micrographs showed that isolated nuclei were encircled by an intact nuclear envelope and stained strongly by the DNA marker 4',6-diamidino-2-phenylindole, but not by the membrane or endosomal markers. Fluorescein isothiocyanate-labeled ANG II and [(125)I]Val(5)-ANG II binding confirmed the presence of ANG II receptors in the nuclei with a predominance of AT(1) receptors. RT-PCR showed that AT(1a) mRNA expression was threefold greater than AT(1b) receptor mRNAs in these nuclei. In freshly isolated nuclei, ANG II increased in vitro [alpha-(32)P]CTP incorporation in a concentration-dependent manner, and the effect was confirmed by autoradiography and RNA electrophoresis. ANG II markedly increased in vitro transcription of mRNAs for transforming growth factor-beta1 by 143% (P < 0.01), macrophage chemoattractant protein-1 by 89% (P < 0.01), and the sodium and hydrogen exchanger-3 by 110% (P < 0.01). These transcriptional effects of ANG II on the nuclei were completely blocked by the AT(1) receptor antagonist losartan (P < 0.01). By contrast, ANG II had no effects on transcription of angiotensinogen and glyceraldehyde-3-phosphate dehydrogenase mRNAs. Because these transcriptional effects of ANG II in isolated nuclei were induced by ANG II in the absence of cell surface receptor-mediated signaling and completely blocked by losartan, we concluded that ANG II may directly stimulate nuclear AT(1a) receptors to induce transcriptional responses that are associated with tubular epithelial sodium transport, cellular growth and hypertrophy, and proinflammatory cytokines.
File Format	HTM / HTML
ISSN	03636143
e-ISSN	15221563
DOI	10.1152/ajpcell.00432.2007
Journal	American Journal of Physiology - Cell Physiology
Issue Number	4
Volume Number	294
Language	English
Publisher	American Physiological Society
Publisher Date	2008-04-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Angiotensin Ii Pharmacology Chemokine Ccl2 Metabolism Kidney Cortex Cytology Receptor, Angiotensin, Type 1 Sodium-hydrogen Antiporter Transforming Growth Factor Beta1 Animals Genetics Rna, Messenger Rats, Sprague-dawley Receptor, Angiotensin, Type 2 Transcription, Genetic Drug Effects Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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Intracellular angiotensin II directly induces in vitro transcription of TGF-β1, MCP-1 and NHE-3 mRNAs in isolated rat renal cortical nuclei via activation of nuclear AT1 receptors

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Intracellular ANG II directly induces in vitro transcription of TGF-beta1, MCP-1, and NHE-3 mRNAs in isolated rat renal cortical nuclei via activation of nuclear AT1a receptors.

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