Interactions of glucocorticoids and cyclic AMP in the tissue-specific regulation of angiotensinogen

Sernia, Conrad; Zeng, Tang; Shinkel, Trixie A.; Kerr, David; Raizada, Mohan K.

doi:10.1038/ki.1994.450

Cited by 5 publications

(2 citation statements)

References 10 publications

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“…Of the hormones and effectors reported to induce AT gene expression in liver cells [32][33][34][35], only the synthetic glucocorticoid Dex produced a spectacular increase (" 12-fold) in AT mRNA levels after a 16 h exposure (Table 1) centrations reported to induce maximal stimulation of both AT gene expression in liver cells [32][33][34][35] and other specific biological effects in Ob1771 adipocytes [12,30], did not cause any change in AT mRNA levels. Similarly, forskolin, a direct activator of adenylate cyclase which increases cAMP levels enabling it to regulate AT secretion in hepatoma cells positively [36], failed to induce any change in AT gene expression, although this agent was clearly lipolytic in these cells [15]. Therefore regulation of AT mRNA accumulation by glucocorticoid in Ob1771 adipocytes was further investigated, and, to determine whether increased levels of AT mRNA were accompanied by increased parallel rates of AT synthesis and secretion, AT was also measured (after its total conversion into angI in the presence of exogenous mouse renin) in cell homogenates and\or conditioned medium of Ob1771 cells.…”

Section: Regulation Of At Mrna In Adipose Cells In Response To Varioumentioning

confidence: 99%

Regulation by glucocorticoids of angiotensinogen gene expression and secretion in adipose cells

Aubert

Darimont

Safonova

et al. 1997

Biochemical Journal

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Adipose cells are an important source of angiotensinogen (AT). Its activation product, angiotensin II, stimulates in vitro and in vivo the production and release of prostacyclin which acts as a potent adipogenic signal in promoting the terminal differentiation of preadipocytes to adipocytes. Since glucocorticoids are known to promote adipose cell differentiation in vitro as well as in vivo, their role in the regulation of AT gene expression and secretion has been investigated in cultured Ob1771 mouse adipose cells. In contrast with liver cells, which are the major source of AT and the target of several hormones for the regulation of its expression, adipose cells are only responsive to glucocorticoids, which are able to up-regulate AT gene expression and AT secretion rapidly and dose-dependently. On exposure to glucocorticoids, accumulation of AT mRNA appears primarily to be due to transcriptional activation of the gene and is parallelled by secretion of the protein. Similar results on AT mRNA expression and AT secretion were obtained using explants of rat adipose tissue ex vivo demonstrating a major if not exclusive mechanism of regulation of AT production by glucocorticoids in mature adipose cells. Together these results provide a potential link between glucocorticoids, AT, the growth of adipose tissue and increased blood pressure.

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Section: Regulation Of At Mrna In Adipose Cells In Response To Varioumentioning

confidence: 99%

Regulation by glucocorticoids of angiotensinogen gene expression and secretion in adipose cells

Aubert

Darimont

Safonova

et al. 1997

Biochemical Journal

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“…mRNAs for AT 1a , AT 1b , AT 2 and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were amplified using primers specific for their respective sequences as described previously (Leung et al 1998b). Angiotensinogen mRNA was detected using primers flanking positions 245-557 of the rat angiotensinogen cDNA as described previously (Sernia et al 1994). The oligonucleotide primers used for amplification of renin mRNA were based on rat renin cDNA as reported (Okura et al 1991).…”

Section: Reverse-transcription Pcr (Rt-pcr)mentioning

confidence: 99%

Expression and localization of the renin-angiotensin system in the rat pancreas

Leung

Chan²,

Tp³

et al. 1999

Journal of Endocrinology

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The possibility of an intrinsic renin-angiotensin system (RAS) in the pancreas has been raised by previous studies in which immunohistochemical examination showed the presence of angiotensin II and its receptor subtypes, type 1 (AT 1 ) and type 2 (AT 2 ). In the present study, gene expression of several key RAS components was investigated by reverse-transcription PCR. mRNA expression for angiotensinogen, renin and angiotensin II receptor subtypes, AT 1a , AT 1b and AT 2 was shown. The presence of angiotensinogen protein, the mandatory component for an intrinsic RAS, was demonstrated by Western blotting and localized by immunohistochemistry to the epithelia and endothelia of pancreatic ducts and blood vessels respectively. Immunoblot analysis detected a predominant protein band of about 60 kDa in the pancreas. This was consistent with the predicted value for angiotensinogen as reported in other tissues. Together with previous findings, the present study shows that the rat pancreas expresses the major RAS component genes, notably angiotensinogen and renin, required for intracellular formation of angiotensin II. The data support the notion of an intrinsic RAS in the rat pancreas which may play a role in the regulation of pancreatic functions.

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