Differential action of AGCF2 upon cell type‐dependent expression of human angiotensinogen gene

Yanai, Kazuyuki; Matsuyama, Shigeki; Murakami, Kazuo; Fukamizu, Akiyoshi

doi:10.1016/s0014-5793(97)00802-8

Cited by 6 publications

(2 citation statements)

References 28 publications

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“…We have identified various regulatory elements and factors that regulate human ANG gene transcription (12)(13)(14)(15)(16)(17)(18)(19). Our previous studies have shown that cis-acting elements located at nucleotides Ϫ1222 to ϩ44 are sufficient for human ANG gene expression in transiently transfected human hepatoma HepG2 cells and in the livers of transgenic mice (20,21) and that HNF-4 plays an important role in hepatic ANG expression (18).…”

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confidence: 99%

Inhibitory Effect of the Small Heterodimer Partner on Hepatocyte Nuclear Factor-4 Mediates Bile Acid-induced Repression of the Human Angiotensinogen Gene

Shimamoto

Ishida

Yamagata

et al. 2004

Journal of Biological Chemistry

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Bile acids are physiological detergents that facilitate excretion, absorption, and transport of fats and sterols in the intestine and liver. It has been revealed recently that bile acids also function as signaling molecules for regulating bile acid metabolism and cholesterol homeostasis (1). A major advance toward understanding the molecular mechanism of bile acid-induced negative feedback regulation of the genes involved in bile acid synthesis has come with the identification of the small heterodimer partner (SHP) 1 as a negative nuclear receptor induced by the farnesoid X receptor, a nuclear receptor of bile acids (2, 3). SHP lacks the highly conserved DNA-binding domain present in other members of the nuclear receptor superfamily (4), and it interacts with a variety of nuclear receptors, including the thyroid hormone receptor (4), the retinoic acid receptor (4), peroxisome proliferator-activated receptor-␣ (5), the retinoid X receptor (6), estrogen receptor-␣ (7, 8), the pregnane X receptor (9), hepatocyte nuclear factor-4 (HNF-4) (10), and the liver receptor homolog that activates the transcription of cholesterol 7␣-hydroxylase (CYP7A1), the rate-limiting enzyme in bile acid biosynthesis (2, 3).Angiotensinogen (ANG), the precursor of vasoactive octapeptide angiotensin II, is mainly synthesized in the liver and secreted into the circulation (11). We have identified various regulatory elements and factors that regulate human ANG gene transcription (12-19). Our previous studies have shown that cis-acting elements located at nucleotides Ϫ1222 to ϩ44 are sufficient for human ANG gene expression in transiently transfected human hepatoma HepG2 cells and in the livers of transgenic mice (20,21) and that HNF-4 plays an important role in hepatic ANG expression (18). The human ANG transgenic mouse exhibits high blood pressure through cross-mating with the line expressing human renin (22).It has been shown that bile duct ligation in animals, an experimental model of liver cirrhosis, results in a decrease in blood pressure and a transient decrease in plasma ANG despite an increase in plasma renin activity (23-25). Interestingly, hepatorenal syndrome, a disease with acute renal failure induced by severe hepatic diseases, is thought to result from the disruption of vasoactive factor control, but its mechanism is ill defined. In hepatorenal syndrome, arterial vasodilation occurs despite high plasma renin activity (26). These observations prompted us to investigate the effect of

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confidence: 99%

Inhibitory Effect of the Small Heterodimer Partner on Hepatocyte Nuclear Factor-4 Mediates Bile Acid-induced Repression of the Human Angiotensinogen Gene

Shimamoto

Ishida

Yamagata

et al. 2004

Journal of Biological Chemistry

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“…AGCE1 was also shown to be required for the activity of an upstream AGT enhancer, ATF-like element (ALE) [44]. In addition to AGCE1, Yanai et al also describes two AGCE2 sites, located upstream and downstream of the transcription initiation site that show a possible cell-type-dependent function [45]. The hepatocyte nuclear factor 4 (HNF4) was also shown to potentiate human AGT (hAGT) promoter activity in HepG2 cells [46].…”

Section: Regulation Of Angiotensinogen Gene Expressionmentioning

confidence: 99%

Angiotensinogen Gene Transcription in Pulmonary Fibrosis

Uhal

Dang

et al. 2012

International Journal of Peptides

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An established body of literature supports the hypothesis that activation of a local tissue angiotensin (ANG) system in the extravascular tissue compartment of the lungs is required for lung fibrogenesis. Transcriptional activation of the angiotensinogen (AGT) gene is believed to be a critical and necessary step in this activation. This paper summarizes the data in support of this theory and discusses transcriptional regulation of AGT, with an emphasis on lung AGT synthesis as a determinant of fibrosis severity. Genetic data linking AGT polymorphisms to the severity of disease in Idiopathic Pulmonary Fibrosis are also discussed.

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Microangiopathy-related cerebral damage and angiotensinogen gene: from epidemiology to biology

Schmidt

Fazekas

Schmidt

2002

Ageing and Dementia Current and Future Concepts

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Differential action of AGCF2 upon cell type‐dependent expression of human angiotensinogen gene

Cited by 6 publications

References 28 publications

Inhibitory Effect of the Small Heterodimer Partner on Hepatocyte Nuclear Factor-4 Mediates Bile Acid-induced Repression of the Human Angiotensinogen Gene

Inhibitory Effect of the Small Heterodimer Partner on Hepatocyte Nuclear Factor-4 Mediates Bile Acid-induced Repression of the Human Angiotensinogen Gene

Angiotensinogen Gene Transcription in Pulmonary Fibrosis

Microangiopathy-related cerebral damage and angiotensinogen gene: from epidemiology to biology

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