Aldosterone Stimulates Epidermal Growth Factor Receptor Expression

Krug, Alexander W.; Großmann, Claudia; Schuster, Claudia; Freudinger, Ruth; Mildenberger, Sigrid; Govindan, Manjapra V.; Gekle, Michael

doi:10.1074/jbc.m308134200

Cited by 99 publications

(93 citation statements)

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“…40 Alternatively, MRs could indirectly modulate AT2R expression, ie, via activation of activating protein-1 (Fos/Jun). This mechanism has been postulated for the aldosteronedependent induction of epidermal growth factor receptor expression 41 and for the cardiac actions of aldosterone. 42 Numerous potential AP1 binding sites were identified in the promoter region of the human, mouse, and rat AT2R genes.…”

Section: Discussionmentioning

confidence: 99%

High-Salt Diet Inhibits Expression of Angiotensin Type 2 Receptor in Resistance Arteries

et al. 2005

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Abstract-Recent studies suggested that type 2 angiotensin receptor (AT2R) could contribute to regulation of blood pressure and/or vascular remodeling. A key question relates to the effects of potential modulators of vascular AT2R expression. In the present work, we evaluated if high salt intake (70 mmol/L NaCl in drinking water) could modulate rat mesenteric artery AT2R function and expression. Angiotensin II dose-response curves were studied in rat perfused pressurized small-diameter arteries in the presence of losartan (AT1R antagonist Key Words: mineralocorticoid Ⅲ sodium Ⅲ hypertension Ⅲ vascular remodeling Ⅲ apoptosis T he renin-angiotensin-aldosterone system (RAAS) regulates vascular tone, body fluid volume, electrolyte balance, hormonal secretion, and neuronal activity. The biological effects of angiotensin II (Ang II), the main effector peptide in the vasculature, are mediated by at least 2 receptor isofoms. 1,2 The type 1 receptor (AT1R) mediates vasoconstriction, sympathetic facilitation, and trophic effects. The type 2 receptor (AT2R) is widely expressed during fetal development, whereas in the adult its expression has been detected in many different vessel types, including mesenteric, coronary, and renal arteries. 3-6 AT2R has opposite effects to those of AT1R, ie, it promotes cell apoptosis and inhibits cell proliferation. 6,7 AT2R also attenuates the pressor action of Ang II 8 and mediates vasodilation. 9,10 Recently, it has been shown that Ang II relaxes small mesenteric arteries via AT2R when AT1R are blocked. [11][12][13] Interestingly, the expression of AT2R is increased in several pathologic conditions such as vascular injury, 14 cardiac remodeling, congestive heart failure, and myocardial infarction. 15,16 It has been suggested that in adults the presence of AT2R in vascular tissues may be playing a role in vascular tone and/or tissue remodeling. [17][18][19] Therefore, a key and complex question that arises is how AT1R and AT2R expression are modulated. Several studies indicate interaction between Ang II and aldosterone, affecting the expression of ATRs. The expression of AT1R appears to be induced by Ang II in vascular smooth muscle, 4 and mineralocorticoids potentiate the action of Ang II in cultured rat vascular smooth muscle cells (VSMCs) by increasing the number of AT1R. 20,21 However, there are few data concerning the physiological regulation of AT2R expression. Dietary sodium depletion, which increases RAAS activity, enhances renal AT2 receptor function 10,22 and expression in both young and mature adult rats, mainly in the glomeruli and interstitial cells. 23 Induction of AT2R-mediated modulation of blood pressure was described in rats fed with a synthetic diet, an effect attributed to the stimulation of the RAAS. 8 Bonnet et al 24 have shown that Ang II infusion in the rat induces the expression of AT2R in the mesenteric vasculature. Nevertheless, it is not clear whether Ang II directly mediates the increased AT2R expression or if it is secondary to direct aldosterone action on arte...

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Section: Discussionmentioning

confidence: 99%

High-Salt Diet Inhibits Expression of Angiotensin Type 2 Receptor in Resistance Arteries

et al. 2005

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“…Mineralocorticoid and catecholamine excess models of secondary hypertension also utilize this pathway. Both are known to stimulate renal EGFR expression [10].…”

Section: Enunciation Of the Hypothesismentioning

confidence: 99%

A Single Initiating Cause of Hypertension; Potential for Primary Prevention

Sambhi¹

2014

J Hypertens

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“…Over-expression of Heparin-binding EGF is detected in ARPKD and EGF antagonistic antibodies suppress the mitogenic activity of cleared cystic fluid [35]. The abundance of EGFR in cells from the renal tubule is responsive to aldosteronedependent transcription [36] and expression of EGFR is necessary to permit the stimulation of rapid signalling responses by aldosterone in CHO cells [37]. The 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 7 activation of ERK1/2 signalling by aldosterone in cells derived from the distal nephron has been described by several groups including our own [38,39] and this response has been linked to trans-activation of EGFR [40].…”

Section: Aldosterone Egfr and Polycystic Kidney Diseasementioning

confidence: 99%