Angiotensin II and 1-7 during aging in Metabolic Syndrome rats. Expression of AT1, AT2 and Mas receptors in abdominal white adipose tissue

Rubio-Ruiz, María Esther; Valle-Mondragón, Leonardo Del; Castrejón-Téllez, Vicente; Carreón‐Torres, Elizabeth; Díaz-Díaz, Eulises; Guarner-Lans, Verónica

doi:10.1016/j.peptides.2014.04.021

Cited by 29 publications

(35 citation statements)

References 52 publications

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“…We postulated that stimulation of the alternative axis within the RAS, related to Ang‐(1‐7) signalling, could provide a counter‐regulatory, anti‐inflammatory effect in early atherosclerosis (Tesanovic et al , ). Both inflammatory cells as well as perivascular adipocytes and fibroblasts express Mas receptors for Ang‐(1‐7) (Rubio‐Ruiz et al , ; Simoes e Silva et al , ). Mas receptor expression was higher in PVAT than in other areas of aorta and it was not significantly increased in ApoE‐/‐ mice, in contrast to reports of the mouse penis (Fraga‐Silva et al , ),…”

Section: Discussionmentioning

confidence: 99%

Anti‐atherosclerotic effect of the angiotensin 1–7 mimetic AVE0991 is mediated by inhibition of perivascular and plaque inflammation in early atherosclerosis

Skiba

Nosalski

Mikołajczyk

et al. 2017

British J Pharmacology

102

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BACKGROUND AND PURPOSEInflammation plays a key role in atherosclerosis. The protective role of angiotensin 1-7 (Ang-(1-7)) in vascular pathologies suggested the therapeutic use of low MW, non-peptide Ang-(1-7) mimetics, such as AVE0991. The mechanisms underlying the vasoprotective effects of AVE0991, a Mas receptor agonist, remain to be explored. EXPERIMENTAL APPROACHWe investigated the effects of AVE0991 on the spontaneous atherosclerosis in apolipoprotein E (ApoE)À/À mice, in the context of vascular inflammation and plaque stability. KEY RESULTSAVE0991 has significant anti-atherosclerotic properties in ApoEÀ/À mice and increases plaque stability, by reducing plaque macrophage content, without effects on collagen. Using the descending aorta of chow-fed ApoEÀ/À mice, before significant atherosclerotic plaque develops, we gained insight to early events in atherosclerosis. Interestingly, perivascular adipose tissue (PVAT) and adventitial infiltration with macrophages and T-cells precedes atherosclerotic plaque or the impairment of endothelium-dependent NO bioavailability (a measure of endothelial function). AVE0991 inhibited perivascular inflammation, by reducing chemokine expression in PVAT and through direct actions on monocytes/macrophages inhibiting their activation, characterized by production of IL-1β, TNF-α, CCL2 and CXCL10, and differentiation to M1 phenotype. Pretreatment with AVE0991 inhibited migration of THP-1 monocytes towards supernatants of activated adipocytes (SW872). Mas receptors were expressed in PVAT and in THP-1 cells in vitro, and the anti-inflammatory effects of AVE0991 were partly Mas dependent. CONCLUSIONS AND IMPLICATIONSThe selective Mas receptor agonist AVE0991 exhibited anti-atherosclerotic and anti-inflammatory actions, affecting monocyte/macrophage differentiation and recruitment to the perivascular space during early stages of atherosclerosis in ApoEÀ/À mice.

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Section: Discussionmentioning

confidence: 99%

Anti‐atherosclerotic effect of the angiotensin 1–7 mimetic AVE0991 is mediated by inhibition of perivascular and plaque inflammation in early atherosclerosis

Skiba

Nosalski

Mikołajczyk

et al. 2017

British J Pharmacology

102

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“…Moreover, the reported sensitivity or limit of quantitation of 3 pmol for the HPLC analysis is not adequate to detect authentic levels of endogenous peptides (16). ANG II and ANG-(1-7) values derived from these methods are typically far higher in plasma (26,33,51,135), kidney (33,110,114), vasculature (48), adipose tissue (33,115), and heart (42) than by RIA, HPLC-RIA, or HPLC-MS methods (Table 1). Indeed, two recent studies quantified mouse renal ANG-(1-7) at Ͼ1,000,000 fmol/g tissue (110) and rat plasma ANG II at Ͼ300,000 pM by HPLC analysis alone (33).…”

Section: Ras Peptidesmentioning

confidence: 99%

“…Indeed, two recent studies quantified mouse renal ANG-(1-7) at Ͼ1,000,000 fmol/g tissue (110) and rat plasma ANG II at Ͼ300,000 pM by HPLC analysis alone (33). Rubio-Ruiz et al (115) reported an ANG-(1-7) concentration of 6,000 pM in serum and Ͼ500,000 fmol/g in adipose tissue from male Wistar rats by capillary electrophoresis.…”

Section: Ras Peptidesmentioning

confidence: 99%

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Biochemical evaluation of the renin-angiotensin system: the good, bad, and absolute?

Chappell

2016

American Journal of Physiology-Heart and Circulatory Physiology

231

256

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“…In addition, a previous study from Rubio-Ruiz et al 24 showed that (1) Mas receptor expression in abdominal white adipose tissue does not differ significantly between MetS and control rats and (2) local Ang(1-7) concentrations in white adipose tissue are higher in MetS rats than in age-matched control rats. These results contradict those reported here.…”

Section: Discussionmentioning

confidence: 85%

Telmisartan Ameliorates Nephropathy in Metabolic Syndrome by Reducing Leptin Release From Perirenal Adipose Tissue

Liu

et al. 2016

Hypertension

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Abstract-Metabolic syndrome (MetS) is associated with nephropathy. Along with common risk factors such as hypertension and hyperglycemia, adipocytokines released from perirenal adipose tissue (PRAT) are implicated in the pathogenesis of MetS nephropathy. The study was designed to elucidate the adverse effects of PRAT-derived leptin on nephropathy and to determine whether the angiotensin II type 1 receptor antagonist telmisartan exerts a renoprotective effect by decreasing the PRAT-derived leptin level in the high-fat diet-induced MetS rat. In MetS rats, PRAT-derived leptin expression increased concomitant with dysfunction of adipogenesis, and the activities of the angiotensin II-angiotensin II type 1 receptor and the angiotensin-converting enzyme 2-angiotensin (1-7)-Mas receptor axes were imbalanced in PRAT. PRAT-derived leptin from MetS rats promoted proliferation of rat glomerular endothelial cells (GERs) by activating the p38 MAPK (mitogenactivated protein kinase) pathway, thereby contributing to the development of nephropathy. Long-term telmisartan treatment improved metabolic parameters and renal function, decreased the amount of PRAT, promoted adipogenesis, increased the expression of angiotensin-converting enzyme 2, restored balanced activities of the angiotensin II-AT1R and angiotensin-converting enzyme 2-angiotensin (1-7)-Mas axes, and exerted an indirect renoprotective effect on MetS rats by decreasing PRAT-derived leptin release. Our results demonstrate a novel link between nephropathy and PRAT in MetS and show that telmisartan confers an underlying protective effect on visceral adipose tissue and the kidney, suggesting that it has potential as a therapeutic agent for the treatment of MetS-associated nephropathy. (Hypertension. 2016;68:478-490.

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Angiotensin II and 1-7 during aging in Metabolic Syndrome rats. Expression of AT1, AT2 and Mas receptors in abdominal white adipose tissue

Cited by 29 publications

References 52 publications

Anti‐atherosclerotic effect of the angiotensin 1–7 mimetic AVE0991 is mediated by inhibition of perivascular and plaque inflammation in early atherosclerosis

Anti‐atherosclerotic effect of the angiotensin 1–7 mimetic AVE0991 is mediated by inhibition of perivascular and plaque inflammation in early atherosclerosis

Biochemical evaluation of the renin-angiotensin system: the good, bad, and absolute?

Telmisartan Ameliorates Nephropathy in Metabolic Syndrome by Reducing Leptin Release From Perirenal Adipose Tissue

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