Alterations of Angiotensin II Receptor Levels in Sutured Wounds in Rat Skin

Abiko, Masami; Rodgers, Kathleen E.; Campeau, Joseph D.; Nakamura, Robert M.; Dizerega, Gefe S.

doi:10.3109/08941939609025862

Cited by 27 publications

(25 citation statements)

References 13 publications

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“…In view of the potential physiological role of a cutaneous RAS, we hypothesized that it may link to mechanisms of tissue repair and remodeling. During the regulation of cell proliferation and differentiation, AT1 and AT2 receptors seem to counteract with each other [6,[10][11][12]17]. Consequently, in skin tissues expressing both AT1 and AT2 receptors, AngII may establish its own regulatory system depending on different expression of these two receptor subtypes.…”

Section: Discussionmentioning

confidence: 95%

Activation of skin renin–angiotensin system in diabetic rats

Hao

Ren²,

Yang³

et al. 2011

Endocr

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The renin-angiotensin system (RAS) is reportedly involved in chronic diabetic complications such as diabetic nephropathy, but changes of the RAS in diabetic skin remain unknown. The aim of this study was to investigate the expression of angiotensin (Ang) II and its type 1 (AT1) and type 2 (AT2) receptors in diabetic skin tissues, and explore the relationship between the local RAS and pathological changes of diabetic skin. Our results showed that thinning of epidermis, degeneration of collagen, fracture of dermal layer, and atrophy/disappearance of subcutaneous fat were observed in diabetic skin. The expression level of AngII was increased in diabetic skin tissues compared to that in controls. mRNA and protein expression of AT1 receptor were also increased while the level of AT2 receptor decreased; the relative expression of AT1 to AT2 receptors was approximately threefold higher in diabetes than in controls. Furthermore, in the culture medium of primary cultured fibroblasts from diabetic skin, the concentration of AngII was significantly higher than that of normal control. The mRNA and protein expression of AT1 receptor was also increased in fibroblasts of diabetic skin compared to controls, while the protein expression of AT2 receptor was decreased. Taken together, our results suggest that the local RAS system is activated in diabetic skin and AngII receptor is likely to mediate the pathological changes of diabetic skin.

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Section: Discussionmentioning

confidence: 95%

Activation of skin renin–angiotensin system in diabetic rats

Hao

Ren²,

Yang³

et al. 2011

Endocr

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“…AT1 and AT2 receptors of Ang II are both expressed in skin, suggesting that skin is not only a source of Ang II but also a target organ. 35 Ang II is known to stimulate fibrous tissue formation and coronary matrix remodelling by promoting TGF-β synthesis via AT1 receptors. 36 AT2 receptor stimulation counteracts AT1 receptor activation, and the effect of Ang II is regulated by the interaction of AT1 and AT2 receptor-mediated signalling in various target tissues.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II regulates collagen metabolism through modulating tissue inhibitor of metalloproteinase-1 in diabetic skin tissues

Ren

Hao

Yang

et al. 2013

Diabetes and Vascular Disease Research

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We investigated the effect of angiotensin II (Ang II) on matrix metalloproteinase-1 (MMP-1)/tissue inhibitor of metalloproteinase-1 (TIMP-1) balance in regulating collagen metabolism of diabetic skin. Skin tissues from diabetic model were collected, and the primary cultured fibroblasts were treated with Ang II receptor inhibitors before Ang II treatment. The collagen type I (Coll I) and collagen type III (Coll III) were measured by histochemistry. The expressions of transforming growth factor-β (TGF-β), MMP-1, TIMP-1 and propeptides of types I and III procollagens in skin tissues and fibroblasts were quantified using polymerase chain reaction (PCR), Western blot or enzyme-linked immunosorbent assay (ELISA). Collagen dysfunction was documented by changed collagen I/III ratio in streptozotocin (STZ)-injected mice compared with controls. This was accompanied by increased expression of TGF-β, TIMP-1 and propeptides of types I and III procollagens in diabetic skin tissues. In primary cultured fibroblasts, Ang II prompted collagen synthesis accompanied by increases in the expressions of TGF-β, TIMP-1 and types I and III procollagens, and these increases were inhibited by losartan, an Ang II type 1 (AT1) receptor blocker, but not affected by PD123319, an Ang II type 2 (AT2) receptor antagonist. These findings present evidence that Ang-II-mediated changes in the productions of MMP-1 and TIMP-1 occur via AT1 receptors and a TGF-β-dependent mechanism.

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“…In rodents, it has been documented that Life Sciences 79 (2006) 475 -483 www.elsevier.com/locate/lifescie there is an increased level of Ang II or Ang-converting enzyme (ACE) in the rat skin (Gyurko et al, 1992;Sun and Weber, 1996) during wound healing, an upregulation of AT 1 or AT 2 receptor in wounded skin (Abiko et al, 1996;Kimura et al, 1992;Viswanathan and Saavedra, 1992), and that the topical administration of Ang II accelerates skin wound healing (Rodgers et al, 1997(Rodgers et al, , 2001(Rodgers et al, , 2003. Interestingly, as previously mentioned, AT 1 and AT 2 receptors play opposite roles in regulation of cellular metabolism and proliferation in skin cells such as skin fibroblasts (Gyurko et al, 1992;Takeda et al, 2004;Min et al, 2004).…”

Section: Introductionmentioning

confidence: 99%