Angiotensin II induces type I collagen gene expression in human dermal fibroblasts through an AP-1/TGF-β1-dependent pathway

Tang, Haihong; Cheng, Dasheng; Jia, Yitao; Ben, Daofeng; Ma, Bing; Lv, Kaiyang; Wei, Duo; Sheng, Zhang; Xia, Zhaofan

doi:10.1016/j.bbrc.2009.05.081

Cited by 28 publications

(21 citation statements)

References 19 publications

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“…Tang et al showed that angiotensin II increases TGF-β expression, and that blockage of TGF-β inhibits angiotensin II-related collagen synthesis. 16 Angiotensin-converting enzyme 1 432 442 384 757 2 330 389 389 752 3 442 346 277 906 4 453 309 304 794 5 474 506 234 688 6 320 330 282 917 7 330 448 213 656 8 304 421 176 693 9 266 314 234 709 10 250 288 192 826 11 320 458 213 805 12 330 464 266 789 13 341 496 272 853 14 373 464 288 896 15 282 357 256 805 16 400 336 309 810 *Values are given as cells per square millimeter.…”

Section: Discussionmentioning

confidence: 97%

Angiotensin-Converting Enzyme Inhibitor Enalapril Reduces Formation of Hypertrophic Scars in a Rabbit Ear Wounding Model

Uzun

Bitik

Hekimoğlu

et al. 2013

Plastic and Reconstructive Surgery

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Section: Discussionmentioning

confidence: 97%

Angiotensin-Converting Enzyme Inhibitor Enalapril Reduces Formation of Hypertrophic Scars in a Rabbit Ear Wounding Model

Uzun

Bitik

Hekimoğlu

et al. 2013

Plastic and Reconstructive Surgery

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“…Angiotensin II has been shown to induce the release of TGF-b from various cell types, including vascular smooth muscle cells (Gibbons et al, 1992;Koibuchi et al, 1993), renal proximal tubular cells (Wolf et al, 1993), glomerular mesangial cells (Kagami et al, 1994), cardiac fibroblasts and myofibroblasts (Fisher and Absher, 1995;Campbell and Katwa, 1997), and dermal fibroblasts (Tang et al, 2009), in a paracrine manner and thereby to regulate various cellular activities. We have now shown that this is also the case in the regulation of keratinocyte migration by angiotensin II.…”

Section: Discussionmentioning

confidence: 99%

Signaling Mechanism Underlying the Promotion of Keratinocyte Migration by Angiotensin II

et al. 2014

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Re-epithelialization begins early during skin wound healing and is regulated by various growth factors and cytokines. Angiotensin II promotes the migration of keratinocytes and thereby contributes to wound healing. We investigated the mechanism by which angiotensin II stimulates human keratinocyte migration. Angiotensin II-induced keratinocyte migration was inhibited by an angiotensin II type 1 receptor (AT 1 R) antagonist (candesartan) or an angiotensin II type 2 receptor (AT 2 R) antagonist (PD123319)

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“…Angiotensin addresses the collagen I and TGF-β 1 expression in dermal fibroblasts. This effect could be suppressed by an angiotensin receptor I antagonist [17]. In rats, the angiotensin receptor II was overexpressed on day 3 after wounding [18, 19].…”

Section: Introductionmentioning

confidence: 99%

Side Effects of Frequently Used Antihypertensive Drugs on Wound Healing in vitro

Besser

Terberger

Bachmann

et al. 2019

Skin Pharmacol Physiol

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Background: The number of patients who has a daily intake of antihypertensive drugs is rising, due to an also rising prevalence of lifestyle diseases. Interestingly, knowledge about effects of these drugs in terms of wound healing is low. Objective: Based on a few differing studies, the idea arose that antihypertensives may have side effects on wound healing. Methods: Five antihypertensive drugs from different substance classes (metoprolol, amlodipine, ramipril, hydrochlorothiazide, candesartan) were investigated, in terms of possible impacts on cell metabolism and migration of human skin fibroblasts and keratinocytes. Additionally, histological and immunohistochemical analyses were performed in a 3-dimensional (3D) wound model addressing the influence on regeneration processes, such as cell migration, metabolic activity, apoptosis and epidermal thickness. Results: Hydrochlorothiazide and ramipril exerted inhibiting effects in nearly all analyses, interestingly, in serum equivalent doses. In contrast, candesartan and amlodipine induced slight positive effects in 2D as well as in 3D models. The previously described positive effects of β-blockers could only partially be confirmed by metoprolol. Antihypertensive drugs affected fibroblasts more than keratinocytes – whether positively or negatively. Conclusion: Antihypertensive drugs have an influence on keratinocytes and fibroblasts; they are not neutral. Candesartan has the most positive effects on skin cells. For angiotensin-converting enzyme inhibitors and thiazide diuretics, wound healing in a 3D model is delayed. β-Receptor blockers seem to improve wound healing to a small extent just like calcium channel blockers. These results should be evaluated in a clinical trial to verify their clinical relevance.

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Angiotensin II induces type I collagen gene expression in human dermal fibroblasts through an AP-1/TGF-β1-dependent pathway

Cited by 28 publications

References 19 publications

Angiotensin-Converting Enzyme Inhibitor Enalapril Reduces Formation of Hypertrophic Scars in a Rabbit Ear Wounding Model

Angiotensin-Converting Enzyme Inhibitor Enalapril Reduces Formation of Hypertrophic Scars in a Rabbit Ear Wounding Model

Signaling Mechanism Underlying the Promotion of Keratinocyte Migration by Angiotensin II

Side Effects of Frequently Used Antihypertensive Drugs on Wound Healing in vitro

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