Synergistic Action of Angiotensin II, Insulin- Like Growth Factor-I, and Transforming Growth Factor-β on Platelet-Derived Growth Factor-BB, Basic Fibroblastic Growth Factor, and Epidermal Growth Factor-Induced DNA Synthesis in Vascular Smooth Muscle Cells

Ko, Yon; Stiebler, Heike; Nickenig, Georg; Wieczorek, A; Vetter, Hans; Sachinidis, Agapios

doi:10.1093/ajh/6.6.496

Cited by 29 publications

(13 citation statements)

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“…Some reports show that TGF-b either induces proliferation (Battegay et al, 1990;Hwang et al, 1992;Stouffer and Owens, 1994) or potentiates growth factor-induced proliferation (Janat and Liau, 1992;Ko et al, 1993), while others have shown a direct inhibition (D'Amore and Smith, 1993;Reddy and Howe, 1993;Grainger et al, 1994), or an inhibition of another growth factor-induced proliferation (Bjorkerud, 1991;Morisaki et al, 1991;Itoh et al, 1993). In our experiments, the effect of TGF-b on NGF secretion by VSM differed from that of PDGF.…”

Section: Resultscontrasting

confidence: 61%

Synergistic increase in nerve growth factor secretion by cultured vascular smooth muscle cells treated with injury-related growth factors

Creedon

Tuttle

1997

J. Neurosci. Res.

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Section: Resultscontrasting

confidence: 61%

Synergistic increase in nerve growth factor secretion by cultured vascular smooth muscle cells treated with injury-related growth factors

Creedon

Tuttle

1997

J. Neurosci. Res.

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“…In mouse, there are two isoforms of AT1R, AT1aR and AT1bR. AT1R has been shown to mediate mitogenesis in cardiac fibroblasts and vascular smooth muscle cells (12,13), whereas in fibroblasts, the activation of AT2R has two opposing effects, inhibition of cell growth (14,15) and promotion of apoptosis (16). Thus, the balance between the expressions of these two receptor types may be crucial in determining the response to Ang II.…”

mentioning

confidence: 99%

A Novel Function of Angiotensin II in Skin Wound Healing

Yahata

Shirakata

Tokumaru

et al. 2006

Journal of Biological Chemistry

124

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The role of angiotensin II (Ang II) in the control of systemic blood pressure and volume homeostasis is well known and has been extensively studied. Recently, Ang II was suggested to also have a function in skin wound healing. In the present study, the in vivo function of Ang II in skin wound healing was investigated using Ang II type 1 receptor (AT1R) knock-out mice. Wound healing in these mice was found to be markedly delayed. Keratinocytes and fibroblasts play important roles in wound healing, and thus the effect of Ang II on the migration of these cells was examined. Ang II stimulated keratinocyte and fibroblast migration in a dose-dependent manner. It has been reported that G protein-coupled receptor (GPCR) activation induces epidermal growth factor (EGF) receptor (EGFR) transactivation through the shedding of heparin-binding EGF-like growth factor (HB-EGF). As AT1R is a GPCR, it was hypothesizedthat Ang II-induced keratinocyte and fibroblast migration is mediated by EGFR transactivation. Ang II induced EGFR phosphorylation, which was inhibited by an AT1R antagonist, HB-EGF neutralizing antibody, and an HB-EGF antagonist in both keratinocytes and in fibroblasts. Moreover, Ang II-induced migration of keratinocytes and fibroblasts was also prevented by these inhibitors. Taken together, these findings clearly demonstrate, for the first time, that Ang II plays an important role in skin wound healing and that it functions by accelerating keratinocyte and fibroblast migration in a process mediated by HB-EGF shedding.

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“…[11][12][13] Fundamentally, studies have demonstrated the importance of the renin-angiotensin-aldosterone system in controlling tissue structure under pathophysiological conditions such as chronic heart failure, hypertension, and renal artery stenosis. 14 -17 For example, in the heart, both angiotensin II (Ang II) and aldosterone increase perivascular collagen deposition and interstitial fibrosis in vivo.…”

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confidence: 99%

Differential Effects of Angiotensin II on Cardiac Cell Proliferation and Intramyocardial Perivascular Fibrosis In Vivo

et al. 1998

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Background-Growth effects of angiotensin II (Ang II) contribute to cardiac remodeling. Remodeling, in turn, may be influenced by proliferation of nonmyocytes. The aims of this study were to determine in vivo which cardiac cell types proliferate in response to Ang II, to evaluate whether proliferation is mediated by the Ang II AT 1 receptor, and to establish whether blood pressure affects cell proliferation by comparing proliferation in the normotensive right atrium and ventricle and pressure-overloaded left ventricle. Methods and Results-Groups of 8 Wistar rats were implanted with miniosmotic pumps releasing 5-bromo-2Ј-deoxyuridine (BrdU) as a cell proliferation marker for 2 weeks. Two groups received Ang II infusions via a second minipump and drinking waterϮlosartan. Two groups received vehicleϮlosartan. Cell proliferation was assessed as the percentage of nuclei that incorporated BrdU. Ang II increased proliferation within medial vascular smooth muscle cells (VSMCs) and in associated adventitial/interstitial fibroblasts of intramyocardial coronary arterioles but decreased proliferation of myoendothelial cells. Despite increased blood pressure, proliferation in atria and ventricles was similar. Aldosterone levels were not significantly elevated, suggesting direct proliferative effects of Ang II. Losartan reduced Ang II-induced VSMC and adventitial fibroblast proliferation but had no effect on myoendothelial cell proliferation. Conclusions-These results indicate direct, differential effects of Ang II on proliferation of atrial and ventricular nonmyocytes. VSMC and fibroblast proliferation is AT 1 receptor-dependent, whereas myoendothelial cells are controlled by an AT 1 -independent mechanism. The effects are independent of aldosterone and blood pressure and have important implications in renin-dependent hypertension and chronic cardiac failure when circulating Ang II is elevated.

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Synergistic Action of Angiotensin II, Insulin- Like Growth Factor-I, and Transforming Growth Factor-β on Platelet-Derived Growth Factor-BB, Basic Fibroblastic Growth Factor, and Epidermal Growth Factor-Induced DNA Synthesis in Vascular Smooth Muscle Cells

Cited by 29 publications

References 0 publications

Synergistic increase in nerve growth factor secretion by cultured vascular smooth muscle cells treated with injury-related growth factors

Synergistic increase in nerve growth factor secretion by cultured vascular smooth muscle cells treated with injury-related growth factors

A Novel Function of Angiotensin II in Skin Wound Healing

Differential Effects of Angiotensin II on Cardiac Cell Proliferation and Intramyocardial Perivascular Fibrosis In Vivo

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