Angiotensin II stimulates two myelin basic protein/microtubule-associated protein 2 kinases in cultured vascular smooth muscle cells.

Tsuda, Terutaka; Kawahara, Yasuhiro; Ishida, Yoshihiro; Koide, Makoto; Shii, Kozui; Yokoyama, Mitsuhiro

doi:10.1161/01.res.71.3.620

Cited by 114 publications

(62 citation statements)

References 61 publications

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“…VSMCs were isolated from rat thoracic aorta by enzymatic dissociation as described previously [7] and used at passage levels [8][9][10][11][12][13][14][15][16]. Ang II and cytochalasin D were obtained from Sigma (St.Louis, MO, USA).…”

Section: Methodsmentioning

confidence: 99%

“…In past immunoblot experiments with antiphosphotyrosine antibody, Ang II induces tyrosine phosphorylation of proteins with apparent molecular masses of 190, 100-120, 70-80, 45 and 40 kDa in VSMCs [7]. The 45-and 40-kDa proteins have been identified as mitogen-activated protein kinase isozymes [9]. These may be involved in the signaling mechanism from the Ang II receptor to the nucleus and play crucial roles in the growth-promoting action of Ang II.…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin II transduces its signal to focal adhesions via angiotensin II type 1 receptors in vascular smooth muscle cells

et al. 1995

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In cultured vascular smooth muscle cells (VSMCs), angiotensin II (Ang II) stimulated tyrosine phosphorylation of several proteins including a cluster of 70-80-kDa proteins as assessed by anti-phosphotyrosine immunoblotting. These 70-80-kDa proteins were identified as a focal adhesion-associated protein, paxillin, by anti-paxillin immunoprecipitation. Ang II-stimulated tyrosine phosphorylation of paxillin was detectable within 1 rain and maximal at around 10 rain and was concentration dependent (half-maximal effect at around 1 nM). Ang II also stimulated tyrosine phosphorylation of focal adhesion kinase in a time-and concentration-dependent manner. The Ang II type 1 (AT1) receptor antagonist, CV-11974, but not the Ang II type 2 receptor antagonist, PD123319, inhibited these reactions. These results indicate that Ang I! transduces its signal to focal adhesions via AT1 receptors in cultured VSMCs.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Angiotensin II transduces its signal to focal adhesions via angiotensin II type 1 receptors in vascular smooth muscle cells

et al. 1995

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“…'.rmal growth factor; NGF, nerve growth factor; PMA, phorboi 12-myristate 13- [14][15][16]. In a preceding report, we have shown that ang II induces tyrosine and serin¢/threonine phosphorylation and activation of two MAP kinases in cultured VSMC [17]. Thus it is likely that MAP kinases play important roles as intermediates in the signalling pathways from the ang II receptors, as well as the growth factor receptors, to the ribosomes and nucleus.…”

Section: Introductionmentioning

confidence: 99%

Involvement of MAP kinase activators in angiotensin II‐induced activation of MAP kinases in cultured vascular smooth muscle cells

Ishida¹,

Kawahara²,

Tsuda³

et al. 1992

FEBS Letters

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In cultured vascular smooth muscle cells (VSMC) angiotensin 11 (ang II) indues tyrosin¢ and serine/thrconine phosphorylation and activation of two mitogen-activated protein (MAP) kinases. When extracts o fang II-stimulated VSMC were fractionated by Mono Q anion-exchange column chromatography, three peaks of the activities which in vitro activate inactive MAP kinases were detected, These MAP kinas¢ activator activities were not detected in extracts of umtimulatcd VSMC, in vitro activation of MAP kinases by the MAP kinas¢ activators was accompanied by tyrosine and serine/threonin¢ phosphorylation of MAP kinasea. These results suggest that the MAP kinase activators are involved in the ang ll-indueed phosphorylation and activation of MAP kinases in VSMC.Angiotensin !1; Mitogen-aetivated protein kinas¢; MAP kinase activator; Protein kina~ C; Vascular smooth muscle eeli

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“…[11][12][13][14] We have previously reported that in isolated perfused rat aortae, increases in perfusion pressure cause a pressure-dependent increase in the activity of MAPKs.…”

mentioning

confidence: 99%

“…[8][9][10] Angiotensin II and endothelins stimulate MAPKs, leading to stimulation of protein synthesis. [11][12][13][14] We have previously reported that in isolated perfused rat aortae, increases in perfusion pressure cause a pressure-dependent increase in the activity of MAPKs.…”

mentioning

confidence: 99%

Mechanical Stretch-Induced Mitogen-Activated Protein Kinase Activation Is Mediated via Angiotensin and Endothelin Systems in Vascular Smooth Muscle Cells.

Hosokawa

Aiuchi

Kambe

et al. 2002

Biological & Pharmaceutical Bulletin

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Vascular smooth muscle hypertrophy in resistance vessels may play an important role in the ethiology of hypertension. [1][2][3][4][5] Mechanical strain plays a pivotal role in the development of vascular hypertrophy in hypertension.6) However, its exact mechanisms remain unknown.Mitogen-activated protein kinases (MAPKs), members of a family of serine/threonine-specific protein kinases, 7) are believed to be involved in the pathway of cell proliferation and thus in vascular structural remodeling.8-10) Angiotensin II and endothelins stimulate MAPKs, leading to stimulation of protein synthesis. [11][12][13][14] We have previously reported that in isolated perfused rat aortae, increases in perfusion pressure cause a pressure-dependent increase in the activity of MAPKs.15) The MAPK activation was inhibited by the angiotensin receptor antagonist losartan and the angiotensinconverting enzyme inhibitor captopril. These findings suggest that pressure loading of the vascular wall per se can activate MAPKs in the vasculature and that the MAPK activation is mediated at least partly via the vascular angiotensin system.We also demonstrated that the pressure loading-induced MAPK activation still occurred in endothelium-denuded aortae.15) Endothelial and vascular smooth muscle cell (VSMC) integrity is thought to be a crucial factor in the maintenance of the structural properties of the vascular wall. 16,17) Thus VSMC may be, at least in part, involved in pressure-induced MAPK activation. Mechanical stress causes MAPK activation in VSMC. 18,19) In VSMC, angiotensin and endothelin systems are present and regulate cell growth. [20][21][22][23][24] The purpose of the present study was to determine, using cultured rat VSMC, whether cyclic stretching causes increases in p42 and p44 MAPK activity and whether angiotensin and endothelin systems in VSMC are involved in stretch-induced MAPK activation. MATERIALS AND METHODSCell Culture Rat aortic VSMC were isolated from the thoracic aortae of Wistar rats (200-250 g) using the method of Ross 25) as described previously. 26) In brief, stripped aortae were placed on polyethylene dishes (diameter 60 mm). Dulbecco's modified Eagle's medium (DMEM) containing 20% fetal calf serum, penicillin 100 U/ml, and streptomycin 100 mg/ml was added to the dishes to cover the aortae. The dishes were kept at 37°C in a humidified atmosphere of 95% air and 5% CO 2 . The cells growing from the explants reached confluence after about 14 d, were harvested by brief exposure to Hanks' medium supplemented with 0.25% trypsin and 0.02% ethylenediaminetetraacetic acid (EDTA)-sodium salt, and transferred to fresh dishes. The properties of the cells cultured showed a typical hills-and-valleys growth pattern and a-actin molecule upon immunohistochemical analysis using mouse anti-a-actin (Zymed Laboratories, Inc.), indicating that the cells were grown from VSMC.Primary cultures of VSMC were plated in 60-mm culture dishes (1ϫ10 5 cells/dish) containing DMEM with 10% fetal calf serum. The cells used in this study were in pas...

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Angiotensin II stimulates two myelin basic protein/microtubule-associated protein 2 kinases in cultured vascular smooth muscle cells.

Abstract: In cultured vascular smooth muscle cells, angiotensin II

Cited by 114 publications

References 61 publications

Angiotensin II transduces its signal to focal adhesions via angiotensin II type 1 receptors in vascular smooth muscle cells

Angiotensin II transduces its signal to focal adhesions via angiotensin II type 1 receptors in vascular smooth muscle cells

Involvement of MAP kinase activators in angiotensin II‐induced activation of MAP kinases in cultured vascular smooth muscle cells

Mechanical Stretch-Induced Mitogen-Activated Protein Kinase Activation Is Mediated via Angiotensin and Endothelin Systems in Vascular Smooth Muscle Cells.

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