Tyrosine phosphorylation increases Ca2+ sensitivity of vascular smooth muscle contraction

Masui, Hidehisa; Wakabayashi, Ichiro

doi:10.1016/s0024-3205(00)00942-5

Cited by 17 publications

(14 citation statements)

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“…A recent study has shown that a part of the Ca 2+ influx pathway involving an L-type Ca 2+ channel is regulated by tyrosine kinase activity in the A10 rat aortic cell line (Nelson et al, 1997). On the contrary, the augmentation by orthovanadate, an activator of tyrosine kinase, of the KCl-induced contraction of the guinea pig aorta, is not mediated by facilitation of transplasmalemmal Ca 2+ entry (Masui and Wakabayashi, 2000). However, it has not been determined whether p38 activation is involved in the Ca 2+ entry mechanism of vascular smooth muscle.…”

Section: Figmentioning

confidence: 99%

Difference in Signal Transduction Mechanisms Involved in 5-Hydroxytryptamine- and U46619-Induced Vasoconstrictions.

Tasaki

Hori

Ozaki

et al. 2003

J. Smooth Muscle Res.

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In order to elucidate the signal transduction pathways of vascular smooth muscle contractions induced by stimulation of receptors for 5-hydroxytryptamine (5-HT) and thromboxane A2 (TXA2), both of which are released from activated platelets, we examined whether protein kinases, such as tyrosine kinase, p38 mitogen-activated protein kinase (MAPK) and protein kinase C (PKC), are involved in the contraction produced by either 5-HT or U46619 (an analog of TXA2) in the rat aorta. Both 5-HT and U46619 induced sustained contractions, which were markedly reduced in the absence of extracellular Ca 2+ . Verapamil (a L-type Ca 2+ channel blocker) markedly inhibited the contractile response to 5-HT, while the U46619-induced contraction was only slightly inhibited by verapamil. Both contractile responses to 5-HT and U46619 were significantly inhibited by calphostin C (a PKC inhibitor). On the other hand, both genistein (5 µM, a tyrosine kinase inhibitor) and SB203580 (a p38 MAPK inhibitor) significantly inhibited 5-HT-induced contractions but had little effects on the contractions induced by U46619. These results suggest that the signal transduction mechanisms involved in the contractions mediated via 5-HT and TXA2 receptors are different as follows. Both the tyrosine kinase and p38 MAPK pathways are involved in 5-HT contraction but not in TXA2 contraction, while both contractions are strongly dependent on transplasmalemmal Ca

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Section: Figmentioning

confidence: 99%

Difference in Signal Transduction Mechanisms Involved in 5-Hydroxytryptamine- and U46619-Induced Vasoconstrictions.

Tasaki

Hori

Ozaki

et al. 2003

J. Smooth Muscle Res.

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“…[26][27][28] Src is a nonreceptor type tyrosine kinase that activates EGFR either directly through phosphorylation at Tyr-845 in the cytoplasm 29,30) or indirectly via the metalloproteinasecatalyzed formation of HB-EGF from pro-HB-EGF. 31) In a previous study using rat thoracic arteries, we showed that OVA-induced vasoconstriction depended on transactivation of EGFR via shedding of pro-HB-EGF.…”

Section: +mentioning

confidence: 99%

Orthovanadate-Induced Vasoconstriction of Rat Mesenteric Arteries Is Mediated by Rho Kinase-Dependent Inhibition of Myosin Light Chain Phosphatase

Ito

Matsuzaki

Sasahara

et al. 2015

Biological & Pharmaceutical Bulletin

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Key words myosin light chain phosphatase; orthovanadate; mesenteric artery Vanadium forms numerous inorganic compounds (vanadyl sulfate, sodium metavanadate, sodium orthovanadate (OVA), vanadium pentoxide) and complexes with organic compounds.1) Because of its structural similarity to phosphate, vanadate possesses various biochemical and pharmacological properties, such as the ability to inhibit ATPases 2) and protein tyrosine phosphatases (PTPases), 3) epidermal growth factor (EGF)-like mitogenic activity, 4) insulin-mimetic properties, 5) anti-apoptotic activities, 6) and antitumor or carcinogenic properties. 7,8) Vanadium compounds exert contractile effects on vascular and non-vascular smooth muscle, such as the guinea pig taenia coli, trachea, and gallbladder smooth muscle.9-11) The contractile effects of vanadates have been considered to be due to inhibition of PTPase, 9,11,12) but not ATPase, 13,14) because genistein, a protein tyrosine kinase inhibitor, attenuates vanadateinduced constriction. Vanadate-induced muscle constriction was regulated by activation of Rho kinase-dependent signaling in ileal longitudinal smooth muscle in guinea pigs, resulting in increased phosphorylation of the myosin light chain (MLC). 15)These reports showed that vanadates inhibited the activity of protein tyrosine phosphatases, leading to Rho kinase-dependent constriction. Recently, we reported that OVA induced Rho kinase-dependent constriction and phosphorylation of the myosin phosphatase target subunit 1 (MYPT1) of myosin light chain phosphatase (MLCP). OVA-induced phosphorylation of MYPT1 was regulated by the EGF receptor (EGFR) and Src, because inhibitors of EGFR and Src abolished phosphorylation of MYPT1.16) Furthermore, metalloproteinase inhibitor TAPI-0 (N-(R)-(2-(hydroxyaminocarbonyl) methyl]-4-methylpentanoyl-L-naphthylalanyl-L-alanine amide) and an inhibitor of heparin/EGF binding abrogated OVA-induced aortic constriction and phosphorylation of EGFR and MYPT1.16) This finding indicated that OVA transactivated EGFR in vascular smooth muscle cells (VSMCs) derived from the rat thoracic aorta. These findings indicate that OVA can influence smooth muscle constriction through EGFR and Rho kinase-dependent inactivation of MLCP. Furthermore, we showed that EGF induced Ca 2+ sensitization in vascular smooth muscle by Rho kinasedependent inactivation of MLCP through the extracellular signal-regulated kinases 1 and 2 (Erk1/2) and Erk1/2 kinase (MEK) pathway. 17) However, it is not clear whether OVA activates MEK and Erk1/2 signaling through the EGFR. In addition, it is unknown whether OVA induces constriction and phosphorylation of MYPT1 in mesenteric arteries in rats. Therefore, in this study, we aimed to determine whether OVA-induced constriction of rat superior mesenteric arteries is mediated by Src, EGFR, mitogen-activated protein kinase (MAPK) s, and Rho kinase.

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“…The resulting increase in [Ca 2ϩ ] i may provoke EGFR transactivation, 1 with subsequent tyrosine phosphorylation events promoting contraction by a mechanism such as increasing the Ca 2ϩ sensitivity of the contractile apparatus. 9 Alternatively, Ang II binding to the AT 1 R may initiate Ca 2ϩ -independent transactivation of the EGFR, which then contributes to the Ang II-induced increase in [Ca 2ϩ ] i as might occur as a result of phospholipase C␥ activation. 10 An important difference between these two scenarios is that one involves EGFRmediated events that favor contraction without altering intracellular Ca 2ϩ homeostasis, whereas the other requires EGFR tyrosine kinase activity to achieve the full [Ca 2ϩ ] i response to Ang II.…”

mentioning

confidence: 99%

Angiotensin II Triggers EGFR Tyrosine Kinase-Dependent Ca ²⁺ Influx in Afferent Arterioles

Che¹,

Carmines²

2002

Hypertension

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Abstract-We previously reported that inhibition of epidermal growth factor receptor tyrosine kinase activity attenuates renal arteriolar contractile responses to angiotensin II. We performed the present experiments to determine if epidermal growth factor receptor tyrosine kinase activity contributes to the afferent arteriolar intracellular [Ca 2ϩ ] response to angiotensin II. Afferent arterioles were dissected from rat kidney and intracellular [Ca 2ϩ ] was monitored with the use of fura-2. In normal Ringer's bath containing 1.5 mmol/L Ca 2ϩ , basal intracellular [Ca 2ϩ ] averaged 95Ϯ7 nmol/L and 100 nmol/L angiotensin II caused a rapid rise (peak ⌬ϭ75Ϯ10 nmol/L) that waned to a plateau averaging 24Ϯ5 nmol/L above baseline. Pretreatment with 100 nmol/L AG1478 (epidermal growth factor receptor tyrosine kinase inhibitor) reduced both the peak and the plateau stages of the angiotensin II response (peak ⌬ϭ42Ϯ7 nmol/L; plateau ⌬ϭ8Ϯ4 nmol/L). A structurally unrelated epidermal growth factor receptor tyrosine kinase inhibitor also suppressed the peak response to angiotensin II, whereas tyrosine phosphatase inhibition enhanced the plateau phase of the response. In the presence of 100 nmol/L extracellular Ca 2ϩ , the angiotensin II response was characterized by a peak of diminished magnitude (⌬ϭ49Ϯ10 nmol/L; PϽ0.05 versus the response in normal Ringer's bath) with no plateau, and this response was unaffected by AG1478. Moreover, angiotensin II stimulation of divalent cation influx (Mn 2ϩ quench of fura-2 fluorescence) was decreased significantly by AG1478. We conclude that epidermal growth factor receptor tyrosine kinase activity contributes to the afferent arteriolar intracellular [Ca 2ϩ ] response to angiotensin II and that this process involves promotion of Ca 2ϩ influx.

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Tyrosine phosphorylation increases Ca2+ sensitivity of vascular smooth muscle contraction

Cited by 17 publications

References 0 publications

Difference in Signal Transduction Mechanisms Involved in 5-Hydroxytryptamine- and U46619-Induced Vasoconstrictions.

Difference in Signal Transduction Mechanisms Involved in 5-Hydroxytryptamine- and U46619-Induced Vasoconstrictions.

Orthovanadate-Induced Vasoconstriction of Rat Mesenteric Arteries Is Mediated by Rho Kinase-Dependent Inhibition of Myosin Light Chain Phosphatase

Angiotensin II Triggers EGFR Tyrosine Kinase-Dependent Ca ²⁺ Influx in Afferent Arterioles

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Tyrosine phosphorylation increases Ca2+ sensitivity of vascular smooth muscle contraction

Cited by 17 publications

References 0 publications

Difference in Signal Transduction Mechanisms Involved in 5-Hydroxytryptamine- and U46619-Induced Vasoconstrictions.

Difference in Signal Transduction Mechanisms Involved in 5-Hydroxytryptamine- and U46619-Induced Vasoconstrictions.

Orthovanadate-Induced Vasoconstriction of Rat Mesenteric Arteries Is Mediated by Rho Kinase-Dependent Inhibition of Myosin Light Chain Phosphatase

Angiotensin II Triggers EGFR Tyrosine Kinase-Dependent Ca 2+ Influx in Afferent Arterioles

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Angiotensin II Triggers EGFR Tyrosine Kinase-Dependent Ca ²⁺ Influx in Afferent Arterioles