Effects of H2O2 on Membrane-Potential and [Ca2+]i of Cultured Rat Arterial Smooth Muscle Cells

Koehler, Peter; Haberland, Catherine; Fingerle, Jürgen; Drews, Gisela; Läng, Florian

doi:10.1006/bbrc.1995.1481

Cited by 53 publications

(26 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our observation of Ca 2ϩ response elicited by H 2 O 2 , at a concentration as low as 10 M, corroborates with the latter studies that suggest that the primary response of PASMCs to a physiological concentration of H 2 O 2 is vasoconstriction. It is also consistent with a previous report in PASMCs (66) and other studies in systemic vascular myocytes (32,52,70) causes direct modification of cysteine residues to form intersubunit cross-linkages within the release channel tetramer (2,18,19) and causes S-glutathionylation in combination with glutathione (12,20). These sulfhydryl modifications enhance RyR activity by altering subunit-subunit interactions and by preventing the inhibitory binding of calmodulin and Mg 2ϩ .…”

Section: Methodssupporting

confidence: 93%

Hydrogen peroxide-induced Ca²⁺mobilization in pulmonary arterial smooth muscle cells

Lin

Yang

Cao

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

March 16, 2007; doi:10.1152/ajplung.00323.2006.-Reactive oxygen species (ROS) generated from NADPH oxidases and mitochondria have been implicated as key messengers for pulmonary vasoconstriction and vascular remodeling induced by agonists and hypoxia. Since Ca 2ϩ mobilization is essential for vasoconstriction and cell proliferation, we sought to characterize the Ca 2ϩ response and to delineate the Ca 2ϩ pathways activated by hydrogen peroxide (H2O2) in rat intralobar pulmonary arterial smooth muscle cells (PASMCs). Exogenous application of 10 M to 1 mM H 2O2 elicited concentration-dependent increase in intracellular Ca 2ϩ concentration in PASMCs, with an initial rise followed by a plateau or slow secondary increase. The initial phase was related to intracellular release. It was attenuated by the inositol trisphosphate (IP 3) receptor antagonist 2-aminoethyl diphenylborate, ryanodine, or thapsigargin, but was unaffected by the removal of Ca 2ϩ in external solution. The secondary phase was dependent on extracellular Ca 2ϩ influx. It was unaffected by the voltage-gated Ca 2ϩ channel blocker nifedipine or the nonselective cation channel blockers SKF-96365 and La 3ϩ , but inhibited concentration dependently by millimolar Ni 2ϩ , and potentiated by the Na ϩ /Ca 2ϩ exchange inhibitor KB-R 7943. H2O2 did not alter the rate of Mn 2ϩ quenching of fura 2, suggesting store-and receptor-operated Ca 2ϩ channels were not involved. By contrast, H2O2 elicited a sustained inward current carried by Na ϩ at Ϫ70 mV, and the current was inhibited by Ni 2ϩ . These results suggest that H2O2 mobilizes intracellular Ca 2ϩ through multiple pathways, including the IP3-and ryanodine receptor-gated Ca 2ϩ stores, and Ni 2ϩ -sensitive cation channels. Activation of these Ca 2ϩ pathways may play important roles in ROS signaling in PASMCs.nonselective cation channels; sodium-calcium exchange; ryanodine receptor; inositol trisphosphate receptor; pulmonary arteries REACTIVE OXYGEN SPECIES (ROS) derived from diverse cellular sources, including NADPH oxidase, mitochondrial electron transport chain (ETC), xanthine oxidase, cytochrome P-450, cyclooxygenase, and nitric oxide synthase, are known to play important roles in the regulation of pulmonary and systemic circulation (15). It has been established that vasoconstrictors/ mitogens, such as angiotensin II, serotonin, endothelin-1, platelet-derived growth factor, and tumor necrosis factor-␣, stimulate the production of superoxide and hydrogen peroxide (H 2 O 2 ) to enhance vasoconstriction and activate redox-sensitive gene transcription to promote proliferation, hypertrophy, migration, and survival of vascular smooth muscle cell (14,34,36,58). Recent studies showed that ROS overproduction is associated with pulmonary remodeling and alterations in vascular reactivity observed in chronic hypoxia, and targeted deletion of gp91 phox subunit prevented these changes in knockout mice, suggesting that ROS generated from NADPH oxidase contribute significantly to the pathogenesis of hypoxic pulmonary hypertens...

show abstract

Section: Methodssupporting

confidence: 93%

Hydrogen peroxide-induced Ca²⁺mobilization in pulmonary arterial smooth muscle cells

Lin

Yang

Cao

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

show abstract

“…In addition, it has been reported that influx of Ca 2+ , after exposure to oxidants, appears to be responsible for the increase in [Ca 2+ ] i of rat aortic smooth muscle cells (Sandirasegarane and Gopalakrishnan 1995). The involvement of intracellular stores has recently been proposed by Krippeit-Drews et al (1995) who showed that hydrogen peroxide produces an early intracellular Ca 2+ increment in some smooth muscle cells, which at least partly results Table 1 Responses of intracellular Ca 2+ concentration (nM) in vascular smooth muscle cells obtained from canine basilar arteries to H 2 O 2 in the absence and presence of extracellular Ca 2+ , 5 µM verapamil, 5×10 -7 M staurosporine, 5×10 -7 M bisindolylmaleimide HCl, 10 -6 M Gö6976, 7.5×10 -5 M genistein, 10 -6 M PD-98059, 5×10 -7 M wortmannin and 10 -5 M LY-294002. The data were obtained 20 s after the reagent treatments.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen peroxide induces contraction and raises [Ca2+]i in canine cerebral arterial smooth muscle: participation of cellular signaling pathways

Zheng

Wang

et al. 1999

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

The effects of hydrogen peroxide (H2O2) on isolated canine basilar arteries, and single smooth muscle cells isolated from these arteries, were investigated in the present study. Exposure of isolated endothelium-intact and denuded arterial rings to H2O2, at concentrations of 2.2x10(-5) M to 4.4x10(-3) M, produced concentration-dependent contractile responses. Removal of the endothelium attenuated, but did not eliminate the contractions. H2O2-induced contractions were inhibited, to different degrees, by preincubation of the vessels with low concentrations of staurosporine or bisindolylmaleimide I HCl [antagonists of protein kinase C (PKC)], Gö6976 (a PKCalpha and PKCbeta1 selective antagonist), genistein (an antagonist of protein tyrosine kinase), PD-98059 (an antagonist of mitogen-activated protein kinase), wortmannin [an antagonist of phosphatidylinositol 3 (PI3)-kinases], and LY-294002 (an antagonist of PI3-kinases). These agents were also found to relax arteries precontracted by H2O2. Removal of extracellular Ca2+ or pretreatment of the vessels with 5.0 microM verapamil markedly attenuated the contractions. Complete inhibition of the contractile response was obtained after buffering intracellular Ca2+ with BAPTA-AM. A variety of specific pharmacological antagonists of several known vasoconstrictors neither inhibited nor attenuated the H2O2-induced contractions. Exposure of smooth muscle cells to H2O2 (4.4x10(-6) M to 4.4x10(-4) M) significantly raised intracellular Ca2+ ([Ca2+]i) within 20 s. This was abolished in the absence of extracellular Ca2+ or after application of 5.0 microM verapamil. Pretreatment of the cells with low concentrations of staurosporine, bisindolylmaleimide I, Gö6976, genistein, PD-98059, wortmannin, and LY-294002 markedly suppressed the H2O2-mediated [Ca2+]i elevation. The present findings suggest that hydrogen peroxide, in vitro, produces endothelium-dependent and independent contractions of canine basilar arteries, which are clearly Ca2+-dependent and are not associated with release of endogenous vasoconstrictors. Several intracellular signal transduction systems, such as PKC (both Ca2+-dependent and Ca2+-independent), protein tyrosine phosphorylation, IP3, mitogen-activated protein kinase and PI3 kinase appear to play a role in the H2O2-induced contractions in cerebral arterial muscle.

show abstract

“…An interrelationship between R OI levels and cellular Ca 2+ concentrations has been prev 3usly reported in various systems. Treatment of several diff¢ rent cell types with H202 induces a considerable increase in c, tosolic free calcium [28][29][30]. This is caused by the release of ir ternal stores rather than by the influx of external Ca 2+ bec:use the effect is also seen in the absence of external Ca 2+.…”

Section: Discussionmentioning

confidence: 99%

Activation of NF‐κB by ER stress requires both Ca²⁺ and reactive oxygen intermediates as messengers

Pahl¹,

Baeuerle²

1996

FEBS Letters

205

115

View full text Add to dashboard Cite

The eukaryotic transcription factor NF-gB is activated by a large variety of stimuli. We have recently shown that ER stress, caused by an aberrant accumulation of membrane proteins within this organdie, also activates NF-gB. Here, we show that activation of NF-gB by ER stress requires an increase in the intracellular levels of both reactive oxygen intermediates (ROIs) and Ca 2+. Two distinct intracellular Ca z+ chelators and a panel of structurally unrelated antioxidants prevented NF-gB activation by various ER stress-eliciting agents, whereas only antioxidants but not the Ca 2+ chelators prevented NF-gB activation by the inflammatory cytokine TNF-c¢. Consistent with an involvement of calcium, the ER-resident Ca2+-ATPase inhihitors thapsigargin and cyclopiazonic acid (CPA), which trigger a rapid efflux of Ca 2+ from the ER, also potently activated NF-gB. Pretreatment with a Ca 2+ chelator abrogated this induction. The Ca 2+ chelator BAPTA-AM inhibited ROI formation in response to thapsigargin and CPA treatment, suggesting that the Ca 2+ increase preceded ROI formation during NF-gB activation. The selective inhibitory effect of the drug tepoxalin suggests that the peroxidase activity of cyclooxygenases or lipoxygenases was responsible for the increased ROI production in response to Ca 2+ release by thapsigargin. l~,,y words." Endoplasmic reticulum; NF-~cB; Ca 2+ ; Radical oxygen intermediate

show abstract

Effects of H2O2 on Membrane-Potential and [Ca2+]i of Cultured Rat Arterial Smooth Muscle Cells

Cited by 53 publications

References 0 publications

Hydrogen peroxide-induced Ca²⁺mobilization in pulmonary arterial smooth muscle cells

Hydrogen peroxide-induced Ca²⁺mobilization in pulmonary arterial smooth muscle cells

Hydrogen peroxide induces contraction and raises [Ca2+]i in canine cerebral arterial smooth muscle: participation of cellular signaling pathways

Activation of NF‐κB by ER stress requires both Ca²⁺ and reactive oxygen intermediates as messengers

Contact Info

Product

Resources

About

Effects of H2O2 on Membrane-Potential and [Ca2+]i of Cultured Rat Arterial Smooth Muscle Cells

Cited by 53 publications

References 0 publications

Hydrogen peroxide-induced Ca2+mobilization in pulmonary arterial smooth muscle cells

Hydrogen peroxide-induced Ca2+mobilization in pulmonary arterial smooth muscle cells

Hydrogen peroxide induces contraction and raises [Ca2+]i in canine cerebral arterial smooth muscle: participation of cellular signaling pathways

Activation of NF‐κB by ER stress requires both Ca2+ and reactive oxygen intermediates as messengers

Contact Info

Product

Resources

About

Hydrogen peroxide-induced Ca²⁺mobilization in pulmonary arterial smooth muscle cells

Hydrogen peroxide-induced Ca²⁺mobilization in pulmonary arterial smooth muscle cells

Activation of NF‐κB by ER stress requires both Ca²⁺ and reactive oxygen intermediates as messengers