The Experts below are selected from a list of 312 Experts worldwide ranked by ideXlab platform

Stephane N Hatem - One of the best experts on this subject based on the ideXlab platform.

  • serca2a controls the mode of agonist induced intracellular ca2 signal Transcription Factor NFAT and proliferation in human vascular smooth muscle cells
    Journal of Molecular and Cellular Cardiology, 2011
    Co-Authors: Regis Bobe, Lahouaria Hadri, Jose J Lopez, Yassine Sassi, Fabrice Atassi, Ioannis Karakikes, Lifan Liang, Isabelle Limon, Annemarie Lompre, Stephane N Hatem
    Abstract:

    In blood vessels, tone is maintained by agonist-induced cytosolic Ca 2+ oscillations of quiescent/ contractile vascular smooth muscle cells (VSMCs). However, in synthetic/proliferative VSMCs, Gq/phosphoinositide receptor-coupled agonists trigger a steady-state increase in cytosolic Ca 2+ followed by a Store Operated Calcium Entry (SOCE) which translates into activation of the proliferation-associated Transcription Factor NFAT. Here, we report that in human coronary artery smooth muscle cells (hCASMCs), the sarco/endoplasmic reticulum calcium ATPase type 2a (SERCA2a) expressed in the contractile form of the hCASMCs, controls the nature of the agonistinduced Ca 2+ transient and the resulting down-stream signaling pathway. Indeed, restoring SERCA2a expression by gene transfer in synthetic hCASMCs 1) increased Ca 2+ storage capacity; 2) modified agonist-induced IP3R Ca 2+ release from steady-state to oscillatory mode (the frequency of agonist-induced IP3R Ca 2+ signal was 11.66 ± 1.40/100 sec in SERCA2a-expressing cells (n=39) vs 1.37 ± 0.20/100 sec in control cell (n=45), p<0.01); 3) suppressed SOCE by preventing interactions between SR calcium sensor STIM1 and pore forming unit ORAI1; 4) inhibited calcium regulated Transcription Factor NFAT and its down-stream physiological function such as proliferation and migration. This study provides evidence for the first time that oscillatory and steady-state patterns of Ca 2+ transients have different effects on calcium-dependent physiological functions in smooth muscle cells.

  • SERCA2a controls the mode of agonist-induced intracellular Ca2+ signal, Transcription Factor NFAT and proliferation in human vascular smooth muscle cells.
    Journal of Molecular and Cellular Cardiology, 2010
    Co-Authors: Regis Bobe, Lahouaria Hadri, Jose J Lopez, Yassine Sassi, Fabrice Atassi, Ioannis Karakikes, Lifan Liang, Isabelle Limon, Annemarie Lompre, Stephane N Hatem
    Abstract:

    In blood vessels, tone is maintained by agonist-induced cytosolic Ca 2+ oscillations of quiescent/ contractile vascular smooth muscle cells (VSMCs). However, in synthetic/proliferative VSMCs, Gq/phosphoinositide receptor-coupled agonists trigger a steady-state increase in cytosolic Ca 2+ followed by a Store Operated Calcium Entry (SOCE) which translates into activation of the proliferation-associated Transcription Factor NFAT. Here, we report that in human coronary artery smooth muscle cells (hCASMCs), the sarco/endoplasmic reticulum calcium ATPase type 2a (SERCA2a) expressed in the contractile form of the hCASMCs, controls the nature of the agonistinduced Ca 2+ transient and the resulting down-stream signaling pathway. Indeed, restoring SERCA2a expression by gene transfer in synthetic hCASMCs 1) increased Ca 2+ storage capacity; 2) modified agonist-induced IP3R Ca 2+ release from steady-state to oscillatory mode (the frequency of agonist-induced IP3R Ca 2+ signal was 11.66 ± 1.40/100 sec in SERCA2a-expressing cells (n=39) vs 1.37 ± 0.20/100 sec in control cell (n=45), p

  • Mutation of δ-Sarcoglycan Is Associated with Ca2+-Dependent Vascular Remodeling in the Syrian Hamster
    American Journal of Pathology, 2007
    Co-Authors: Larissa Lipskaia, Stephane N Hatem, Caroline Pinet, Yves Fromes, Isabelle Cantaloube, Alain Coulombe, Annemarie Lompre
    Abstract:

    We examined whether mutation of the δ-sarcoglycan gene, which causes dilated cardiomyopathy, also alters the vascular smooth muscle cell (VSMC) phenotype and arterial function in the Syrian hamster CHF 147. Thoracic aorta media thickness showed marked variability in diseased hamsters with zones of atrophy and hypertrophied segments. CHF-147 VSMCs displayed a proliferating/“synthetic” phenotype characterized by the absence of the smooth muscle myosin heavy chain SM2, dystrophin, and Ca2+-handling proteins, and the presence of cyclin D1. In freshly isolated VSMCs from CHF 147 hamsters, voltage-independent basal Ca2+ channels showed enhanced activity similar to that in proliferating wild-type (WT) cells. The Transcription Factor NFAT (nuclear Factor of activated T cells) was spontaneously active in freshly isolated CHF 147 VSMCs, as in proliferating VSMCs from WT hamsters. Mibefradil inhibited B-type channels, NFAT activity, and VSMC proliferation. CHF 147 hamsters had abundant apoptotic cells distributed in patches along the aorta, and clusters of inactive mitochondria were observed in 25% of isolated CHF 147 cells, whereas no such clusters were seen in WT cells. In conclusion, mutation of the δ-sarcoglycan gene increases plasma membrane permeability to Ca2+, activates the Ca2+-regulated Transcription Factor NFAT, and leads to spontaneous mitochondrial aggregation, causing abnormal VSMC proliferation and apoptosis.

Jonathan G Murphy - One of the best experts on this subject based on the ideXlab platform.

Annemarie Lompre - One of the best experts on this subject based on the ideXlab platform.

  • serca2a controls the mode of agonist induced intracellular ca2 signal Transcription Factor NFAT and proliferation in human vascular smooth muscle cells
    Journal of Molecular and Cellular Cardiology, 2011
    Co-Authors: Regis Bobe, Lahouaria Hadri, Jose J Lopez, Yassine Sassi, Fabrice Atassi, Ioannis Karakikes, Lifan Liang, Isabelle Limon, Annemarie Lompre, Stephane N Hatem
    Abstract:

    In blood vessels, tone is maintained by agonist-induced cytosolic Ca 2+ oscillations of quiescent/ contractile vascular smooth muscle cells (VSMCs). However, in synthetic/proliferative VSMCs, Gq/phosphoinositide receptor-coupled agonists trigger a steady-state increase in cytosolic Ca 2+ followed by a Store Operated Calcium Entry (SOCE) which translates into activation of the proliferation-associated Transcription Factor NFAT. Here, we report that in human coronary artery smooth muscle cells (hCASMCs), the sarco/endoplasmic reticulum calcium ATPase type 2a (SERCA2a) expressed in the contractile form of the hCASMCs, controls the nature of the agonistinduced Ca 2+ transient and the resulting down-stream signaling pathway. Indeed, restoring SERCA2a expression by gene transfer in synthetic hCASMCs 1) increased Ca 2+ storage capacity; 2) modified agonist-induced IP3R Ca 2+ release from steady-state to oscillatory mode (the frequency of agonist-induced IP3R Ca 2+ signal was 11.66 ± 1.40/100 sec in SERCA2a-expressing cells (n=39) vs 1.37 ± 0.20/100 sec in control cell (n=45), p<0.01); 3) suppressed SOCE by preventing interactions between SR calcium sensor STIM1 and pore forming unit ORAI1; 4) inhibited calcium regulated Transcription Factor NFAT and its down-stream physiological function such as proliferation and migration. This study provides evidence for the first time that oscillatory and steady-state patterns of Ca 2+ transients have different effects on calcium-dependent physiological functions in smooth muscle cells.

  • SERCA2a controls the mode of agonist-induced intracellular Ca2+ signal, Transcription Factor NFAT and proliferation in human vascular smooth muscle cells.
    Journal of Molecular and Cellular Cardiology, 2010
    Co-Authors: Regis Bobe, Lahouaria Hadri, Jose J Lopez, Yassine Sassi, Fabrice Atassi, Ioannis Karakikes, Lifan Liang, Isabelle Limon, Annemarie Lompre, Stephane N Hatem
    Abstract:

    In blood vessels, tone is maintained by agonist-induced cytosolic Ca 2+ oscillations of quiescent/ contractile vascular smooth muscle cells (VSMCs). However, in synthetic/proliferative VSMCs, Gq/phosphoinositide receptor-coupled agonists trigger a steady-state increase in cytosolic Ca 2+ followed by a Store Operated Calcium Entry (SOCE) which translates into activation of the proliferation-associated Transcription Factor NFAT. Here, we report that in human coronary artery smooth muscle cells (hCASMCs), the sarco/endoplasmic reticulum calcium ATPase type 2a (SERCA2a) expressed in the contractile form of the hCASMCs, controls the nature of the agonistinduced Ca 2+ transient and the resulting down-stream signaling pathway. Indeed, restoring SERCA2a expression by gene transfer in synthetic hCASMCs 1) increased Ca 2+ storage capacity; 2) modified agonist-induced IP3R Ca 2+ release from steady-state to oscillatory mode (the frequency of agonist-induced IP3R Ca 2+ signal was 11.66 ± 1.40/100 sec in SERCA2a-expressing cells (n=39) vs 1.37 ± 0.20/100 sec in control cell (n=45), p

  • Mutation of δ-Sarcoglycan Is Associated with Ca2+-Dependent Vascular Remodeling in the Syrian Hamster
    American Journal of Pathology, 2007
    Co-Authors: Larissa Lipskaia, Stephane N Hatem, Caroline Pinet, Yves Fromes, Isabelle Cantaloube, Alain Coulombe, Annemarie Lompre
    Abstract:

    We examined whether mutation of the δ-sarcoglycan gene, which causes dilated cardiomyopathy, also alters the vascular smooth muscle cell (VSMC) phenotype and arterial function in the Syrian hamster CHF 147. Thoracic aorta media thickness showed marked variability in diseased hamsters with zones of atrophy and hypertrophied segments. CHF-147 VSMCs displayed a proliferating/“synthetic” phenotype characterized by the absence of the smooth muscle myosin heavy chain SM2, dystrophin, and Ca2+-handling proteins, and the presence of cyclin D1. In freshly isolated VSMCs from CHF 147 hamsters, voltage-independent basal Ca2+ channels showed enhanced activity similar to that in proliferating wild-type (WT) cells. The Transcription Factor NFAT (nuclear Factor of activated T cells) was spontaneously active in freshly isolated CHF 147 VSMCs, as in proliferating VSMCs from WT hamsters. Mibefradil inhibited B-type channels, NFAT activity, and VSMC proliferation. CHF 147 hamsters had abundant apoptotic cells distributed in patches along the aorta, and clusters of inactive mitochondria were observed in 25% of isolated CHF 147 cells, whereas no such clusters were seen in WT cells. In conclusion, mutation of the δ-sarcoglycan gene increases plasma membrane permeability to Ca2+, activates the Ca2+-regulated Transcription Factor NFAT, and leads to spontaneous mitochondrial aggregation, causing abnormal VSMC proliferation and apoptosis.

Regis Bobe - One of the best experts on this subject based on the ideXlab platform.

  • serca2a controls the mode of agonist induced intracellular ca2 signal Transcription Factor NFAT and proliferation in human vascular smooth muscle cells
    Journal of Molecular and Cellular Cardiology, 2011
    Co-Authors: Regis Bobe, Lahouaria Hadri, Jose J Lopez, Yassine Sassi, Fabrice Atassi, Ioannis Karakikes, Lifan Liang, Isabelle Limon, Annemarie Lompre, Stephane N Hatem
    Abstract:

    In blood vessels, tone is maintained by agonist-induced cytosolic Ca 2+ oscillations of quiescent/ contractile vascular smooth muscle cells (VSMCs). However, in synthetic/proliferative VSMCs, Gq/phosphoinositide receptor-coupled agonists trigger a steady-state increase in cytosolic Ca 2+ followed by a Store Operated Calcium Entry (SOCE) which translates into activation of the proliferation-associated Transcription Factor NFAT. Here, we report that in human coronary artery smooth muscle cells (hCASMCs), the sarco/endoplasmic reticulum calcium ATPase type 2a (SERCA2a) expressed in the contractile form of the hCASMCs, controls the nature of the agonistinduced Ca 2+ transient and the resulting down-stream signaling pathway. Indeed, restoring SERCA2a expression by gene transfer in synthetic hCASMCs 1) increased Ca 2+ storage capacity; 2) modified agonist-induced IP3R Ca 2+ release from steady-state to oscillatory mode (the frequency of agonist-induced IP3R Ca 2+ signal was 11.66 ± 1.40/100 sec in SERCA2a-expressing cells (n=39) vs 1.37 ± 0.20/100 sec in control cell (n=45), p<0.01); 3) suppressed SOCE by preventing interactions between SR calcium sensor STIM1 and pore forming unit ORAI1; 4) inhibited calcium regulated Transcription Factor NFAT and its down-stream physiological function such as proliferation and migration. This study provides evidence for the first time that oscillatory and steady-state patterns of Ca 2+ transients have different effects on calcium-dependent physiological functions in smooth muscle cells.

  • SERCA2a controls the mode of agonist-induced intracellular Ca2+ signal, Transcription Factor NFAT and proliferation in human vascular smooth muscle cells.
    Journal of Molecular and Cellular Cardiology, 2010
    Co-Authors: Regis Bobe, Lahouaria Hadri, Jose J Lopez, Yassine Sassi, Fabrice Atassi, Ioannis Karakikes, Lifan Liang, Isabelle Limon, Annemarie Lompre, Stephane N Hatem
    Abstract:

    In blood vessels, tone is maintained by agonist-induced cytosolic Ca 2+ oscillations of quiescent/ contractile vascular smooth muscle cells (VSMCs). However, in synthetic/proliferative VSMCs, Gq/phosphoinositide receptor-coupled agonists trigger a steady-state increase in cytosolic Ca 2+ followed by a Store Operated Calcium Entry (SOCE) which translates into activation of the proliferation-associated Transcription Factor NFAT. Here, we report that in human coronary artery smooth muscle cells (hCASMCs), the sarco/endoplasmic reticulum calcium ATPase type 2a (SERCA2a) expressed in the contractile form of the hCASMCs, controls the nature of the agonistinduced Ca 2+ transient and the resulting down-stream signaling pathway. Indeed, restoring SERCA2a expression by gene transfer in synthetic hCASMCs 1) increased Ca 2+ storage capacity; 2) modified agonist-induced IP3R Ca 2+ release from steady-state to oscillatory mode (the frequency of agonist-induced IP3R Ca 2+ signal was 11.66 ± 1.40/100 sec in SERCA2a-expressing cells (n=39) vs 1.37 ± 0.20/100 sec in control cell (n=45), p

Mark L Dellacqua - One of the best experts on this subject based on the ideXlab platform.