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Distinct roles of PMCA isoforms in Ca2+ homeostasis of bladder smooth muscle: evidence from PMCA gene-ablated mice.

Distinct roles of PMCA isoforms in Ca2+ homeostasis of bladder smooth muscle: evidence from PMCA gene-ablated mice. Research Abstract Details 

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  • Distinct roles of PMCA isoforms in Ca2+ homeostasis of bladder smooth muscle: evidence from PMCA gene-ablated mice. Abstract Text:

    li liuLi Liu,yukisato ishidaYukisato Ishida,gbolahan okunadeGbolahan Okunade,gail j pyne-geithmanGail J Pyne-Geithman,gary e shullGary E Shull,richard j paulRichard J Paul,

    We previously showed that plasma membrane Ca(2+)-ATPase (PMCA) activity accounted for 25-30% of relaxation in bladder smooth muscle (8). Among the four PMCA isoforms only PMCA1 and PMCA4 are expressed in smooth muscle. To address the role of these isoforms, we measured cytosolic Ca(2+) ([Ca(2+)](i)) using fura-PE3 and simultaneously measured contractility in bladder smooth muscle from wild-type (WT), Pmca1(+/-), Pmca4(+/-), Pmca4(-/-), and Pmca1(+/-)Pmca4(-/-) mice. There were no differences in basal [Ca(2+)](i) values between bladder preparations. KCl (80 mM) elicited both larger forces (150-190%) and increases in [Ca(2+)](i) (130-180%) in smooth muscle from Pmca1(+/-) and Pmca1(+/-)Pmca4(-/-) bladders than those in WT or Pmca4(-/-). The responses to carbachol (CCh: 10 muM) were also greater in Pmca1(+/-) (120-150%) than in WT bladders. In contrast, the responses in Pmca4(-/-) and Pmca1(+/-)Pmca4(-/-) bladders to CCh were significantly smaller (40-50%) than WT. The rise in half-times of force and [Ca(2+)](i) increases in response to KCl and CCh, and the concomitant half-times of their decrease upon washout of agonist were prolonged in Pmca4(-/-) (130-190%) and Pmca1(+/-)Pmca4(-/-) (120-250%) bladders, but not in Pmca1(+/-) bladders with respect to WT. Our evidence indicates distinct isoform functions with the PMCA1 isoform involved in overall Ca(2+) clearance, while PMCA4 is essential for the [Ca(2+)](i) increase and contractile response to the CCh receptor-mediated signal transduction pathway.

    Distinct roles of PMCA isoforms in Ca2+ homeostasis of bladder smooth muscle: evidence from PMCA gene-ablated mice. Publishing Authors By Initials

    l liuL Liu,y ishidaY Ishida,g okunadeG Okunade,gj pyne-geithmanGJ Pyne-Geithman,ge shullGE Shull,rj paulRJ Paul,

    For similar urogenital system: urinary tract: urinary bladder research abstracts see: urogenital system: urinary tract: urinary bladder research

    PUBMED ID PMID:

    MEDLINE DATE:

    Distinct roles of PMCA isoforms in Ca2+ homeostasis of bladder smooth muscle: evidence from PMCA gene-ablated mice. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: American journal of physiology. Cell physiology

    VOLUME: 292

    Page Numbers: C423-31

    Journal Abbreviation: Am. J. Physiol., Cell Physiol.

    ISSN: 0363-6143

    DAY: 6

    MONTH: 09

    YEAR: 2006

    Distinct roles of PMCA isoforms in Ca2+ homeostasis of bladder smooth muscle: evidence from PMCA gene-ablated mice. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901225

    Distinct roles of PMCA isoforms in Ca2+ homeostasis of bladder smooth muscle: evidence from PMCA gene-ablated mice. Keywords Mesh Terms:

    KEYWORDS: Urinary Bladder

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Distinct roles of PMCA isoforms in Ca2+ homeostasis of bladder smooth muscle: evidence from PMCA gene-ablated mice. Information

    Substance Name: Plasma Membrane Calcium-Transporting ATP

    Registry Number: EC 3.6.3.8

    Grant and Affiliation Information for Distinct roles of PMCA isoforms in Ca2+ homeostasis of bladder smooth muscle: evidence from PMCA gene-ablated mice.

    AFFILIATION: Molecular and Cellular Physiology, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267-0576, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: HL 66044

    ACRONYM: HL

    MEDLINETA: Am J Physiol Cell Physiol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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