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Status: Bibliographieeintrag

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Verfasst von:Sproßmann, Franz [VerfasserIn]   i
 Pankert, Patrick [VerfasserIn]   i
 Sausbier, Ulrike [VerfasserIn]   i
 Wirth, Angela [VerfasserIn]   i
 Zhou, Xiao-Bo [VerfasserIn]   i
 Madlung, Johannes [VerfasserIn]   i
 Zhao, Hong [VerfasserIn]   i
 Bucurenciu, Iancu [VerfasserIn]   i
 Jakob, Andreas [VerfasserIn]   i
 Lamkemeyer, Tobias [VerfasserIn]   i
 Neuhuber, Winfried [VerfasserIn]   i
 Offermanns, Stefan [VerfasserIn]   i
 Shipston, Michael J. [VerfasserIn]   i
 Korth, Michael [VerfasserIn]   i
 Nordheim, Alfred [VerfasserIn]   i
 Ruth, Peter [VerfasserIn]   i
 Sausbier, Matthias [VerfasserIn]   i
Titel:Inducible knockout mutagenesis reveals compensatorymechanisms elicited by constitutive BK channeldeficiency in overactive murine bladder
Verf.angabe:Franz Sprossmann, Patrick Pankert, Ulrike Sausbier, Angela Wirth, Xiao-Bo Zhou, Johannes Madlung, Hong Zhao, Iancu Bucurenciu, Andreas Jakob, Tobias Lamkemeyer, Winfried Neuhuber, Stefan Offermanns, Michael J. Shipston, Michael Korth, Alfred Nordheim, Peter Ruth and Matthias Sausbier
E-Jahr:2009
Jahr:25 February 2009
Umfang:18 S.
Fussnoten:Gesehen am 11.11.2019
Titel Quelle:Enthalten in: Vereinigung der Europäischen Biochemischen GesellschaftenThe FEBS journal
Ort Quelle:Oxford [u.a.] : Wiley-Blackwell, 2005
Jahr Quelle:2009
Band/Heft Quelle:276(2009), 6, Seite 1680-1697
ISSN Quelle:1742-4658
Abstract:The large-conductance, voltage-dependent and Ca2+-dependent K+ (BK) channel links membrane depolarization and local increases in cytosolic free Ca2+ to hyperpolarizing K+ outward currents, thereby controlling smooth muscle contractility. Constitutive deletion of the BK channel in mice (BK−/−) leads to an overactive bladder associated with increased intravesical pressure and frequent micturition, which has been revealed to be a result of detrusor muscle hyperexcitability. Interestingly, time-dependent and smooth muscle-specific deletion of the BK channel (SM-BK−/−) caused a more severe phenotype than displayed by constitutive BK−/− mice, suggesting that compensatory pathways are active in the latter. In detrusor muscle of BK−/− but not SM-BK−/− mice, we found reduced L-type Ca2+ current density and increased expression of cAMP kinase (protein kinase A; PKA), as compared with control mice. Increased expression of PKA in BK−/− mice was accompanied by enhanced β-adrenoceptor/cAMP-mediated suppression of contractions by isoproterenol. This effect was attenuated by about 60-70% in SM-BK−/− mice. However, the Rp isomer of adenosine-3′,5′-cyclic monophosphorothioate, a blocker of PKA, only partially inhibited enhanced cAMP signaling in BK−/− detrusor muscle, suggesting the existence of additional compensatory pathways. To this end, proteome analysis of BK−/− urinary bladder tissue was performed, and revealed additional compensatory regulated proteins. Thus, constitutive and inducible deletion of BK channel activity unmasks compensatory mechanisms that are relevant for urinary bladder relaxation.
DOI:doi:10.1111/j.1742-4658.2009.06900.x
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1111/j.1742-4658.2009.06900.x
 Volltext: https://febs.onlinelibrary.wiley.com/doi/abs/10.1111/j.1742-4658.2009.06900.x
 DOI: https://doi.org/10.1111/j.1742-4658.2009.06900.x
Datenträger:Online-Ressource
Sprache:eng
Bibliogr. Hinweis:Erscheint auch als : Druck-Ausgabe: Inducible knockout mutagenesis reveals compensatorymechanisms elicited by constitutive BK channeldeficiency in overactive murine bladder. - 2009
Sach-SW:cAMP/PKA signaling
 overactive urinary bladder
 proteomic adaptation
 smooth muscle-specific BK channel knockout mice
 time-dependent BK channel deletion
K10plus-PPN:1681559455
Verknüpfungen:→ Zeitschrift

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