title: Sarcoplasmic reticulum Ca2+ release in neonatal rat cardiac myocytes.
abstract: In the neonatal mammalian heart, the role of ryanodine receptor (=Ca(2+) release channel)-mediated sarcoplasmic reticulum (SR) Ca(2+) release for excitation-contraction coupling is still a matter of debate. Using an adenoviral system, we overexpressed separately the junctional SR proteins triadin, junctin, and calsequestrin, which are probably involved in regulation of ryanodine receptor function. Infection of neonatal rat cardiac myocytes with triadin, junctin, or calsequestrin viruses, controlled by green fluorescent protein expression, resulted in an increased protein level of the corresponding transgenes. Measurement of Ca(2+) transients of infected cardiac myocytes revealed unchanged peak amplitudes under basal conditions but with overexpression of calsequestrin and triadin caffeine-releasable SR Ca(2+) content was increased. Our results demonstrate that an increased expression of triadin or calsequestrin is associated with an increased SR Ca(2+) storage but unchanged Ca(2+) signaling in neonatal rat cardiac myocytes. This is consistent with an ancillary role of the sarcoplasmic reticulum in excitation-contraction coupling in the developing mammalian heart.
authors.affiliation: Institut für Pharmakologie und Toxikologie, Medizinische Fakultät, Martin-Luther-Universität Halle-Wittenberg, 06112 Halle (Saale), Germany. ulrich.gergs@medizin.uni-halle.de
authors.forename: Ulrich
authors.initials: U
authors.lastname: Gergs
authors.forename: Uwe
authors.initials: U
authors.lastname: Kirchhefer
authors.forename: Jan
authors.initials: J
authors.lastname: Buskase
authors.forename: Katharina
authors.initials: K
authors.lastname: Kiele-Dunsche
authors.forename: Igor B
authors.initials: IB
authors.lastname: Buchwalow
authors.forename: Larry R
authors.initials: LR
authors.lastname: Jones
authors.forename: Wilhelm
authors.initials: W
authors.lastname: Schmitz
authors.forename: Otto
authors.initials: O
authors.lastname: Traub
authors.forename: Joachim
authors.initials: J
authors.lastname: Neumann
mesh_terms: D000256:Adenoviridae; D000818:Animals; D000831:Animals, Newborn; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000502:physiology; D002135:Calcium-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D002155:Calsequestrin / Q000235:genetics / Q000378:metabolism; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D056966:Excitation Contraction Coupling / Q000187:drug effects / Q000502:physiology*; D005786:Gene Expression Regulation; D005822:Genetic Vectors; D006321:Heart / Q000187:drug effects / Q000502:physiology; D017136:Ion Transport / Q000187:drug effects / Q000502:physiology*; D009124:Muscle Proteins / Q000235:genetics / Q000378:metabolism; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D011993:Recombinant Fusion Proteins / Q000235:genetics / Q000378:metabolism; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000187:drug effects* / Q000378:metabolism*; D014161:Transduction, Genetic
chemical_list: D002135:Calcium-Binding Proteins; D002155:Calsequestrin; D002352:Carrier Proteins; D009124:Muscle Proteins; D011993:Recombinant Fusion Proteins; D019837:Ryanodine Receptor Calcium Release Channel; C070048:triadin; D002110:Caffeine; D002118:Calcium