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On the fate of skeletal myoblasts in a cardiac environment: down‐regulation of voltage‐gated ion channels
Author(s) -
Ott H. C.,
Berjukow S.,
Marksteiner R.,
Margreiter E.,
Böck G.,
Laufer G.,
Hering S.
Publication year - 2004
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.060186
Subject(s) - myocyte , ion channel , skeletal muscle , voltage gated ion channel , chemistry , microbiology and biotechnology , biophysics , medicine , biology , biochemistry , receptor
We have analysed the voltage‐gated ion channels and fusion competence of skeletal muscle myoblasts labelled with green fluorescent protein (GFP) and the membrane dye PKH transplanted into the infarcted myocardium of syngenic rats. After cell transplantation the animals were killed and GFP + –PKH + myoblasts enzymatically isolated for subsequent studies of ionic currents through voltage‐gated sodium, calcium and potassium channels. A down‐regulation of all three types of ion channels after engraftment was observed. The fraction of cells with calcium (68%) and sodium channels (65%) declined to zero within 24 h and 1 week, respectively. Down‐regulation of potassium currents (90% in control) occurred within 2 weeks to about 30%. Before injection myoblasts expressed predominantly transient outward potassium channels whereas after isolation from the myocardium exclusively rapid delayed rectifier channels. The currents recovered completely between 1 and 6 weeks under cell culture conditions. The down‐regulation of ion channels and changes in potassium current kinetics suggest that the environment provided by infarcted myocardium affects expression of voltage‐gated ion channels of skeletal myoblasts.