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Overexpression of neuronal calcium sensor‐1 alters contractile function in adult rat ventricular myocytes
Author(s) -
Telemaque Sabine,
Liu Daniel SD,
Grain Terrie,
Liu MeeiYueh,
Liu S. Jesse
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1446-a
Subject(s) - myocyte , contraction (grammar) , calcium , medicine , stimulation , endocrinology , long term potentiation , chemistry , rest (music) , biology , receptor
Neuronal‐calcium sensor‐1 (NCS‐1), a small calcium binding protein, has been shown to interact with ion channels (including Ca channels) in neuronal cells. We have previously reported that NCS‐1 was also present in rat cardiomyocytes. The present study examined whether NCS‐1 overexpression in ventricular myocytes alters the contractile function. Isolated adult rat ventricular myocytes were infected with an adenovirus construct expressing NCS‐1 (MOI: 100). At 48 hours after infection, myocytes were rinsed with control culture medium, and cell shortening was elicited in normal Tyrode's solution with field stimulation. The kinetics of steady‐state cell shortening and the post‐rest potentiation were monitored, and compared with those of non‐infected time‐control myocytes. Our results show that the rise time (10–90% of time‐to‐peak) and half‐width (50% of duration) of cell shortening in NCS‐1‐infected cells were significantly reduced (31.1±0.9 and 57.3±2.3 ms vs. 37.5±1.5 and 68.7±2.8 ms in control cells, respectively, n=23 from 5 hearts). However, the decay time (10–90% of relaxation) was not significantly altered in the NCS‐1‐infected cells. Post‐rest potentiation in NCS‐1 cells was significantly increased after a 60‐sec rest period (P=0.037, n=18), but not after a 30‐sec rest (P=0.076, n=22). Taken together, our data suggest that NCS‐1 alters the contractile function by facilitating contraction, with a slight alteration of sarcoplasmic reticular function in adult rat ventricular myocytes.