TY - JOUR
T1 - The involvement of Ca2+ and myosin light chain kinase in collagen-induced platelet activation
AU - Lokeshwar, Vinata B.
AU - Bourguignon, Lilly Y.W.
N1 - Funding Information:
We gratefully acknowledge Dr. Gerard J. Bourguignon's assistance in the preparation of this paper. We would also like to thank Ms. Silvia Fajardo for technical help during the course of these experiments. This work was supported in part by United states Public Health Services Grant GM 36353 and by grants from the American Heart Association (AHA) and American Lung Association (ALA). V.B. Lokeshwar is a postdoctoral fellow of AHA and L.Y.W. Bourguignon is an Established Investigator of AHA and ALA.
PY - 1992
Y1 - 1992
N2 - In this study we have used several complementary biochemical and immunological techniques to examine the involvement of Ca2+ and myosin light chain kinase in collagen-induced platelet activation. Our results indicate that collagen stimulates a rapid influx of external Ca2+ (within the first 1-5 min of treatment) which is followed by phosphorylation of myosin light chains (within 10 min of treatment) and granule secretion (within 15 min of treatment). In addition, we have found that certain Ca2+ channel entry blockers (e.g. nifedipine and bepridil) or calmodulin antagonists (e.g. W-7) specifically inhibit collagen-induced Ca2+ influx, myosin light chain phosphorylation and subsequent granule secretion. These data suggest that Ca2+/calmodulin-dependent myosin light chain kinase-mediated myosin light chain phosphorylation is necessary for regulating the actomyosin-related contractility required for normal platelet function.
AB - In this study we have used several complementary biochemical and immunological techniques to examine the involvement of Ca2+ and myosin light chain kinase in collagen-induced platelet activation. Our results indicate that collagen stimulates a rapid influx of external Ca2+ (within the first 1-5 min of treatment) which is followed by phosphorylation of myosin light chains (within 10 min of treatment) and granule secretion (within 15 min of treatment). In addition, we have found that certain Ca2+ channel entry blockers (e.g. nifedipine and bepridil) or calmodulin antagonists (e.g. W-7) specifically inhibit collagen-induced Ca2+ influx, myosin light chain phosphorylation and subsequent granule secretion. These data suggest that Ca2+/calmodulin-dependent myosin light chain kinase-mediated myosin light chain phosphorylation is necessary for regulating the actomyosin-related contractility required for normal platelet function.
UR - http://www.scopus.com/inward/record.url?scp=0026616948&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0026616948&partnerID=8YFLogxK
U2 - 10.1016/S0309-1651(06)80168-2
DO - 10.1016/S0309-1651(06)80168-2
M3 - Article
C2 - 1423657
AN - SCOPUS:0026616948
SN - 0309-1651
VL - 16
SP - 883
EP - 897
JO - Cell Biology International Reports
JF - Cell Biology International Reports
IS - 9
ER -