TY - JOUR
T1 - Calphostin C as a rapid and strong inducer of apoptosis in human coronary artery smooth muscle cells
AU - Krueger, Kristopher D.
AU - Hunter, William J.
AU - DelCore, Michael G.
AU - Agrawal, Devendra K.
N1 - Funding Information:
This work was supported by a grant from the Nebraska Department of Health, Cancer and Smoking-related Diseases Research Program.
PY - 2003/12
Y1 - 2003/12
N2 - Vascular smooth muscle cells (VSMCs) play a major role in the development of atherosclerotic and restenotic lesions. The apoptotic process has been implicated in the development of this pathology. In this study, we characterized the induction of apoptosis by calphostin C (CC), a protein kinase C (PKC) inhibitor, in primary human coronary artery smooth muscle cells in the presence and absence of insulin-like growth factor-I (IGF-I). Additionally, we investigated the signal transduction pathways important for IGF-I mediated protection. Calphostin C induced apoptosis, as measured by terminal deoxy-UTP nick-end labeling (TUNEL), in a time- and dose-dependent manner, approaching 20% within 6 h of 50 nM calphostin C treatment. The amount of apoptosis increased to 44.58±8.08%, 47.54±1.66% and 78.1±11.9% after 8, 10 and 12 h of treatment, respectively (p
AB - Vascular smooth muscle cells (VSMCs) play a major role in the development of atherosclerotic and restenotic lesions. The apoptotic process has been implicated in the development of this pathology. In this study, we characterized the induction of apoptosis by calphostin C (CC), a protein kinase C (PKC) inhibitor, in primary human coronary artery smooth muscle cells in the presence and absence of insulin-like growth factor-I (IGF-I). Additionally, we investigated the signal transduction pathways important for IGF-I mediated protection. Calphostin C induced apoptosis, as measured by terminal deoxy-UTP nick-end labeling (TUNEL), in a time- and dose-dependent manner, approaching 20% within 6 h of 50 nM calphostin C treatment. The amount of apoptosis increased to 44.58±8.08%, 47.54±1.66% and 78.1±11.9% after 8, 10 and 12 h of treatment, respectively (p
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U2 - 10.1016/S1567-5769(03)00206-6
DO - 10.1016/S1567-5769(03)00206-6
M3 - Article
C2 - 14636826
AN - SCOPUS:0242628283
VL - 3
SP - 1751
EP - 1759
JO - International Immunopharmacology
JF - International Immunopharmacology
SN - 1567-5769
IS - 13-14
ER -