Calphostin C as a rapid and strong inducer of apoptosis in human coronary artery smooth muscle cells

Kristopher D. Krueger; William J. Hunter; Michael G. DelCore; Devendra K. Agrawal

doi:10.1016/S1567-5769(03)00206-6

Calphostin C as a rapid and strong inducer of apoptosis in human coronary artery smooth muscle cells

Kristopher D. Krueger, William J. Hunter, Michael G. DelCore, Devendra K. Agrawal

Department of Medicine

Research output: Contribution to journal › Article

7 Scopus citations

Abstract

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

Original language	English (US)
Pages (from-to)	1751-1759
Number of pages	9
Journal	International Immunopharmacology
Volume	3
Issue number	13-14
DOIs	https://doi.org/10.1016/S1567-5769(03)00206-6
State	Published - Dec 2003

All Science Journal Classification (ASJC) codes

Immunology and Allergy
Immunology
Pharmacology

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Krueger, K. D., Hunter, W. J., DelCore, M. G., & Agrawal, D. K. (2003). Calphostin C as a rapid and strong inducer of apoptosis in human coronary artery smooth muscle cells. International Immunopharmacology, 3(13-14), 1751-1759. https://doi.org/10.1016/S1567-5769(03)00206-6

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abstract = "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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