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β 2 ‐glycoprotein I protects J774A.1 macrophages and human coronary artery smooth muscle cells against apoptosis
Author(s) -
Lin KaeYuan,
Wang HsuehHsiao,
Lai ShiauTing,
Pan JuPin,
Chiang AnNa
Publication year - 2004
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20314
Subject(s) - apoptosis , vascular smooth muscle , nitric oxide , microbiology and biotechnology , chemistry , glycoprotein , programmed cell death , biology , smooth muscle , biochemistry , endocrinology
Abstract β 2 ‐Glycoprotein I (β 2 ‐GPI) is a plasma glycoprotein with multifactorial relevance to clinical consequences. It was previously indicated that β 2 ‐GPI can selectively bind to apoptotic cells. This study was designed to determine the role of β 2 ‐GPI in apoptosis. Using an immunohistochemical study, we observed that β 2 ‐GPI was co‐localized with the apoptotic macrophages and smooth muscle cells (SMCs) of human coronary arteries. The contribution of β 2 ‐GPI to apoptotic death was then investigated in vascular cells. Two nitric oxide (NO) donors, S ‐nitrosoglutathione (GSNO) and S ‐nitroso‐ N ‐acetyl penicillamine (SNAP) were used in this study to trigger apoptosis in J774A.1 macrophages and human coronary artery smooth muscle cells (HCASMC). Cell viability was significantly improved in β 2 ‐GPI‐treated cells. It was also possible to detect a remarkable inhibitory effect by β 2 ‐GPI on the NO‐induced apoptosis by preventing nuclear shrinkage. Furthermore, the NO‐induced apoptosis was associated with increase in caspase‐3 activity and in the protein levels of caspase‐3, c‐Fos, and c‐Jun. However, all these apoptosis‐related events were inhibited in vascular cells treated with 200 μg/ml β 2 ‐GPI. This is the first study to show that β 2 ‐GPI may be important in the prevention of apoptosis in vascular cells. © 2004 Wiley‐Liss, Inc.