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Am J Physiol Heart Circ Physiol 270: H1462-H1468, 1996;
0363-6135/96 $5.00
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AJP - Heart and Circulatory Physiology, Vol 270, Issue 4 1462-H1468, Copyright © 1996 by American Physiological Society

ARTICLES

Cyclical strain increases monocyte chemotactic protein-1 secretion in human endothelial cells

B. S. Wung, J. J. Cheng, Y. J. Chao, J. Lin, Y. J. Shyy and D. L. Wang
Cardiovascular Division, Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, Republic of China.

The effects of mechanical strain on monocyte chemotactic protein-1 (MCP-1) secretion were examined on human endothelial cells (ECs) grown on a flexible membrane base. MCP-1 release into culture medium from strained ECs was demonstrated to be time and strain dose dependent. Northern blot analysis demonstrated a mainly serum-independent 1.8-fold induction of MCP-1 mRNA levels in ECs strained at 15 kPa compared with unstrained controls. ECs treated with actinomycin D abolished this strain-induced expression. Strained ECs at the periphery of wells showed higher MCP-1 gene expression than ECs at the center. Pretreatment of ECs with either cytochalasin D or phalloidin did not abolish strain-induced gene expression. ECs pretreated with stretch-activated ion channel blocker gadolinium or with ryanodine to deplete intracellular stored Ca2+ strongly inhibited the strain-induced MCP-1 levels. We conclude that 1) cyclical strain can modulate the secretion of MCP-1 in a dose-dependent manner, 2) strain-induced MCP-1 production is mediated by increasing MCP-1 mRNA levels via transcription, 3) cytoskeletal rearrangement is not essential for this strain-induced MCP-1 expression, and 4) both Ca2+ influx via stretch-activated ion channels and intracellular Ca2+ release contribute to the strain-induced effect. Such strain-induced MCP-1 secretion might contribute to the trapping of monocytes in the subendothelial space to initiate atherogenesis.


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