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KMID : 0613820180280121516
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Journal of Life Science
2018 Volume.28 No. 12 p.1516 ~ p.1522
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Pathophysiological Regulation of Vascular Smooth Muscle Cells by Prostaglandin F2α-dependent Activation of Phospholipase C-β3
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Kang Ki-Ung
Oh Jun-Young
Lee Yun-Ha
Lee Hye-Sun
Jin Seo-Yeon
Bae Sun-Sik
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Abstract
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Atherosclerosis is an obstructive vessel disease mainly caused by chronic arterial inflammation to which the proliferation and migration of vascular smooth muscle cells (VSMCs) is the main pathological response. In the present study, the primary responsible inflammatory cytokine and its signaling pathway was investigated. The proliferation and migration of VSMCs was significantly enhanced by the prostaglandin F2α (PGF2α), while neither was affected by tumor necrosis factor α. Prostacyclin I2 was seen to enhance the proliferation of VSMCs while simultaneously suppressing their migration. Both prostaglandin D2 and prostaglandin E2 significantly enhanced the migration of VSMCs, however, proliferation was not affected by either of them. The proliferation and migration of VSMCs stimulated by PGF2α progressed in a dose-dependent manner; the EC50 value of both proliferation and migration was 0.1 μM. VSMCs highly expressed the phospholipase isoform C-β3 (PLC-β3) while others such as PLC-β1, PLC-β2, and PLC-β4 were not expressed. Inhibition of the PLCs by U73122 completely blocked the PGF2α-induced migration of VSMCs, and, in addition, silencing PLC-β3 significantly diminished the PGF2α-induced proliferation and migration of VSMCs. Given these results, we suggest that PGF2α plays a crucial role in the proliferation and migration of VSMCs, and activation of PLC-β3 could be involved in their PGF2α-dependent migration.
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KEYWORD
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Atherosclerosis, migration, proliferation, prostaglandin, VSMC
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