TRAIL promotes the survival,migration and proliferation of vascular smooth muscle cells |
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Authors: | Email author" target="_blank">P?SecchieroEmail author C?Zerbinati E?Rimondi F?Corallini D?Milani V?Grill G?Forti S?Capitani G?Zauli |
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Institution: | (1) Department of Morphology and Embryology, University of Ferrara, Via Fossato di Mortara 66, 44100 Ferrara, Italy;(2) Department of Normal Human Morphology, University of Trieste, Via Manzoni 16, 34138 Trieste, Italy;(3) Division of Cardiac Surgery, Cardiosurgery Complex Structure, Hospital Riuniti of Trieste , via di Cattinara, 34138 Trieste, Italy |
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Abstract: | Human and rat primary sub-cultured vascular smooth muscle cells (VSMCs) showed clear expression of the
death receptors TRAIL-R1 and TRAIL-R2; however, recombinant soluble TRAIL did not induce cell death when added to
these cells. TRAIL tended to protect rat VSMCs from apoptosis induced either by inflammatory cytokines tumor
necrosis factor- + interleukin-1 + interferon- or by prolonged serum withdrawal, and promoted a
significant increase in VSMC proliferation and migration. Of note, all the biological effects induced by TRAIL
were significantly inhibited by pharmacological inhibitors of the ERK pathway. Western blot analysis consistently
showed that TRAIL induced a significant activation of ERK1/2, and a much weaker phosphorylation of Akt, while it
did not affect the p38/MAPK pathway. Taken together, these data strengthen the notion that the TRAIL/TRAIL-R
system likely plays a role in the biology of the vascular system by affecting the survival, migration and
proliferation of VSMCs.Received 6 May 2004; received after revision 7 June 2004; accepted 8 June 2004 |
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Keywords: | VSMCs TRAIL signal transduction apoptosis migration proliferation |
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