Differential Effects of Intravenous Anesthetics on PDGF-BB-Induced Vascular Smooth Muscle Cell Migration
Background: Intravenous anesthetics are used during the perioperative and/or postoperative period in critically ill patients. Vascular smooth muscle cells (VSMCs) play important roles in vascular injury repair or restenosis after intervention. We previously reported that platelet-derived growth fact...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Cell Physiol Biochem Press GmbH & Co KG
2014-06-01
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| Series: | Cellular Physiology and Biochemistry |
| Subjects: | |
| Online Access: | http://www.karger.com/Article/FullText/362961 |
| Summary: | Background: Intravenous anesthetics are used during the perioperative and/or postoperative period in critically ill patients. Vascular smooth muscle cells (VSMCs) play important roles in vascular injury repair or restenosis after intervention. We previously reported that platelet-derived growth factor (PDGF)-BB induces VSMC migration via extracellular signal-regulated kinase (ERK) and Akt in a VSMC line, A10 cells. In the present study, we investigated the effects of intravenous anesthetics on PDGF-BB-induced VSMC migration and the mechanism. Methods: VSMCs migration was assessed using Boyden chamber, and phosphorylation of each protein kinase was analyzed by Western blotting. Results: Propofol or midazolam but not ketamine or dexmedetomidine suppressed PDGF-BB-induced A10 cells migration in a concentration-dependent manner. The suppressive effects on migration were observed also in human aortic smooth muscle cells. Propofol or midazolam did not affect phosphorylation of PDGF receptor β in A10 cells. Propofol or midazolam failed to affect PDGF-BB-induced phosphorylation of ERK or Akt. On the other hand, propofol or midazolam attenuated PDGF-BB-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK), but did not affect phosphorylation of stress-activated protein kinase/c-Jun N-terminal kinase. Both ketamine and dexmedetomidine had no effect on the phosphorylation of p38 MAPK induced by PDGF-BB. Conclusion: These results strongly suggest that propofol or midazolam inhibits VSMC migration by PDGF-BB via suppression of p38 MAPK activation. Propofol or midazolam may affect VSMC function in critically ill patients. |
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| ISSN: | 1015-8987 1421-9778 |