Smooth muscle cell response to mechanical injury involves intracellular calcium release and ERK1/ERK2 phosphorylation
Author
Summary, in English
We have investigated possible signaling pathways coupled to injury-induced ERK1/2 activation and the subsequent initiation of vascular rat smooth muscle cell migration and proliferation. Aortic smooth muscle cells were cultured to confluency and subjected to in vitro injury under serum-free conditions. In fluo-4-loaded cells, injury induced a rapid wave of intracellular Ca(2+) release that propagated about 200 microm in radius from the injured zone, reached a peak in about 20 s, and subsided to the baseline within 2 min. The wave was abolished by prior treatment with the sarcoplasmic reticulum ATPase inhibitor thapsigargin, but not by omission of extracellular Ca(2+). ERK1/2 activation reached a peak at 10 min after injury and was inhibited by the MEK1 inhibitor PD98059, as well as by thapsigargin, fluphenazine, genistein, and the Src inhibitor PP2. These inhibitors also reduced [(3)H]thymidine incorporation and migration of cells into the injured area determined at 48 h after injury. These results show that mechanical injury to vascular smooth muscle cells induces a Ca(2+) wave which is dependent on intracellular Ca(2+) release. Furthermore, the injury activates ERK1/2 phosphorylation as well as cell migration and replication.
Department/s
- Department of Experimental Medical Science
- Vascular Physiology
- Islet cell physiology
- Vessel Wall Biology
Publishing year
2001
Language
English
Pages
88-96
Publication/Series
Experimental Cell Research
Volume
269
Issue
1
Document type
Journal article
Publisher
Academic Press
Topic
- Cell and Molecular Biology
Keywords
- smooth muscle cells
- Ca2+
- ERK1/2
- injury
- migration
- proliferation
Status
Published
Research group
- Vascular Physiology
- Islet cell physiology
- Vessel Wall Biology
ISBN/ISSN/Other
- ISSN: 1090-2422