Smooth muscle cell response to mechanical injury involves intracellular calcium release and ERK1/ERK2 phosphorylation
(2001) In Experimental Cell Research 269(1). p.88-96- Abstract
- 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... (More)
- 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1120806
- author
- Moses, Sara LU ; Dreja, Karl LU ; Lindqvist, Anders LU ; Lövdahl, Cecilia ; Hellstrand, Per LU and Hultgårdh, Anna LU
- organization
- publishing date
- 2001
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- smooth muscle cells, Ca2+, ERK1/2, injury, migration, proliferation
- in
- Experimental Cell Research
- volume
- 269
- issue
- 1
- pages
- 88 - 96
- publisher
- Academic Press
- external identifiers
-
- pmid:11525642
- scopus:0035840152
- ISSN
- 1090-2422
- DOI
- 10.1006/excr.2001.5308
- language
- English
- LU publication?
- yes
- id
- 59e22287-25bf-430d-9512-72791d0a26e2 (old id 1120806)
- date added to LUP
- 2016-04-01 11:56:51
- date last changed
- 2022-04-21 00:09:07
@article{59e22287-25bf-430d-9512-72791d0a26e2,
abstract = {{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.}},
author = {{Moses, Sara and Dreja, Karl and Lindqvist, Anders and Lövdahl, Cecilia and Hellstrand, Per and Hultgårdh, Anna}},
issn = {{1090-2422}},
keywords = {{smooth muscle cells; Ca2+; ERK1/2; injury; migration; proliferation}},
language = {{eng}},
number = {{1}},
pages = {{88--96}},
publisher = {{Academic Press}},
series = {{Experimental Cell Research}},
title = {{Smooth muscle cell response to mechanical injury involves intracellular calcium release and ERK1/ERK2 phosphorylation}},
url = {{http://dx.doi.org/10.1006/excr.2001.5308}},
doi = {{10.1006/excr.2001.5308}},
volume = {{269}},
year = {{2001}},
}