Abstract
Previously, we reported that hyposmotic swelling evoked transient vascular smooth muscle cell (SMC) contraction that was completely abolished by L-type Ca2+ channel blockers. In contrast, sustained contraction revealed in hyper- and isoosmotically-shrunken SMCs was insensitive to L-type channel blockers and was diminished in Ca2+-free medium by only 30-50%. Several research groups reported cell volume-dependent cytoskeleton network rearrangements. This study examines the role of cytoskeleton proteins in cell volume-dependent contraction of endothelium-denuded vascular smooth muscle rings (VSMR) from the rat thoracic aorta. Hyperosmotic shrinkage and hyposmotic swelling were triggered by modulation of medium osmolality; isosmotic shrinkage was induced by VSMR transfer from hypo- to isosmotic medium. The relative content of globular (G) and fibrillar (F) actin was estimated by fluorescence microscopy. Hyperosmotic shrinkage and hyposmotic swelling led to elevation of the F-actin/G-actin ratio by 2.5- and 1.8-fold respectively. Contraction of shrunken and swollen VSMR was insensitive to modulators of microtubules such as vinblastine, colchicine and docetaxel. Microfilament disassembly by cytochalasin B resulted in dramatic attenuation of the maximal amplitude of contraction of hyperosmotically-shrunken and hyposmotically-swollen VSMR, and almost completely abolished the contraction triggered by isosmotic shrinkage. These data suggest that both L-type Ca2+ channel-mediated contraction of swollen vascular SMC and Ca2+ o-insensitive contractions of shrunken cells are triggered by reorganization of the microfilament network caused by elevation of the F-actin/G-actin ratio.
| Original language | English |
|---|---|
| Pages (from-to) | 29-36 |
| Number of pages | 8 |
| Journal | Cellular Physiology and Biochemistry |
| Volume | 21 |
| Issue number | 1-3 |
| DOIs | |
| Publication status | Published - 2008 |
| Externally published | Yes |
Fingerprint
Keywords
- Cell volume
- Contraction
- Microfilaments
- Microtubules
- Smooth muscle
ASJC Scopus subject areas
- Physiology
- Cell Biology
Cite this
Vascular smooth muscle contraction evoked by cell volume modulation : Role of the cytoskeleton network. / Koltsova, Svetlana V.; Gusakova, Svetlana V.; Anfinogenova, Yana J.; Baskakov, Mikhail B.; Orlov, Sergei N.
In: Cellular Physiology and Biochemistry, Vol. 21, No. 1-3, 2008, p. 29-36.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Vascular smooth muscle contraction evoked by cell volume modulation
T2 - Role of the cytoskeleton network
AU - Koltsova, Svetlana V.
AU - Gusakova, Svetlana V.
AU - Anfinogenova, Yana J.
AU - Baskakov, Mikhail B.
AU - Orlov, Sergei N.
PY - 2008
Y1 - 2008
N2 - Previously, we reported that hyposmotic swelling evoked transient vascular smooth muscle cell (SMC) contraction that was completely abolished by L-type Ca2+ channel blockers. In contrast, sustained contraction revealed in hyper- and isoosmotically-shrunken SMCs was insensitive to L-type channel blockers and was diminished in Ca2+-free medium by only 30-50%. Several research groups reported cell volume-dependent cytoskeleton network rearrangements. This study examines the role of cytoskeleton proteins in cell volume-dependent contraction of endothelium-denuded vascular smooth muscle rings (VSMR) from the rat thoracic aorta. Hyperosmotic shrinkage and hyposmotic swelling were triggered by modulation of medium osmolality; isosmotic shrinkage was induced by VSMR transfer from hypo- to isosmotic medium. The relative content of globular (G) and fibrillar (F) actin was estimated by fluorescence microscopy. Hyperosmotic shrinkage and hyposmotic swelling led to elevation of the F-actin/G-actin ratio by 2.5- and 1.8-fold respectively. Contraction of shrunken and swollen VSMR was insensitive to modulators of microtubules such as vinblastine, colchicine and docetaxel. Microfilament disassembly by cytochalasin B resulted in dramatic attenuation of the maximal amplitude of contraction of hyperosmotically-shrunken and hyposmotically-swollen VSMR, and almost completely abolished the contraction triggered by isosmotic shrinkage. These data suggest that both L-type Ca2+ channel-mediated contraction of swollen vascular SMC and Ca2+ o-insensitive contractions of shrunken cells are triggered by reorganization of the microfilament network caused by elevation of the F-actin/G-actin ratio.
AB - Previously, we reported that hyposmotic swelling evoked transient vascular smooth muscle cell (SMC) contraction that was completely abolished by L-type Ca2+ channel blockers. In contrast, sustained contraction revealed in hyper- and isoosmotically-shrunken SMCs was insensitive to L-type channel blockers and was diminished in Ca2+-free medium by only 30-50%. Several research groups reported cell volume-dependent cytoskeleton network rearrangements. This study examines the role of cytoskeleton proteins in cell volume-dependent contraction of endothelium-denuded vascular smooth muscle rings (VSMR) from the rat thoracic aorta. Hyperosmotic shrinkage and hyposmotic swelling were triggered by modulation of medium osmolality; isosmotic shrinkage was induced by VSMR transfer from hypo- to isosmotic medium. The relative content of globular (G) and fibrillar (F) actin was estimated by fluorescence microscopy. Hyperosmotic shrinkage and hyposmotic swelling led to elevation of the F-actin/G-actin ratio by 2.5- and 1.8-fold respectively. Contraction of shrunken and swollen VSMR was insensitive to modulators of microtubules such as vinblastine, colchicine and docetaxel. Microfilament disassembly by cytochalasin B resulted in dramatic attenuation of the maximal amplitude of contraction of hyperosmotically-shrunken and hyposmotically-swollen VSMR, and almost completely abolished the contraction triggered by isosmotic shrinkage. These data suggest that both L-type Ca2+ channel-mediated contraction of swollen vascular SMC and Ca2+ o-insensitive contractions of shrunken cells are triggered by reorganization of the microfilament network caused by elevation of the F-actin/G-actin ratio.
KW - Cell volume
KW - Contraction
KW - Microfilaments
KW - Microtubules
KW - Smooth muscle
UR - http://www.scopus.com/inward/record.url?scp=38349170448&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=38349170448&partnerID=8YFLogxK
U2 - 10.1159/000113744
DO - 10.1159/000113744
M3 - Article
C2 - 18209469
AN - SCOPUS:38349170448
VL - 21
SP - 29
EP - 36
JO - Cellular Physiology and Biochemistry
JF - Cellular Physiology and Biochemistry
SN - 1015-8987
IS - 1-3
ER -