Vascular smooth muscle contraction evoked by cell volume modulation

Role of the cytoskeleton network

Svetlana V. Koltsova, Svetlana V. Gusakova, Yana J. Anfinogenova, Mikhail B. Baskakov, Sergei N. Orlov

Research output: Contribution to journalArticle

10 Citations (Scopus)

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 languageEnglish
Pages (from-to)29-36
Number of pages8
JournalCellular Physiology and Biochemistry
Volume21
Issue number1-3
DOIs
Publication statusPublished - 2008
Externally publishedYes

Fingerprint

Muscle Contraction
Cytoskeleton
Cell Size
Vascular Smooth Muscle
Actins
docetaxel
Actin Cytoskeleton
Smooth Muscle Myocytes
Tubulin Modulators
Cytochalasin B
Vinblastine
Colchicine
Thoracic Aorta
Fluorescence Microscopy
Osmolar Concentration
Endothelium
Research
Proteins

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 journalArticle

Koltsova, Svetlana V. ; Gusakova, Svetlana V. ; Anfinogenova, Yana J. ; Baskakov, Mikhail B. ; Orlov, Sergei N. / Vascular smooth muscle contraction evoked by cell volume modulation : Role of the cytoskeleton network. In: Cellular Physiology and Biochemistry. 2008 ; Vol. 21, No. 1-3. pp. 29-36.
@article{bf4871929acd425cbe4ce7e2f342710f,
title = "Vascular smooth muscle contraction evoked by cell volume modulation: Role of the cytoskeleton network",
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.",
keywords = "Cell volume, Contraction, Microfilaments, Microtubules, Smooth muscle",
author = "Koltsova, {Svetlana V.} and Gusakova, {Svetlana V.} and Anfinogenova, {Yana J.} and Baskakov, {Mikhail B.} and Orlov, {Sergei N.}",
year = "2008",
doi = "10.1159/000113744",
language = "English",
volume = "21",
pages = "29--36",
journal = "Cellular Physiology and Biochemistry",
issn = "1015-8987",
publisher = "S. Karger AG",
number = "1-3",

}

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

VL - 21

SP - 29

EP - 36

JO - Cellular Physiology and Biochemistry

JF - Cellular Physiology and Biochemistry

SN - 1015-8987

IS - 1-3

ER -