Nonmuscle myosin, force maintenance, and the tonic contractile phenotype in smooth muscle

Albert Y. Rhee, Ozgur Ogut, Frank V. Brozovich

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Recent studies have demonstrated that nonmuscle (NM) myosin II forms filaments and can generate and maintain force in smooth muscle tissue [Lofgren et al. (2003) J Gen Physiol 121:301-310; Morano et al. (2000) Nat Cell Biol 2:371-375]. To further investigate the mechanical contribution of NM myosin to force maintenance during smooth muscle contraction, we utilized a selective inhibitor of the NM myosin ATPase, blebbistatin [Straight et al. (2003) Science 299:1743-1747]. Force and myosin light chain (MLC 20) phosphorylation were measured during KCl stimulation of small strips of intact mouse bladder and aorta at 22°C. The bladder strips contracted with a typical phasic force response, characterized by a large, rapid, transient increase in force followed by a decline to a lower, steady-state level. The addition of blebbistatin did not alter the peak force, but decreased force maintenance. KCl depolarization of aortic strips resulted in a tonic contraction; force increased to a sustained steady state. Similar to the bladder tissue, blebbistatin substantially decreased the steady-state force in the aorta. Blebbistatin did not influence the MLC 20 phosphorylation transient in either tissue type. Additionally, blebbistatin did not change the maximum shortening velocity (V max) during KCl depolarization of the aorta. Our results also suggest that NMIIA and NMIIB isoforms are differentially expressed. The expression of NMIIA is more prominent in the bladder, while NMIIB expression is predominant in the aorta. These results suggest that NM myosin contributes to the mechanism of force maintenance in smooth muscle, and could suggest that the expression of NMIIB is a factor for determining the tonic contractile phenotype.

Original languageEnglish (US)
Pages (from-to)766-774
Number of pages9
JournalPflugers Archiv European Journal of Physiology
Volume452
Issue number6
DOIs
StatePublished - Sep 2006

Fingerprint

Myosins
Smooth Muscle
Muscle
Maintenance
Aorta
Phenotype
Urinary Bladder
Phosphorylation
Depolarization
Tissue
Myosin Type II
Myosin Light Chains
Muscle Contraction
Protein Isoforms
blebbistatin
Muscles

Keywords

  • Blebbistatin
  • Latch
  • MLC phosphorylation
  • Myosin
  • Shortening velocity

ASJC Scopus subject areas

  • Physiology

Cite this

Nonmuscle myosin, force maintenance, and the tonic contractile phenotype in smooth muscle. / Rhee, Albert Y.; Ogut, Ozgur; Brozovich, Frank V.

In: Pflugers Archiv European Journal of Physiology, Vol. 452, No. 6, 09.2006, p. 766-774.

Research output: Contribution to journalArticle

Rhee, Albert Y. ; Ogut, Ozgur ; Brozovich, Frank V. / Nonmuscle myosin, force maintenance, and the tonic contractile phenotype in smooth muscle. In: Pflugers Archiv European Journal of Physiology. 2006 ; Vol. 452, No. 6. pp. 766-774.
@article{a281e01f61a1481ba5c91622ce493bb8,
title = "Nonmuscle myosin, force maintenance, and the tonic contractile phenotype in smooth muscle",
abstract = "Recent studies have demonstrated that nonmuscle (NM) myosin II forms filaments and can generate and maintain force in smooth muscle tissue [Lofgren et al. (2003) J Gen Physiol 121:301-310; Morano et al. (2000) Nat Cell Biol 2:371-375]. To further investigate the mechanical contribution of NM myosin to force maintenance during smooth muscle contraction, we utilized a selective inhibitor of the NM myosin ATPase, blebbistatin [Straight et al. (2003) Science 299:1743-1747]. Force and myosin light chain (MLC 20) phosphorylation were measured during KCl stimulation of small strips of intact mouse bladder and aorta at 22°C. The bladder strips contracted with a typical phasic force response, characterized by a large, rapid, transient increase in force followed by a decline to a lower, steady-state level. The addition of blebbistatin did not alter the peak force, but decreased force maintenance. KCl depolarization of aortic strips resulted in a tonic contraction; force increased to a sustained steady state. Similar to the bladder tissue, blebbistatin substantially decreased the steady-state force in the aorta. Blebbistatin did not influence the MLC 20 phosphorylation transient in either tissue type. Additionally, blebbistatin did not change the maximum shortening velocity (V max) during KCl depolarization of the aorta. Our results also suggest that NMIIA and NMIIB isoforms are differentially expressed. The expression of NMIIA is more prominent in the bladder, while NMIIB expression is predominant in the aorta. These results suggest that NM myosin contributes to the mechanism of force maintenance in smooth muscle, and could suggest that the expression of NMIIB is a factor for determining the tonic contractile phenotype.",
keywords = "Blebbistatin, Latch, MLC phosphorylation, Myosin, Shortening velocity",
author = "Rhee, {Albert Y.} and Ozgur Ogut and Brozovich, {Frank V.}",
year = "2006",
month = "9",
doi = "10.1007/s00424-006-0091-4",
language = "English (US)",
volume = "452",
pages = "766--774",
journal = "Pfl{\"u}gers Archiv - European Journal of Physiology",
issn = "0031-6768",
publisher = "Springer Verlag",
number = "6",

}

TY - JOUR

T1 - Nonmuscle myosin, force maintenance, and the tonic contractile phenotype in smooth muscle

AU - Rhee, Albert Y.

AU - Ogut, Ozgur

AU - Brozovich, Frank V.

PY - 2006/9

Y1 - 2006/9

N2 - Recent studies have demonstrated that nonmuscle (NM) myosin II forms filaments and can generate and maintain force in smooth muscle tissue [Lofgren et al. (2003) J Gen Physiol 121:301-310; Morano et al. (2000) Nat Cell Biol 2:371-375]. To further investigate the mechanical contribution of NM myosin to force maintenance during smooth muscle contraction, we utilized a selective inhibitor of the NM myosin ATPase, blebbistatin [Straight et al. (2003) Science 299:1743-1747]. Force and myosin light chain (MLC 20) phosphorylation were measured during KCl stimulation of small strips of intact mouse bladder and aorta at 22°C. The bladder strips contracted with a typical phasic force response, characterized by a large, rapid, transient increase in force followed by a decline to a lower, steady-state level. The addition of blebbistatin did not alter the peak force, but decreased force maintenance. KCl depolarization of aortic strips resulted in a tonic contraction; force increased to a sustained steady state. Similar to the bladder tissue, blebbistatin substantially decreased the steady-state force in the aorta. Blebbistatin did not influence the MLC 20 phosphorylation transient in either tissue type. Additionally, blebbistatin did not change the maximum shortening velocity (V max) during KCl depolarization of the aorta. Our results also suggest that NMIIA and NMIIB isoforms are differentially expressed. The expression of NMIIA is more prominent in the bladder, while NMIIB expression is predominant in the aorta. These results suggest that NM myosin contributes to the mechanism of force maintenance in smooth muscle, and could suggest that the expression of NMIIB is a factor for determining the tonic contractile phenotype.

AB - Recent studies have demonstrated that nonmuscle (NM) myosin II forms filaments and can generate and maintain force in smooth muscle tissue [Lofgren et al. (2003) J Gen Physiol 121:301-310; Morano et al. (2000) Nat Cell Biol 2:371-375]. To further investigate the mechanical contribution of NM myosin to force maintenance during smooth muscle contraction, we utilized a selective inhibitor of the NM myosin ATPase, blebbistatin [Straight et al. (2003) Science 299:1743-1747]. Force and myosin light chain (MLC 20) phosphorylation were measured during KCl stimulation of small strips of intact mouse bladder and aorta at 22°C. The bladder strips contracted with a typical phasic force response, characterized by a large, rapid, transient increase in force followed by a decline to a lower, steady-state level. The addition of blebbistatin did not alter the peak force, but decreased force maintenance. KCl depolarization of aortic strips resulted in a tonic contraction; force increased to a sustained steady state. Similar to the bladder tissue, blebbistatin substantially decreased the steady-state force in the aorta. Blebbistatin did not influence the MLC 20 phosphorylation transient in either tissue type. Additionally, blebbistatin did not change the maximum shortening velocity (V max) during KCl depolarization of the aorta. Our results also suggest that NMIIA and NMIIB isoforms are differentially expressed. The expression of NMIIA is more prominent in the bladder, while NMIIB expression is predominant in the aorta. These results suggest that NM myosin contributes to the mechanism of force maintenance in smooth muscle, and could suggest that the expression of NMIIB is a factor for determining the tonic contractile phenotype.

KW - Blebbistatin

KW - Latch

KW - MLC phosphorylation

KW - Myosin

KW - Shortening velocity

UR - http://www.scopus.com/inward/record.url?scp=33748375128&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33748375128&partnerID=8YFLogxK

U2 - 10.1007/s00424-006-0091-4

DO - 10.1007/s00424-006-0091-4

M3 - Article

VL - 452

SP - 766

EP - 774

JO - Pflügers Archiv - European Journal of Physiology

JF - Pflügers Archiv - European Journal of Physiology

SN - 0031-6768

IS - 6

ER -