Temporal spatial expression and function of non-muscle myosin II isoforms IIA and IIB in scar remodeling

Jennifer E. Bond, Trung Ho, Maria Angelica Selim, Cedric L. Hunter, Edith V. Bowers, Howard Levinson

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Scar contracture is believed to be caused by the cell contractility during the remodeling phase of wound healing. Cell contractility is mediated by non-muscle myosin II (NMMII) and actin, but the temporal-spatial expression profile of NMMII isoforms A and B (IIA and IIB) during the remodeling phase and the role of NMMII in scar fibroblast tissue remodeling are unknown. Human scar tissue immunostained for IIA and IIB showed that both isoforms were highly expressed in scar tissue throughout the remodeling phase of repair and expression levels returned to normal after the remodeling phase. Human scar tissue immunostained for Β-, γ- and α-smooth muscle actin showed that all isoforms were consistently expressed throughout the remodeling phase of repair. The Β- and γ-smooth muscle actin were widely expressed throughout the dermis, but α-smooth muscle actin was only locally expressed within the dermis. In vitro, fibroblasts explanted from scar tissue were shown to express more IIA than fibroblasts explanted from normal tissue and scar fibroblasts contracted collagen lattices to a greater extent than normal fibroblasts. Blebbistatin was used to demonstrate the function of NMMII in collagen lattice contraction. In normal tissue, fibroblasts are stress-shielded from external tensile stress by the extracellular matrix. After dermal injury and during remodeling, fibroblasts are exposed to a matrix of increased stiffness. The effect of matrix stiffness on IIA and IIB expression was examined. IIA expression was greater in fibroblasts cultured in collagen lattices with increasing stiffness, and in fibroblasts cultured on glass slides compared with polyacrylamide gels with stiffness of 1 kPa. In conclusion, NMMII and actin isoform expression changes coordinately with the remodeling phase of repair, and NMMII is increased as matrix stiffness increases. As NMMII expression increases, so does the fibroblast contractility.

Original languageEnglish (US)
Pages (from-to)499-508
Number of pages10
JournalLaboratory Investigation
Volume91
Issue number4
DOIs
StatePublished - Apr 2011
Externally publishedYes

Fingerprint

Myosin Type II
Cicatrix
Protein Isoforms
Fibroblasts
Actins
Smooth Muscle
Collagen
Dermis
Contracture
Wound Healing
Glass
Extracellular Matrix

Keywords

  • non-muscle myosin II
  • scar contracture
  • tissue remodeling

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Cell Biology
  • Molecular Biology

Cite this

Temporal spatial expression and function of non-muscle myosin II isoforms IIA and IIB in scar remodeling. / Bond, Jennifer E.; Ho, Trung; Selim, Maria Angelica; Hunter, Cedric L.; Bowers, Edith V.; Levinson, Howard.

In: Laboratory Investigation, Vol. 91, No. 4, 04.2011, p. 499-508.

Research output: Contribution to journalArticle

Bond, Jennifer E. ; Ho, Trung ; Selim, Maria Angelica ; Hunter, Cedric L. ; Bowers, Edith V. ; Levinson, Howard. / Temporal spatial expression and function of non-muscle myosin II isoforms IIA and IIB in scar remodeling. In: Laboratory Investigation. 2011 ; Vol. 91, No. 4. pp. 499-508.
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