Sphingosylphosphorylcholine induces α-smooth muscle actin expression in human lung fibroblasts and fibroblast-mediated gel contraction via S1P 2 receptor and Rho/Rho-kinase pathway

X. Q. Wang, L. J. Mao, Q. H. Fang, T. Kobayashi, H. J. Kim, H. Sugiura, S. Kawasaki, S. Togo, K. Kamio, Xiang-de Liu, S. I. Rennard

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Chronic airway diseases like COPD and asthma are usually accompanied with airway fibrosis. Myofibroblasts, which are characterized by expression of smooth muscle actin (α-SMA), play an important role in a variety of developmental and pathological processes, including fibrosis and wound healing. Sphingosylphosphorylcholine (SPC), a sphingolipid metabolite, has been implicated in many physiological and pathological conditions. The current study tested the hypothesis that SPC may modulate tissue remodeling by affecting the expression of α-SMA in human fetal lung fibroblast (HFL-1) and fibroblast mediated gel contraction. The results show that SPC stimulates α-SMA expression in HFL-1 and augments HFL-1 mediated collagen gel contraction in a time- and concentration-dependent manner. The α-SMA protein expression and fibroblast gel contraction induced by SPC was not blocked by TGF-β1 neutralizing antibody. However, it was significantly blocked by S1P2 receptor antagonist JTE-013, the Rho-specific inhibitor C3 exoenzyme, and a Rho-kinase inhibitor Y-27632. These findings suggest that SPC stimulates α-SMA protein expression and HFL-1 mediated collagen gel contraction via S1P2 receptor and Rho/Rho kinase pathway, and by which mechanism, SPC may be involved in lung tissue remodeling.

Original languageEnglish (US)
Pages (from-to)23-30
Number of pages8
JournalProstaglandins and Other Lipid Mediators
Volume108
DOIs
StatePublished - Jan 1 2014

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Lysosphingolipid Receptors
rho-Associated Kinases
Fibroblasts
Smooth Muscle
Muscle
Actins
Gels
Lung
Fibrosis
Collagen
Tissue
Sphingolipids
Myofibroblasts
Pathologic Processes
Metabolites
Neutralizing Antibodies
Wound Healing
Chronic Obstructive Pulmonary Disease
sphingosine phosphorylcholine
Proteins

Keywords

  • Fibroblast
  • SPC
  • Tissue repair

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Pharmacology
  • Cell Biology

Cite this

Sphingosylphosphorylcholine induces α-smooth muscle actin expression in human lung fibroblasts and fibroblast-mediated gel contraction via S1P 2 receptor and Rho/Rho-kinase pathway . / Wang, X. Q.; Mao, L. J.; Fang, Q. H.; Kobayashi, T.; Kim, H. J.; Sugiura, H.; Kawasaki, S.; Togo, S.; Kamio, K.; Liu, Xiang-de; Rennard, S. I.

In: Prostaglandins and Other Lipid Mediators, Vol. 108, 01.01.2014, p. 23-30.

Research output: Contribution to journalArticle

Wang, X. Q. ; Mao, L. J. ; Fang, Q. H. ; Kobayashi, T. ; Kim, H. J. ; Sugiura, H. ; Kawasaki, S. ; Togo, S. ; Kamio, K. ; Liu, Xiang-de ; Rennard, S. I. / Sphingosylphosphorylcholine induces α-smooth muscle actin expression in human lung fibroblasts and fibroblast-mediated gel contraction via S1P 2 receptor and Rho/Rho-kinase pathway In: Prostaglandins and Other Lipid Mediators. 2014 ; Vol. 108. pp. 23-30.
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abstract = "Chronic airway diseases like COPD and asthma are usually accompanied with airway fibrosis. Myofibroblasts, which are characterized by expression of smooth muscle actin (α-SMA), play an important role in a variety of developmental and pathological processes, including fibrosis and wound healing. Sphingosylphosphorylcholine (SPC), a sphingolipid metabolite, has been implicated in many physiological and pathological conditions. The current study tested the hypothesis that SPC may modulate tissue remodeling by affecting the expression of α-SMA in human fetal lung fibroblast (HFL-1) and fibroblast mediated gel contraction. The results show that SPC stimulates α-SMA expression in HFL-1 and augments HFL-1 mediated collagen gel contraction in a time- and concentration-dependent manner. The α-SMA protein expression and fibroblast gel contraction induced by SPC was not blocked by TGF-β1 neutralizing antibody. However, it was significantly blocked by S1P2 receptor antagonist JTE-013, the Rho-specific inhibitor C3 exoenzyme, and a Rho-kinase inhibitor Y-27632. These findings suggest that SPC stimulates α-SMA protein expression and HFL-1 mediated collagen gel contraction via S1P2 receptor and Rho/Rho kinase pathway, and by which mechanism, SPC may be involved in lung tissue remodeling.",
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AU - Sugiura, H.

AU - Kawasaki, S.

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AU - Liu, Xiang-de

AU - Rennard, S. I.

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