TGF-β1 latency associated peptide promotes remodeling of healing cutaneous wounds in the rat

M. Varedi, Ella Englander

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Background: The process of wound healing involves integrated events including inflammation, granulation tissue formation, matrix deposition and remodeling. Growth factors play a key role in the process. Among them transforming growth factor-β1 (TGF-β1) is known to accelerate tissue repair by promoting the synthesis and deposition of extracellular matrix proteins. However, persistence or overactivity of TGF-β1 during the remodeling phase can potentially lead to fibrosis. The primary objective of this study was, therefore, to determine the effects of TGF-β1 inactivation, by its latency associated peptide (LAP), on the cutaneous healing wounds. Methods: Excisional wounds were generated on the back of male adult rats. Wounds received TGF-β1 or LAP during the post-inflammatory phase. Expression of type I collagen and a-smooth muscle actin was evaluated by Western blotting. Wound maturation was further assessed by histology and immunohistochemical methods using specific antibody for proliferating cell nuclear antigen (PCNA). Results: Wounds treated with TGF-β1 showed a marked increase in the level of type I collagen, whereas no significant changes were observed in the wounds treated with LAP as compared to that in control. Expression of α-smooth muscle actin was markedly reduced in the wounds treated with LAP but was slightly increased in the wounds treated with TGF-β1. Both neodermis and newly-formed epidermis exhibited a higher degree of maturation in the LAP-treated wounds as compared to TGF-β1 treated wounds. Conclusion: Local administration of LAP seems to be beneficial to tissue remodeling. It promotes wound maturation and, may prevent fibrosis and hypertrophic scarring.

Original languageEnglish (US)
Pages (from-to)65-69
Number of pages5
JournalIranian Journal of Medical Sciences
Volume31
Issue number2
StatePublished - 2006

Fingerprint

Transforming Growth Factors
Wound Healing
Skin
Peptides
Wounds and Injuries
Collagen Type I
Smooth Muscle
Actins
Fibrosis
Granulation Tissue
Extracellular Matrix Proteins
Proliferating Cell Nuclear Antigen
Epidermis
Cicatrix
Intercellular Signaling Peptides and Proteins
Histology
Western Blotting
Inflammation
Antibodies

Keywords

  • Fibrosis
  • Latency associated peptide
  • TGF-β1
  • Wound healing

ASJC Scopus subject areas

  • Medicine(all)

Cite this

TGF-β1 latency associated peptide promotes remodeling of healing cutaneous wounds in the rat. / Varedi, M.; Englander, Ella.

In: Iranian Journal of Medical Sciences, Vol. 31, No. 2, 2006, p. 65-69.

Research output: Contribution to journalArticle

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abstract = "Background: The process of wound healing involves integrated events including inflammation, granulation tissue formation, matrix deposition and remodeling. Growth factors play a key role in the process. Among them transforming growth factor-β1 (TGF-β1) is known to accelerate tissue repair by promoting the synthesis and deposition of extracellular matrix proteins. However, persistence or overactivity of TGF-β1 during the remodeling phase can potentially lead to fibrosis. The primary objective of this study was, therefore, to determine the effects of TGF-β1 inactivation, by its latency associated peptide (LAP), on the cutaneous healing wounds. Methods: Excisional wounds were generated on the back of male adult rats. Wounds received TGF-β1 or LAP during the post-inflammatory phase. Expression of type I collagen and a-smooth muscle actin was evaluated by Western blotting. Wound maturation was further assessed by histology and immunohistochemical methods using specific antibody for proliferating cell nuclear antigen (PCNA). Results: Wounds treated with TGF-β1 showed a marked increase in the level of type I collagen, whereas no significant changes were observed in the wounds treated with LAP as compared to that in control. Expression of α-smooth muscle actin was markedly reduced in the wounds treated with LAP but was slightly increased in the wounds treated with TGF-β1. Both neodermis and newly-formed epidermis exhibited a higher degree of maturation in the LAP-treated wounds as compared to TGF-β1 treated wounds. Conclusion: Local administration of LAP seems to be beneficial to tissue remodeling. It promotes wound maturation and, may prevent fibrosis and hypertrophic scarring.",
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N2 - Background: The process of wound healing involves integrated events including inflammation, granulation tissue formation, matrix deposition and remodeling. Growth factors play a key role in the process. Among them transforming growth factor-β1 (TGF-β1) is known to accelerate tissue repair by promoting the synthesis and deposition of extracellular matrix proteins. However, persistence or overactivity of TGF-β1 during the remodeling phase can potentially lead to fibrosis. The primary objective of this study was, therefore, to determine the effects of TGF-β1 inactivation, by its latency associated peptide (LAP), on the cutaneous healing wounds. Methods: Excisional wounds were generated on the back of male adult rats. Wounds received TGF-β1 or LAP during the post-inflammatory phase. Expression of type I collagen and a-smooth muscle actin was evaluated by Western blotting. Wound maturation was further assessed by histology and immunohistochemical methods using specific antibody for proliferating cell nuclear antigen (PCNA). Results: Wounds treated with TGF-β1 showed a marked increase in the level of type I collagen, whereas no significant changes were observed in the wounds treated with LAP as compared to that in control. Expression of α-smooth muscle actin was markedly reduced in the wounds treated with LAP but was slightly increased in the wounds treated with TGF-β1. Both neodermis and newly-formed epidermis exhibited a higher degree of maturation in the LAP-treated wounds as compared to TGF-β1 treated wounds. Conclusion: Local administration of LAP seems to be beneficial to tissue remodeling. It promotes wound maturation and, may prevent fibrosis and hypertrophic scarring.

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