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Biochem Biophys Res Commun. 2015 Jan 16;456(3):792-8. doi: 10.1016/j.bbrc.2014.12.037. Epub 2014 Dec 13.

Proteoglycan from salmon nasal cartridge [corrected] promotes in vitro wound healing of fibroblast monolayers via the CD44 receptor.

Author information

1
Department of Physiology, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan.
2
Department of Physiology, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan; Mechanobiology Laboratory, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan; Mechanobiology Institute Singapore, National University of Singapore, Singapore 117411, Singapore. Electronic address: msokabe@med.nagoya-u.ac.jp.

Erratum in

  • Biochem Biophys Res Commun. 2015 Aug 14;464(1):367.

Abstract

Proteoglycans (PGs) are involved in various cellular functions including cell growth, adhesion, and differentiation; however, their physiological roles are not fully understood. In this study, we examined the effect of PG purified from salmon nasal cartilage (SNC-PG) on wound closure using tissue-cultured cell monolayers, an in vitro wound-healing assay. The results indicated that SNC-PG significantly promoted wound closure in NIH/3T3 cell monolayers by stimulating both cell proliferation and cell migration. SNC-PG was effective in concentrations from 0.1 to 10μg/ml, but showed much less effect at higher concentrations (100-1000μg/ml). The effect of SNC-PG was abolished by chondroitinase ABC, indicating that chondroitin sulfates (CSs), a major component of glycosaminoglycans (GAGs) in SNC-PG, are crucial for the SNC-PG effect. Furthermore, chondroitin 6-sulfate (C-6-S), a major CS of SNC-PG GAGs, could partially reproduce the SNC-PG effect and partially inhibit the binding of SNC-PG to cells, suggesting that SNC-PG exerts its effect through an interaction between the GAGs in SNC-PG and the cell surface. Neutralization by anti-CD44 antibodies or CD44 knockdown abolished SNC-PG binding to the cells and the SNC-PG effect on wound closure. These results suggest that interactions between CS-rich GAG-chains of SNC-PG and CD44 on the cell surface are responsible for the SNC-PG effect on wound closure.

KEYWORDS:

CD44; Chondroitin sulfate; Proteoglycan; Salmon nasal cartilage; Wound healing

PMID:
25514035
DOI:
10.1016/j.bbrc.2014.12.037
[Indexed for MEDLINE]

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