Open AccessGalectin‐3 regulation of wound healing and fibrotic processes: insights for chronic skin wound therapeutics
Author(s) -
McLeod Karrington,
Walker John T.,
Hamilton Douglas W.
Publication year - 2018
Publication title -
journal of cell communication and signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 44
eISSN - 1873-961X
pISSN - 1873-9601
DOI - 10.1007/s12079-018-0453-7
Subject(s) - wound healing , myofibroblast , matricellular protein , dermis , galectin 3 , fibrosis , galectin , s100a9 , inflammation , skin repair , microbiology and biotechnology , angiogenesis , macrophage polarization , cancer research , medicine , downregulation and upregulation , fibroblast , biology , immunology , macrophage , pathology , extracellular matrix , cell culture , biochemistry , genetics , gene , in vitro
A member of the lectin family, galectin‐3 is a 250 amino‐acid protein that contains a C‐terminus carbohydrate recognition domain (CRD) that recognizes β‐galactosides. Considered to have certain common properties associated with matricellular proteins, galectin‐3 is expressed in the dermis and epidermis in healthy skin and is upregulated in skin healing, peaking at day 1 post wounding in mice. Galectin‐3 has been implicated in several processes central to the wound healing response, specifically in the regulation of inflammation, macrophage polarization, angiogenesis, fibroblast to myofibroblast transition and re‐epithelialization. However, it appears that many of the effects of Galectin‐3 are highly tissue specific and context dependent. Genetic deletion of galectin‐3 shows different effects in skin compared to lung, heart, and kidney remodeling. In this review, we will compare galectin‐3 functions in these tissues. Furthermore, we will discuss, based on its identified regulation of cell processes, whether in an exogenous form, galectin‐3 could represent a novel therapeutic for impaired skin healing.