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Induction of keratinocyte migration by ECa 233 is mediated through FAK/Akt, ERK, and p38 MAPK signaling
Author(s) -
Singkhorn Sawana,
Tantisira Mayuree H.,
Tanasawet Supita,
Hutamekalin Pilaiwanwadee,
Wongtawatchai Tulaporn,
Sukketsiri Wanida
Publication year - 2018
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.6075
Subject(s) - hacat , protein kinase b , rhoa , wound healing , mapk/erk pathway , cell migration , p38 mitogen activated protein kinases , pi3k/akt/mtor pathway , microbiology and biotechnology , keratinocyte , signal transduction , centella , cancer research , rac1 , cell growth , chemistry , medicine , biology , cell culture , cell , immunology , traditional medicine , biochemistry , genetics
Centella asiatica is widely considered the most important medicinal plant for treating and relieving skin diseases. Recently developed standardized extract of Centella asiatica ECa 233 has demonstrated positive effects on wound healing of incision and burn wound in rats. However, knowledge associated with wound healing mechanism of ECa 233 was scare. Therefore, this study aimed to investigate the effect and underlying molecular mechanisms of ECa 233 on the migration of a human keratinocyte cell line (HaCaT) using scratch wound healing assay. Formation of filopodia, a key protein in cell migration as well as signaling pathways possibly involved were subsequently assessed. It was found that HaCaT cell migration was significantly enhanced by ECa 233 in a concentration‐ and time‐dependent manner. The filopodia formations were accordingly increased in exposure to ECa 233 at concentrations of 0.1–100 μg/ml. Furthermore, ECa 233 was found to significantly upregulate the expression of Rac1 and RhoA and to induce phosphorylation of FAK and Akt as well as ERK and p38 MAPK. Taken all together, it is suggestive that ECa 233 induces cell migration and subsequently promotes wound healing activity, through the activation of FAK, Akt, and MAPK signaling pathways thereby supporting the role of ECa 233 to be further developed for the clinical treatment of wound.