Galectin-3 protects keratinocytes from UVB-induced apoptosis by enhancing AKT activation and suppressing ERK activation

Jun Saegusa, Daniel K. Hsu, Wei Liu, Ichiro Kuwabara, Yasuko Kuwabara, Lan Yu, Fu-Tong Liu

Research output: Contribution to journalArticle

37 Scopus citations

Abstract

Keratinocytes undergo apoptosis in a variety of physiological and pathological conditions. Galectin-3 is a member of a family of β-galactoside-binding animal lectins expressed abundantly in keratinocytes and other epithelial cells. Here, we have studied the regulatory role of galectin-3 in keratinocyte apoptosis by using cells from gene-targeted galectin-3 null (gal3-/-) mice. We showed that galectin-3 mRNA was transiently upregulated in ultraviolet-B (UVB)-irradiated wild-type keratinocytes. We found that gal3-/- keratinocytes were significantly more sensitive to apoptosis induced by UVB as well as various other stimuli, both in vitro and in vivo, than wild-type cells. Moreover, we demonstrated that increased apoptosis in gal3-/- keratinocytes was attributable to higher extracellular signal-regulated kinase (ERK) activation and lower AKT activation after UVB irradiation. We conclude that endogenous galectin-3 is an anti-apoptotic molecule in keratinocytes functioning by suppressing ERK activation and enhancing AKT activation and may play a role in the development of apoptosis-related skin diseases.

Original languageEnglish (US)
Pages (from-to)2403-2411
Number of pages9
JournalJournal of Investigative Dermatology
Volume128
Issue number10
DOIs
StatePublished - Oct 2008

ASJC Scopus subject areas

  • Dermatology

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