1. Decrease of galectin-3 in keratinocytes: A potential diagnostic marker and a critical contributor to the pathogenesis of psoriasis.
- Author
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Shi, Zhen-rui, Tan, Guo-zhen, Cao, Cui-xiang, Han, Yan-fang, Meng, Zhen, Man, Xiao-yong, Jiang, Ze-xin, Zhang, Yu-ping, Dang, Ning-ning, Wei, Kai-hua, Bu, Ding-fang, Liu, Fu-tong, and Wang, Liangchun
- Subjects
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GALECTINS , *KERATINOCYTES , *PSORIASIS , *SKIN inflammation , *GENETIC overexpression - Abstract
Psoriasis-specific proteins dysregulated in keratinocytes and involved in the pathophysiological process of psoriasis remains elusive. We report here that epidermal galectin-3 expression is significantly downregulated in lesional skin, but not in non-lesional skin in psoriasis patients, nor in a group of diseases known as psoriasiform dermatitis clinically and histologically similar to psoriasis. The deficiency of epidermal galectin-3 is sufficient to promote development of psoriatic lesions, as evidenced by more severe skin inflammation in galectin-3 knockout (gal3 −/− ) mice, compared to wild-type mice, after imiquimod treatment, and in skin from gal3 −/− mice grafted onto wildtype mice. The development of psoriatic-like lesions is attributable to 1) the spontaneously tuning up of psoriasis signatures in keratinocytes through JNK pathway; and 2) neutrophil accumulation caused by the enhanced leukocyte-recruiting capacity associated with overexpression of S100A7-9 and CXCL-1, 8 in keratinocytes with impaired galectin-3 expression. Psoriasis-like skin inflammation is significantly improved in gal-3 −/− mice both by inhibition of neutrophils accumulation with a selective CXCR2 antagonist of SB225002, and by intracutaneous injection of recombinant galectin-3. Overall, these findings offer promising galectin-3-related diagnostic and therapeutic resolutions of psoriasis. [ABSTRACT FROM AUTHOR]
- Published
- 2018
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