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LITAF, HHEX, and DUSP1 expression in mesenchymal stem cells from patients with psoriasis.

Authors :
Chang WJ
Niu XP
Hou RX
Li JQ
Liu RF
Wang Q
Wang CF
Li XH
Yin GH
Zhang KM
Source :
Genetics and molecular research : GMR [Genet Mol Res] 2015 Dec 02; Vol. 14 (4), pp. 15793-801. Date of Electronic Publication: 2015 Dec 02.
Publication Year :
2015

Abstract

Psoriasis is a common chronic relapsing inflammatory skin disease, in which mesenchymal stem cells (MSCs) have been hypothesized to play an important role in abnormal localized inflammation and vascular proliferation observed in skin lesions. Previous studies have revealed abnormal gene expression patterns, DNA methylation status, and cytokine secretion of MSCs in psoriatic skin lesions, as well as some gene expression abnormalities related to inflammation and angiogenesis. We further verified the gene and protein expressions of inflammation-related lipopolysaccharide-induced tumor necrosis factor-alpha transcription factor (LITAF), dual-specificity protein phosphatase 1 (DUSP1), and angiogenesis-related hematopoietically expressed homeobox (HHEX) in MSCs derived from the skin lesions of psoriasis patients. The gene expression of LITAF, DUSP1, and HHEX in dermal MSCs was measured at the mRNA level using reverse transcription-polymerase chain reaction and the corresponding protein expression levels were analyzed by western blotting analysis. The gene and protein expression levels of LITAF, HHEX, and DUSP1 in dermal MSCs were significantly lower in psoriasis patients compared to controls. Amplification and western blotting results were consistent with our previously reported gene chip data. Our results suggest that dermal MSCs in psoriatic skin lesions may be involved in the development, progression, and regulation of localized inflammatory abnormalities by reducing the expression of LITAF, HHEX, and DUSP1, which are related to inflammation and angiogenesis.

Details

Language :
English
ISSN :
1676-5680
Volume :
14
Issue :
4
Database :
MEDLINE
Journal :
Genetics and molecular research : GMR
Publication Type :
Academic Journal
Accession number :
26634547
Full Text :
https://doi.org/10.4238/2015.December.1.31