RT Journal Article
SR Electronic
T1 TRB3 is elevated in psoriasis vulgaris lesions and mediates HaCaT cells proliferation in vitro
JF Journal of Investigative Medicine
JO J Investig Med
FD BMJ Publishing Group Ltd
SP jim-2017-000453
DO 10.1136/jim-2017-000453
A1 Xiao-Jing Yu
A1 Tie-Jun Song
A1 Lu-Wei Zhang
A1 Ying Su
A1 Ke-Yu Wang
A1 Qing Sun
YR 2017
UL http://hw-f5-jim.highwire.org/content/early/2017/08/07/jim-2017-000453.abstract
AB Psoriasis is a chronic skin disease characterized by abnormal keratinocyte proliferation and differentiation, inflammation, and angiogenesis. Overexpression of tribbles homolog3 (TRB3), which belongs to the tribbles family of pseudokinases, has been found in several human tumors and metabolic diseases, but its role in psoriasis has not been fully clarified. The aim of this study is to investigate the expression of TRB3 in psoriasis and explore its roles in the proliferation of keratinocytes. Twenty-four patients with psoriasis vulgaris were recruited for the study. Diagnosis of psoriasis was based on clinical and histologic examinations. Immunohistochemistry and real-time reverse transcription PCR (RT-PCR) were performed to determine protein and messenger RNA (mRNA) expression of TRB3 in psoriasis lesions. 5-Bromo-2-deoxyUridine (BrdU) incorporation assay were performed for cell proliferation. Cell cycle distribution was assessed by flow cytometry analysis. The levels of TRB3 is elevated in psoriatic lesions compared with psoriatic non-lesions. The HaCat cells expressed the TRB3 gene. We found TRB3 silencing to significantly inhibit HaCat cell proliferation. Furthermore, the specific knockdown of TRB3 slowed down the cell cycle at the gap 0/first gap phase. In conclusion, our data suggest that TRB3 is overexpressed in lesions of patients with psoriasis and may be involved in the abnormal proliferation of keratinocytes. Therefore, TRB3 may be a potential therapeutic target for psoriasis.