Possible Role of lncRNA MEG3-microRNA-21 and Endoplasmic Reticulum (ER) Stress Proteins in the Pathogenesis of Psoriasis Vulgaris.

Abstract

Background: Psoriasis is a chronic inflammatory immune mediated disease arising from interaction between genetic risk variants and the environment. Maternally expressed gene3 (MEG3) is a long noncoding RNA (lncRNA) known for gene transcription regulation and inhibiting proliferation. MEG3 competes with microRNA (miRNA-21) influencing cell proliferation and apoptosis balance. Endoplasmic reticulum (ER) stress proteins promote cell survival via unfolded protein response (UPR) influenced by MEG3. We aimed to detect the possible role of MEG3, miRNA-21 and ER stress proteins in pathogenesis of psoriasis vulgaris.

Methods: Human GRP78, ATF6, caspase3 tissue levels were assayed by Enzyme Linked Immunosorbent Assay (ELISA). Assessment of long non-coding MEG3 and miRNA 21 expressions was done by quantitative real time polymerase chain reaction (qRT-PCR).

Results: Expression of MEG3 was significantly downregulated, while miRNA-21 was remarkably upregulated, ER stress proteins GRP78, ATF6, and caspase 3 all showed low levels in homogenized psoriatic lesions when compared to normal skin. miRNA 21 and MEG3 were identified as possible diagnostic markers for psoriasis vulgaris.

Discussion: MEG3 is barely expressed in psoriatic lesions while miRNA-21 expression is remarkably elevated but when correlated to each other there was unexpected positive correlation. MEG3 and miRNA-21 were identified as possible diagnostic markers for psoriasis. Undifferentiated psoriatic lesions have very weak UPR.