Roles of miR-31 and endothelin-1 in psoriasis vulgaris: pathophysiological functions and potential biomarkers

Title:

Roles of miR-31 and endothelin-1 in psoriasis vulgaris: pathophysiological functions and potential biomarkers

Creator:

Borska, L., Andrys, C., Chmelarova, M., Kovarikova, H., Krejsek, J., Hamakova, K., Beranek, M., Palicka, V., Kremlacek, J., Borsky, P., and Fiala, Z.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:c0f97da3-b710-4493-a8e3-17c1c873a649
uuid:c0f97da3-b710-4493-a8e3-17c1c873a649

Subject:

miR-31, Endothelin-1, keratinocyte, and psoriasis

Type:

article, model:article, and TEXT

Description:

Psoriatic lesions are characterized by hyperproliferation, aberrant differentiation of keratinocytes resistant to apoptosis and inflammation. miR-31 plays pro-proliferative, pro-differentiative and pro-inflammatory roles and modulates apoptosis in psoriatic keratinocytes. Endothelin-1 (ET-1) is produced by psoriatic keratinocytes and suppresses apoptosis. Inflammation increases the production of ET-1, which in turn leads to the chronic stimulation of keratinocyte proliferation. The aim of this study was to identify the putative link between two potential biomarkers (miR-31 and ET-1) in patients with psoriasis. The study design included experimental group (29 patients with psoriasis), and the control group (22 blood donors). The PASI score evaluated the state of the disease (median: 18.6; interquartile range 14.5-20.9). Both, the serum level of ET-1 and the whole blood level of miR-31 were significantly increased (p<0.001 and p<0.05, respectively) in patients compared to the controls. However, a significant negative relationship between ET-1 and miR-31 was observed (Spearman’s rho=-037, p=0.05). It is possible that a negative feedback loop will be present between miR-31 and ET-1. Our results indicate that miR-31 and ET-1, potential biomarkers of the disease, play significant roles in the pathophysiology of psoriasis.

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2017 Volume:66 | Number:6

Harvested from:

CDK

Metadata only:

false