MicroRNA-155 regulates monocyte chemokine and chemokine receptor expression in Rheumatoid Arthritis.

ABSTRACT:

Objective

To test the hypothesis that miR-155 regulates monocyte migratory potential via modulation of chemokine and chemokine receptor expression in RA, and thereby is associated with disease activity.

Methods

The miR-155 copy-numbers in monocytes from peripheral blood (PB) of healthy (n?=?22), RA (n?=?24) and RA SF (n?=?11) were assessed by real time-PCR using synthetic miR-155 as a quantitative standard. To evaluate the functional impact of miR-155, human monocytes were transfected with control or miR-155 mimic, and the effect on transcript levels, and production of chemokines was evaluated by Taqman low-density arrays and multiplex assays. A comparative study evaluated constitutive chemokine receptor expression in miR-155^-/- and wild-type murine (CD115?⁺?Ly6C?⁺?Ly6G^-) monocytes.

Results

Compared with healthy monocytes, the miR-155 copy-number was higher in RA, peripheral blood (PB) and SF monocytes (PB P?-/- monocytes showed downregulated CCR7 and upregulated CCR2 expression.

Conclusion

Given the observed correlations with disease activity, these data provide strong evidence that miR-155 can contribute to RA pathogenesis by regulating chemokine production and pro-inflammatory chemokine receptor expression, thereby promoting inflammatory cell recruitment and retention in the RA synovium.

SUBMITTER: Elmesmari A 

PROVIDER: S-EPMC5088623 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature