Abstract
Pristane-induced arthritis (PIA) in mice is an experimental model that resembles human rheumatoid arthritis, a chronic autoimmune disease that affects joints and is characterized by synovial inflammation and articular cartilage and bone destruction. AIRmax and AIRmin mouse lines differ in their susceptibility to PIA, and linkage analysis in this model mapped arthritis severity QTLs in chromosomes 5 and 8. miRNAs are a class of small RNA molecules that have been extensively studied in the development of arthritis. We analyzed miRNA and gene expression profiles in peritoneal cells of AIRmax and AIRmin lines, in order to evaluate the genetic architecture in this model. Susceptible AIRmax mice showed higher gene (2025 vs 1043) and miRNA (240 vs 59) modulation than resistant AIRmin mice at the onset of disease symptoms. miR-132-3p/212-3p, miR-106-5p, miR-27b-3p, and miR-25-3p were among the miRNAs with the highest expression in susceptible animals, showing a negative correlation with the expression of predicted target genes (Il10, Cd69, and Sp1r1). Our study showed that global gene and miRNA expression profiles in peritoneal cells of susceptible AIRmax and resistant AIRmin lines during pristane-induced arthritis are distinct, evidencing interesting targets for further validation.
Highlights
Rheumatoid arthritis (RA) is a chronic autoimmune disease that affects joints and causes persistent synovial inflammation and articular cartilage bone destruction [1]
Mouse lines genetically selected to maximal (AIRmax) or minimal (AIRmin) acute inflammatory response induced by s.c. injection of polyacrylamide beads [5, 6] differ widely in their susceptibility/resistance to Pristane-induced arthritis (PIA) [7]
We investigated the differences in miRNA expression by peritoneal cells of pristane-treated AIRmax and AIRmin mice and their involvement in the expression of their potential target genes by microarrays
Summary
Rheumatoid arthritis (RA) is a chronic autoimmune disease that affects joints and causes persistent synovial inflammation and articular cartilage bone destruction [1]. Mouse lines genetically selected to maximal (AIRmax) or minimal (AIRmin) acute inflammatory response induced by s.c. injection of polyacrylamide beads [5, 6] differ widely in their susceptibility/resistance to PIA [7]. These mice have been extensively used to study the genetic susceptibility to various experimental disease models and the acute inflammatory response [8,9,10]. In the PIA model, genome mapping detected significant QTLs for PIA severity in chromosomes 5 (Prtia2) and 8 (Prtia3) and suggestive QTLs in chromosomes 7, 17, and 19 [11]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
