RT Journal Article
SR Electronic
T1 Expression of Peroxisome Proliferator-activated Receptors α, β, γ, and H- and L-Prostaglandin D Synthase During Osteoarthritis in the Spontaneous Hartley Guinea Pig and Experimental Dog Models
JF The Journal of Rheumatology
JO J Rheumatol
FD The Journal of Rheumatology
SP 877
OP 890
DO 10.3899/jrheum.120738
VO 40
IS 6
A1 Sarah-Salwa Nebbaki
A1 Fatima Ezzahra El Mansouri
A1 Hassan Afif
A1 Mohit Kapoor
A1 Mohamed Benderdour
A1 Jean-Pierre Pelletier
A1 Johanne Martel-Pelletier
A1 Hassan Fahmi
YR 2013
UL http://www.jrheum.org/content/40/6/877.abstract
AB Objective. To investigate the expression of peroxisome proliferator-activated receptors (PPAR) α, β, and γ, and hematopoietic and lipocalin-type prostaglandin D synthase (H- and L-PGDS) over the course of osteoarthritis (OA) in the spontaneous Hartley guinea pig and the anterior cruciate ligament transection dog models. Methods. Guinea pigs were sacrificed at 2 (control group), 4, 8, and 12 months of age (n = 5 per group). Non-operated (control) and operated dogs were sacrificed at 4, 8, and 12 weeks postsurgery. Cartilage was evaluated histologically using the Osteoarthritis Research Society International (OARSI) guidelines. The expression of PPAR-α, β, γ, and H- and L-PGDS was evaluated by real-time PCR and immunohistochemistry. The nonparametric Spearman test was used for correlation analysis. Results. PPAR-α, β, and γ were detected in medial tibial plateau from control animals in both the spontaneous and surgical models. Levels of PPAR-α and β did not change over the course of OA, whereas PPAR-γ levels decreased during progression of disease. We also observed that the expression of H-PGDS remained unchanged, whereas L-PGDS increased over the course of OA. PPAR-γ levels correlated negatively, whereas L-PGDS levels correlated positively, with the histological score of OA. Conclusion. The level of PPAR-γ decreased, whereas level of L-PGDS increased during the progression of OA. These data suggest that reduced expression of PPAR-γ may contribute to the pathogenesis of OA, whereas enhanced expression of L-PGDS may be part of a reparative process.