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In vitro  studies have shown that Rela/p65, a key subunit mediating NF-κB signalling, is involved in chondrogenic differentiation, cell survival and catabolic enzyme production. Here, we analyse  in vivo  functions of Rela in embryonic limbs and adult articular cartilage, and find that Rela protects chondrocytes from apoptosis through induction of anti-apoptotic genes including  Pik3r1 . During skeletal development, homozygous knockout of  Rela  leads to impaired growth through enhanced chondrocyte apoptosis, whereas heterozygous knockout of  Rela  does not alter growth. In articular cartilage, homozygous knockout of  Rela  at 7 weeks leads to marked acceleration of osteoarthritis through enhanced chondrocyte apoptosis, whereas heterozygous knockout of  Rela  results in suppression of osteoarthritis development through inhibition of catabolic gene expression. Haploinsufficiency or a low dose of an IKK inhibitor suppresses catabolic gene expression, but does not alter anti-apoptotic gene expression. The biphasic regulation of chondrocytes by Rela contributes to understanding the pathophysiology of osteoarthritis.

Biphasic regulation of chondrocytes by Rela through induction of anti-apoptotic and catabolic target genes