ArticleImmunity, inflammation and disease2026
PRKACB Attenuates Chondrocyte Loss and Inflammation in Osteoarthritis.
Article in Immunity, inflammation and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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- PRKACB Attenuates Chondrocyte Loss and Inflammation in Osteoarthritis.Immunity, inflammation and disease · 2026Article
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Abstract
backgroundPrevious work revealed that protein kinase cAMP-dependent catalytic β (PRKACB) may play a crucial role in osteoarthritis (OA) development. However, the mechanism by which PRKACB plays a role in OA still needs to be further investigated. Our aim was to explore the mechanism of PRKACB in a human chondrocyte inflammatory injury model.
methodsHuman CHON-001 chondrocytes were treated with 10 ng/mL IL-1β for 12 h to establish an in vitro model of chondrocyte inflammatory injury. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Flow cytometry (FCM) was conducted to assess apoptosis. Western blot assays were carried out to measure cleaved caspase-3, caspase-3, PRKACB, collagen II, aggrecan, phosphorated protein kinase A (p-PKA), PKA, cAMP response element-binding protein (CREB) and p-CREB protein expression levels. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) assay was used to measure PRKACB gene expression. Interleukin 6 (IL-6), IL-1β, and tumor necrosis factor alpha (TNF-α) levels were measured by enzyme-linked immunosorbent assay (ELISA).
resultsPRKACB expression was decreased in IL-1β-treated CHON-001 cells. Transfection of a PRKACB plasmid increased PRKACB expression in CHON-001 cells. IL-1β significantly inhibited CHON-001 cell viability; induced apoptosis; increased cleaved caspase-3 expression and the cleaved caspase-3/caspase-3 ratio; promoted TNF-α, IL-6 and IL-8 secretion; and decreased the expression levels of collagen II and aggrecan. However, these effects could be suppressed by the PRKACB plasmid. Moreover, we also found that PRKACB activated the PKA/CREB signaling pathway. H89 (a PKA inhibitor) distinctly reversed the effect of PRKACB on IL-1β-induced CHON-001 cells.
conclusionPRKACB can increase cell viability and reduce inflammation by activating the PKA/CREB signaling pathway, and PRKACB is a novel target for OA treatment.
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