Interleukin-1{beta} induces fibroblast growth factor 2 expression and subsequently promotes endothelial progenitor cell angiogenesis in chondrocytes

Arthritis is a process of chronic inflammation that results in joint damage. Interleukin-1β (IL-1β) is an inflammatory cytokine that acts as a key mediator of cartilage degradation, and is abundantly expressed in arthritis. Neovascularization is one of the pathological characteristics of arthritis. However, the role of IL-1β in the angiogenesis of chondrocytes remains unknown. Here, we demonstrate that stimulating chondrocytes (ATDC5) with IL-1β increased the expression of fibroblast growth factor (FGF)-2, a potent angiogenic inducer, and then promoted endothelial progenitor cell (EPC) tube formation and migration. In addition, FGF-2 neutralizing antibody abolished ATDC5-conditional medium-mediated angiogenesis in vitro , as well as its angiogenic effects in the chick chorioallantoic membrane (CAM) assay and Matrigel plug nude mice model in vivo . Immunohistochemistry (IHC) staining from collagen-induced arthritis (CIA) mouse model also demonstrate that arthritis increased expression of IL-1β and FGF-2, as well as EPCs homing in articular cartilage. Moreover, IL-1β-induced FGF-2 expression via the type-1 interleukin-1 receptor (IL-1RI), reactive oxygen species (ROS) generation, AMP-activated protein kinase (AMPK), p38, and nuclear factor kappa B (NF-B) pathway has been demonstrated. Based on the above findings, we conclude that IL-1β promotes FGF-2 expression in chondrocytes through the ROS/AMPK/p38/NF-B signaling pathway and subsequently ...
Source: Clinical Science - Category: Biomedical Science Authors: Tags: PublishAheadOfPrint Source Type: research