THE EFFECT OF INTERLEUKIN-1Β INDUCTION ON CHONDROCYTES

Abstract

IL-1β is a glycoprotein molecule produced and secreted in an inactive form called pro-IL-1β. IL-1β stimulates the synthesis and activity matrikmetalloproteinase (MMPs), one of which is MMP-13 and it also synthesis the other enzymes that cause cartilage degradation. IL-1β has the ability to suppress the synthesis of type 2 collagen, proteoglycans and inhibit TGF-beta serves to stimulate the proliferation of chondrocytes. Chondrocytes are cells contained in avascular tissue, synthesize all the elements contained in the cartilage matrix. The changes that occurred during the chondrocytes in vitro conditions also occur in the body of patients with osteoarthritis (OA). This research is a true experimental by using post-test only control group design, The aim of this research  is to know the changes of chondrocytes and secretion of MMP-13 after being given recombinant human IL-1β. The result showed chondrocytes become hypertrophic, the cells swollen and the secretion of MMP-13 increased, the results are analized used un-paired t test obtained (p = 0.000), there are differences in the secretion of MMP-13 between groups were given IL-1β with a group were not given IL-1β. Chondrocytes induced IL-1β to produce MMP-13 and type X collagen which shows dedifferentiation toward hypertrophic phenotype. Stimulation of IL-1β activates several MAPK kinase (MAPKK) will then phosphorylates and activates MAPK, p38, c-jun N-terminal kinase (JNK) and extracelullar signal-regulated kinase (ERK) which will translocate into the nucleus. Next, MAPK phosphorylates and activates several transcription factors (ATF-2, c-jun, Elk-1 and Ets-1) that play a role in the transcription of MMP will further increase in the expression of Nuclear factor kappa B (NFkB) and activator protein 1 (AP- 1) and the secretion of proinflammatory cytokines occurs stimulation were able to induce chondrocytes to synthesize the MMPs and stimulates the normal chondrocytes becomes hypertrophic