Interleukin-4 reversed the Interleukin-1-inhibited proteoglycan synthesis through the inhibition of NO release: a possible involvement of intracellular calcium ion

F Nishisaka; S Sohen; H Fukuoka; Y Okamoto; M Matukawa; K Fukuda; C Hamanishi

doi:10.1016/s0928-4680(00)00061-4

Interleukin-4 reversed the Interleukin-1-inhibited proteoglycan synthesis through the inhibition of NO release: a possible involvement of intracellular calcium ion

Pathophysiology. 2001 Mar;7(4):289-293. doi: 10.1016/s0928-4680(00)00061-4.

Authors

F Nishisaka¹, S Sohen, H Fukuoka, Y Okamoto, M Matukawa, K Fukuda, C Hamanishi

Affiliation

¹ Department of Orthopedic Surgery, Kinki University School of Medicine, 377-2 Ohnohigashi, Osaka-sayama, 589-8511, Osaka, Japan

PMID: 11228400
DOI: 10.1016/s0928-4680(00)00061-4

Abstract

Interleukin-1 (IL-1) causes cartilage degradation through nitric oxide (NO) synthesis. Although Interleukin-4 (IL-4) antagonizes the IL-1-mediated cartilage degradation, the precise mechanisms are not clear. We examined the effect of IL-4 on NO synthesis in parallel with intracellular Ca levels ([Ca(2+)]i) and proteoglycan (PG) synthesis. IL-4-inhibited IL-1-enhanced NO release in a dose-dependent manner. IL-1-enhanced [Ca(2+)]i in the chondrocytes, and IL-4 attenuated this increase. IL-4 reversed IL-1-inhibited PG synthesis. Accordingly, IL-4 reversed the IL-1-inhibited PG synthesis through the inhibition of NO release. An increase in [Ca(2+)]i with IL-1 is possibly involved in this action.