Resistin stimulates expression of chemokine genes in chondrocytes via combinatorial regulation of c/EBPβ and NF-κB

12Citations
Citations of this article
9Readers
Mendeley users who have this article in their library.

Abstract

© 2014 by the authors; licensee MDPI, Basel, Switzerland. To further investigate the regulation role of two chemokine genes CCL3 and CCL4 in chondrocytes in response to resistin, human primary chondrocytes and T/C-28a2 cells were cultured. The function of resistin on the chemokine genes, and the expression of C/EBPβ, NF-κB isoforms were tested using qPCR. The methods used to investigate timed co-regulation of C/EBPβ and NF-κB were NF-κB inhibitor (IKK-NBD) and C/EBPβ inhibitor (SB303580) treatments, and subcellular localization, with or without resistin stimulation. Results showed that resistin could increase the up-regulation of chemokine genes independently. Resistin increased the expression of C/EBPβ and NF-κB isoforms. C/EBPβ regulated basal activity and steadily increased over time up to 24h with resistin. NF-κB was up-regulated upon induction with resistin, peaking at 4 h. C/EBPβ and NF-κBco-enhanced the chemokines expression; inhibition of their activity was additive. Thetiming of activation in chondrocytes was confirmed by subcellular localization of C/EBPβ and c-rel. Chondrocytes react to resistin in a non-restricted cell-specific manner, utilizing C/EBPβ and NF-κB in a combinatorial regulation of chemokine gene expression. The activity of C/EBPβ is augmented by a transient increase in activity of NF-κB, and both transcription factors act independently on the chemokine genes, CCL3 and CCL4. Thus, resistin stimulates CCL3 and CCL4 through combinatorial regulation of C/EBPβ and NF-κB in chondrocytes.

Cite

CITATION STYLE

APA

Zhang, Z., Zhang, Z., Kang, Y., Hou, C., Duan, X., Sheng, P., … Liao, W. (2014). Resistin stimulates expression of chemokine genes in chondrocytes via combinatorial regulation of c/EBPβ and NF-κB. International Journal of Molecular Sciences, 15(10), 17242–17255. https://doi.org/10.3390/ijms151017242

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free