| First Author | Chai SP | Year | 2009 |
| Journal | Biochim Biophys Acta | Volume | 1790 |
| Issue | 3 | Pages | 213-8 |
| PubMed ID | 19162127 | Mgi Jnum | J:148738 |
| Mgi Id | MGI:3846292 | Doi | 10.1016/j.bbagen.2008.12.002 |
| Citation | Chai SP, et al. (2009) Endothelin-1 stimulates interleukin-6 secretion from 3T3-L1 adipocytes. Biochim Biophys Acta 1790(3):213-8 |
| abstractText | BACKGROUND: Since both endothelin-1 (ET-1) and interleukin-6 (IL-6) may induce insulin resistance and adipose tissue is a major contributor of circulating IL-6, we examined the effects of ET-1 on IL-6 secretion from 3T3-L1 adipocytes. METHODS: IL-6 release was measured by ELISA. RT-PCR and real-time PCR analyses were used to determine cellular IL-6 mRNA levels. A luciferase reporter driven by promoter (-1310/+198) of mouse IL-6 gene was transfected into 3T3-L1 adipocytes to monitor IL-6 transcription. RESULTS: Treatment of adipocytes with ET-1 dose- and time-dependently increased IL-6 secretion. The stimulatory effect of ET-1 on IL-6 secretion was abolished by actinomycin D and ET-1 induced an increase in IL-6 mRNA levels. ET-1 was able to enhance the IL-6 promoter activity and its stimulatory effect was inhibited by GF109203X, U0126, salicylate, dominant negative CREB and mithramycin A. Thus it appears that ET-1 may stimulate IL-6 secretion mainly through an enhanced IL-6 transcription, by a mechanism involving both protein kinase C and p42/p44 mitogen-activated protein kinase, and probably downstream NF-kappaB, CREB and Sp1 transcription factors. GENERAL SIGNIFICANCE: This study demonstrates that ET-1 is able to increase IL-6 secretion from adipocytes and raises the possibility that ET-1-induced insulin resistance may be mediated by IL-6. |
