Effect of tumor necrosis factor-α on resistin expression in 3T3-L1 adipocytes and its mechanism

Yang Zaigang , Zhang Muxun , Xu Lijun , Zhang Jianhua , Wang Hohgwei

Current Medical Science ›› 2005, Vol. 25 ›› Issue (3) : 121 -123.

PDF
Current Medical Science ›› 2005, Vol. 25 ›› Issue (3) : 121 -123. DOI: 10.1007/BF02873554
Article

Effect of tumor necrosis factor-α on resistin expression in 3T3-L1 adipocytes and its mechanism

Author information +
History +
PDF

Abstract

In order to investigate the effect of tumor necrosis factor-α (TNFα) on resistin expression in 3T3-L1 adipocytes, and further explore its mechanisms, the differentiated 3T3-L1 adipocytes were incubated with 0, 1, 10, 100 ng/mL TNFα respectively for 24 h, and then the expression of resistin was determined. The differentiated 3T3-L1 adipocytes were incubated with 100 ng/mL TNFα for 3, 6, 24 h respectively, and then the expression of resistin mRNA was analyzed. 3T3-L1 adipocytes were induced to differentiate into mature adipocytes. The cells were randomly divided into 4 groups for culture. In the control group, no drugs were added. Cells of TNFα group were treated with 100 ng/mL TNFα. In Ro-31-8220 group, 5 μmol/L protein kinase C inhibitor Ro-31-8220 was added. With TNFα+Ro-31-8220 group, 100 ng/mL TNFα were added 1 h after the addition of 5 μmol/L Ro-31-8220. All adipocytes were cultured for 24 h. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were employed to detect the expression of resistin gene. Our results showed that resistin protein and mRNA in 3T3-L1 adipocytes were inhibited by TNFα at different concentrations (P<0.01), and the inhibitory effect increased with the concentration (P<0.01). At the same concentrations, the inhibitory effect increased with time (P<0.01). Ro-31-8220 could inhibit its expression and the inhibitive effect remained unchanged with addition of TNFα(P>0.05). It was concluded that TNFα could inhibit the expression of resistin in 3T3-L1 adipocytes. The mechanism may be that the expression of resistin is partly controlled by protein kinase C signal conduction pathway.

Keywords

tumor necrosis factor-α / resistin / 3T3-L1 adipocyte / mechanism

Cite this article

Download citation ▾
Yang Zaigang, Zhang Muxun, Xu Lijun, Zhang Jianhua, Wang Hohgwei. Effect of tumor necrosis factor-α on resistin expression in 3T3-L1 adipocytes and its mechanism. Current Medical Science, 2005, 25(3): 121-123 DOI:10.1007/BF02873554

登录浏览全文

4963

注册一个新账户 忘记密码

References

[1]

SteppanC M, BaileyS T, BhatS, et al. . The hormone resistin links obesity to diabetes. Nature, 2001, 409307-307

[2]

FelipeF, BonetM L, RibotJ, et al. . Modulation of resistin expression by retinoic acid and vitamin A status. Diabetes, 2004, 53(4): 882-882

[3]

DelhantyP J, MesottenD, McdougallF, et al. . Growth hormone rapidly induces resistin gene expression in white adipose tissue of spontaneous dwarf rats. Endocrinology, 2002, 1432445-2445

[4]

NobuhiroS, HideyukiS, TakehideO, et al. . Humoral regulation of resistin expression in 3T3-L1 and mouse adipose cells. Diabetes, 2002, 511737-1737

[5]

KochanZ, KarbowskaJ. Dehydroepiandrosterone upregulates resistin gene expression in white adipose tissue. Mol Cell Endocrinol, 2004, 218(1–2): 57-57

[6]

MathiasM, JohannesK, SusanneN, et al. . Tumor necrosis factor-α is a negative regulator of resistin gene expression and secretion. Biochem Biophy Res Commun, 2001, 2881027-1027

[7]

FasshauerM, KleinJ, NeumannS, et al. . Isoproterenol inhibits resistin gene expression through a G(S)-protein-coupled pathway in 3T3-L1 adipocytes. FEBS Lett, 2001, 500(1–2): 60-60

[8]

SongH, ShojimaN, SakodaH, et al. . Resistin is regulated by C/EBPα, PPARs, and signal-transducing molecules. Biochem Biophys Res Commun, 2002, 299(2): 291-291

AI Summary AI Mindmap
PDF

84

Accesses

0

Citation

Detail

Sections
Recommended

AI思维导图

/