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PPARγ激动剂干预对激活星形胶质细胞Jagged1的影响

Effect of PPARγ agonist on Jagged1 mRNA expression in activated astrocytes
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摘要 目的观察过氧化物酶体增殖物激活受体γ(PPARγ)激动剂吡格列酮干预对激活星形胶质细胞产生Jagged1的影响。方法采用脂多糖(LPS)刺激纯化的星形胶质细胞,将不同梯度浓度吡格列酮(0.01,0.1,1.0,10.0μm)和转化生长因子β1(10 ng/ml)共刺激星形胶质细胞6 h,提取细胞RNA。结果吡格列酮呈浓度依存性抑制LPS激活星形胶质细胞中Jagged1的mRNA表达(P<0.05)。结论吡格列酮抑制星形胶质细胞Jagged1的产生,Jagged1/Notch通路的激活可能随之减弱,有利于多发性硬化的髓鞘修复。 Objective To investigate the effect of peroxisome proliferator-activated receptor-gamma（PPARγ） agonist on Jagged1 mRNA expression in activated astrocytes.Methods Astrocyte activated by LPS was treated by pioglitazone with different concentrations（0.01,0.1,1.0,10.0 μm）and TGF-β1（10 ng/ml） for 6 hours.Then the Jagged1 mRNA was extracted and the expression of Jagged1 mRNA was evaluated with fluorescent quantixative RT-PCR.Results Pioglitazone inhibited the Jagged1 mRNA expression of astrocytes in a concentration-dependent manner（P〈0.05）.Conclusion Pioglitazone inhibits Jagged1 mRNA expression of astrocytes,which leads to reducing the activation of Jagged1/Notch1 pathway and facilitating the repair of myelin sheath of multiple sclerosis.
作者 曾彦英 陈伟贤 高霞 王峥 顾冰洁 王松 季晓辉
机构地区 南京医科大学第一附属医院老年医学科 南京医科大学免疫与微生物教研室
出处 《江苏医药》 CAS CSCD 北大核心 2011年第15期1737-1739,共3页 Jiangsu Medical Journal
基金 江苏省卫生厅"135"工程重点学科基金(200131) 江苏省高校自然科学研究计划自筹经费项目(08KJD320004)
关键词 过氧化物酶体增殖物激活受体Γ 星形胶质细胞 Jaggedl基因 转化生长因子Β1 Peroxisome proliferator-activated receptor-gamma Astrocyte Jagged1 gene Transforming growth factor-β1
分类号 R741 [医药卫生—神经病学与精神病学]
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参考文献12

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二级参考文献35

  • 1Zhang Y, Zhang J, Navrazhina K, et al. TGFbetal induces Jagged1 expression in astrocytes via ALK5 and Smad3 and regulates the balance between oligodendrocyte progenitor proliferation and differentiation[J]. Glia, 2010, 58(8) : 964- 974.
  • 2Zhang Y, Argaw AT, Gurfein BT, et al. Notch1 signaling plays a role in regulating precursor differentiation during CNS[J]. Proc Natl Acad Sci, 2009, 106(45): 19162-19167.
  • 3Seifert T, Bauer J, Weissert R, et al. Notchl and its ligand Jagged1 are,present in remyelination in a T-cell- and antibody-mediated model of inflammatory demyelination[J]. Acta Neuropathol, 2007, 113(2) :195-203.
  • 4John GR, Shankar SL, Shafit-Zagardo B, et al. Multiple sclerosis: re-expression of a developmental pathway that restricts oligodendrocyte maturation[J]. Nat Med, 2002, 8 (10): 1115-1121.
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  • 7Aharoni R, Herschkovitz A, Eilam R, et al. Demyelination arrest and remyelination induced by glatiramer acetate treatment of experimental autoimmune encephalomyelitis [J ]. Proc Natl Aead Sci, 2008, 105(32):11358-11363.
  • 8Seifert T, Bauer J, Weissert R, et al. Notch1 and its ligand Jaggedl are present in remyelination in a T-cell- and antibody-mediated model of inflammatory demyelination[J]. Acta Neuropathol, 2007, 113(2) : 195-203.
  • 9Jurynczyk failure to M, Jurewicz A, Bielecki B, et al. Overcoming repair demyelination in EAE: gamma-secretase inhibition of Notch signaling[J]. J Neurol Sci, 2008, 265 (2) :5-11.
  • 10Zhao C, Fancy SP, Kotter MR, et al. Mechanisms of CNS remyelination-the key to therapeutic advances. J Neurol Sci, 2005,233 ( 1-2 ) :1 87-91.

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江苏医药
2011年 第15期

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