tgf

Conclusion TGF � � 1 may involve in regulation of ocular growth.

结论视网膜tgf- β1的变化可能与FDM的 形成有关,tgf- β1可能参与眼球生长调控.

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Expression of TGF � � 1 mRNA was evaluated by RT PCR.

RT?PCR方法测定肺组织内TGF?β1的表达.

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Survival rate for positive staining group of TGF | � � RI was better than negative group ( P & lt ; 0.01 ).

TGFβ R 阳性者术后3、5年生存率优于阴性者.

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TGF-� � 1 in Ctrl group did not return to the reference value until 8 weeks after trauma.

对照组TGF - β1水平直至骨折后8周时,才回落至正常水平.

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Expression of TGF � � 1 was evaluated by RT PCR technique.

逆转录聚合酶链反应(RT?PCR)方法测定肺组织内TGF?β1的表达.

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The results also suggest that MCP-1 induced EMT may involve the TGF-� � 1-independant pathway of the cells.

同时提示MCP1诱导的转分化可能涉及非TGFβ依赖的细胞信号传导途径,需进一步研究.

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ConclusionThere is an additive effect but no synergism between IGF-I and TGF-� � 1 on EMT.

IGF-I 和TGF - β1对诱导HKC转化无协同作用.

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Simvastatin may effectively attenuate DN progression through down-regulating the expression of TGF-� � via p 38 MAPK.

斯伐他汀可能通过抑制p38MAPK磷酸化而减少TGF - β的蛋白表达.

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Methods: Using cell culture and Western blot, the TGF-� � 1-induced expression of FN and ILK was tested.

方法培养人肾小管上皮细胞(HKC),用蛋白印迹方法检测TGF - β1诱导HKC合成 FN和表达ILK的作用.

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Results TGF � � 1 expression was found in both cytoplasm and extracellular stroma.

结果:tgfβ在宫颈鳞癌细胞浆及细胞外基质中均可见表达.

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Conclusions: CPL can inhibit the transcription of TGF-� � _ 1.

结论: CPL可 明显下调实验性肝纤维化大鼠肝组织TGF - β_1mRNA的表达.

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The expression of TGF � � _ 1 in BEC increased in both COPD ( 0.785±0.071 ) and chronic bronchitis ( 0.559±0.051 ) groups compared to control ( 0.195±0.029 ) ( P < 0.05 ).

COPD 组、慢支组气道上皮细胞TGF-β1的表达明显高于对照组 ( 0.195±0.029 ),差异有显著性P<0.05.

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In all cell lines TGF a induced total EGFR protein levels higher than EGF (? P? < 0.05 ).

各细胞系EGFR蛋白水平TGFα组明显高于EGF组 ( P<0.05 ).

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Conclusion: TGF-� � directly induces the expression of CTGF and ECM components in HMCs.

结论: HMCs可表达CTGF. TGF - β可诱导体外培养的HMCsCTGF及 ECM成分高表达.

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C-ski is transcriptional co-repressors that inhibit transforming growth factor-beta ( TGF-beta ) signaling through interaction with Smad 3, Smad 2 protein.

同时,近些年研究表明TGF -beta 信号系统是导致瘢痕形成的重要原因,而Smad3和Smad2做为TGF -beta 途径重要的信号因子,在瘢痕形成中具有重要作用, 因此,抑制Smad3和Smad2成为了减轻瘢痕形成的新途径.

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