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[佩罗尼氏病中的基因表达谱及转化生长因子-β1干预的影响]

[Gene expression profiles and effects of transforming growth factor-beta1 intervention in Peyronie's disease].

作者信息

Wang Zhong, Liu Jing-fang, Zhou Zhi-heng, Zhang Yuan-fang, Wang Wen-jian, Zhang Peng, Selcuk Yucel, Guiting Lin, Lin Ching-shwun

机构信息

Department of Urology, Huashan Hospital, Fudan University, Shanghai 200040, China.

出版信息

Zhonghua Wai Ke Za Zhi. 2004 Feb 7;42(3):182-6.

Abstract

OBJECTIVE

To demonstrate molecular insight into the pathology of Peyronie's disease (PD). A preliminary profile of differential gene expression between the PD plaque and control tunica albuginea was obtained with DNA microarrays. Also, to investigate the effect of intervention in PD cells, transforming growth factor-beta1 (TGF-beta1) was recruited to treat PD cell lines.

METHODS

Three PD plaques and control tunica albugineas were constructed and studied. cDNA probes were prepared from RNA isolated from those cells and hybridized with the Clontech Atlas 3.6 Array. Relative changes of greater than 2.0 defined up-regulation and down-regulation, respectively. The expression of selected individual gene MCP-1 and the effect of TGF-beta1 on MCP-1 were analyzed by reverse transcriptase-polymerase chain reaction.

RESULTS

Some up-regulated genes in the PD plaque detected by the Clontech assay were screened, one of them was monocyte chemotactic protein. One involved the pathogenesis of PD as a downstream gene and responded to the TGF-beta1 treatment but not CTGF. The results were also confirmed by TR-PCR in all the types of cell.

CONCLUSIONS

The cell lines from plaque tissue and normal tunica from men with PD were successfully established. The findings indicate a potential role for MCP-1 over expression in the pathogenesis of PD as a downstream gene regulated by some genes and could be a new therapeutic target in PD. The information may allow a better understanding of the basic mechanisms involved in the etiology and pathogenesis of PD. Furthermore, it may permit some strategies of therapeutic interventions combine routine methods with Chinese herbal medicine.

摘要

目的

深入了解佩罗尼氏病(PD)的病理分子机制。通过DNA微阵列获得了PD斑块与对照白膜之间差异基因表达的初步概况。此外,为了研究对PD细胞干预的效果,引入转化生长因子-β1(TGF-β1)来处理PD细胞系。

方法

构建并研究了三个PD斑块和对照白膜。从这些细胞中分离的RNA制备cDNA探针,并与Clontech Atlas 3.6阵列杂交。大于2.0的相对变化分别定义为上调和下调。通过逆转录聚合酶链反应分析选定的单个基因MCP-1的表达以及TGF-β1对MCP-1的影响。

结果

筛选出了通过Clontech检测在PD斑块中一些上调的基因,其中之一是单核细胞趋化蛋白。作为下游基因之一参与了PD的发病机制,并对TGF-β1治疗有反应,但对CTGF无反应。所有类型细胞中的TR-PCR也证实了该结果。

结论

成功建立了来自PD男性患者斑块组织和正常白膜的细胞系。研究结果表明,MCP-1过表达作为某些基因调控的下游基因在PD发病机制中具有潜在作用,可能成为PD的一个新治疗靶点。这些信息可能有助于更好地理解PD病因和发病机制中涉及的基本机制。此外,可能允许一些治疗干预策略将常规方法与中药相结合。

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