An oligonucleotide microarray study on gene expression profile in mouse testis of experimental cryptorchidism

To investigate the germ cell apoptosis under body temperature in testis, we analyzed the gene expression patterns on day 1, day 4, day 7, day 14, day 28 and normal control adult mouse testis after experimental cryptorchidism (EC) using Affymetrix MOE430A microarray. Our data showed that EC led to th...

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Published inFrontiers in bioscience Vol. 11; no. 1; pp. 2465 - 2482
Main Authors Li, Yin-Chuan, Hu, Xiao-Qian, Xiao, Li-Juan, Hu, Zhao-Yuan, Guo, Jian, Zhang, Ke-Ying, Song, Xin-Xin, Liu, Yi-Xun
Format Journal Article
LanguageEnglish
Published United States 01.09.2006
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Summary:To investigate the germ cell apoptosis under body temperature in testis, we analyzed the gene expression patterns on day 1, day 4, day 7, day 14, day 28 and normal control adult mouse testis after experimental cryptorchidism (EC) using Affymetrix MOE430A microarray. Our data showed that EC led to the oxidative stress and gene expression fluctuation in the first 28 days, both of which were highly coincident in timing. Cryptorchid testis showed more effective antioxidative capability in the first 4 days, and suddenly lowered the capability from day 5 on, then gradually restored the antioxidation from day 10 to day 14, and turned to worse on day 28 again. The extensive high gene expression on day 4 after EC and the up-rising of oxidative stress level on day 5 and the abrupt down-regulation of the gene on day 7 were closely related. From the chip data, we have found that the high level of reactive oxidative species (ROS) was not only related to the dysfunction or abnormality of the direct origin of ROS generation, but also related to the abnormality of the more upstream physiological events in energy metabolism, lipid metabolism. The selective regulation of metabolic substrate transporter in different cell population implied the existence of various regulation of the selective signal pathways among different cell populations by EC.
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ISSN:1093-9946
1093-4715
DOI:10.2741/1983