MiR-200a was shown to be upregulated in the corpus cavernosum （CC） of rats with aging-related erectile dysfunction （A-ED） in our previous study. Among its target genes, SIRT1 was also reported as a protective fact...MiR-200a was shown to be upregulated in the corpus cavernosum （CC） of rats with aging-related erectile dysfunction （A-ED） in our previous study. Among its target genes, SIRT1 was also reported as a protective factor in erectile function by our groups previously. Thus, miR-200a might attenuate the erectile function in A-ED via SIRT1 inhibition. In the present study, three animal groups were included： aged rats with ED （group AE, n = 8）, aged rats with normal erectile function （group AN, n = 8）, and young rats as normal controls （group YN, n = 8）. CCs from each group were collected for histological and molecular measurements to validate the dysregulation of miR-200a and SIRT1. After that, the cavernous endothelial cells （CECs） from CC of aged rats with normal erectile function were transfected with miR-200a in vitro. Then the expression of SIRT1 and molecules within the eNOS/NO/PKG pathway were measured to investigate whether the transfection could imitate the attenuated process of erectile function in the aged. As a result, miR-200a was upregulated while the SIRT1, the levels of eNOS and cGMP were all downregulated in the CCs from AE group. After transfection in vitro, the miR-200a was upregulated while the SIRT1 and levels of eNOS and cGMP were obviously downregulated. Finally, based on the results of our previous study, we further verify that up-regulation of miR-200a could participate in the mechanisms of A-ED via SIRT1 inhibition, and mainly attenuate endothelial function via influencing the eNOS/NO/PKG pathway.展开更多
基金ACKNOWLEDGMENT This work was supported by grant from the National Natural Science Foundation of China （81170563 ）, and funded by Key Proj oct supported by Medical Science and Technology development Foundation, Nanjing Department of Health （YKK12096）, and by Key Project supported by Science and Technology development Foundation, Nanjing Medical University （2014NJMUZD053）.
文摘MiR-200a was shown to be upregulated in the corpus cavernosum （CC） of rats with aging-related erectile dysfunction （A-ED） in our previous study. Among its target genes, SIRT1 was also reported as a protective factor in erectile function by our groups previously. Thus, miR-200a might attenuate the erectile function in A-ED via SIRT1 inhibition. In the present study, three animal groups were included： aged rats with ED （group AE, n = 8）, aged rats with normal erectile function （group AN, n = 8）, and young rats as normal controls （group YN, n = 8）. CCs from each group were collected for histological and molecular measurements to validate the dysregulation of miR-200a and SIRT1. After that, the cavernous endothelial cells （CECs） from CC of aged rats with normal erectile function were transfected with miR-200a in vitro. Then the expression of SIRT1 and molecules within the eNOS/NO/PKG pathway were measured to investigate whether the transfection could imitate the attenuated process of erectile function in the aged. As a result, miR-200a was upregulated while the SIRT1, the levels of eNOS and cGMP were all downregulated in the CCs from AE group. After transfection in vitro, the miR-200a was upregulated while the SIRT1 and levels of eNOS and cGMP were obviously downregulated. Finally, based on the results of our previous study, we further verify that up-regulation of miR-200a could participate in the mechanisms of A-ED via SIRT1 inhibition, and mainly attenuate endothelial function via influencing the eNOS/NO/PKG pathway.
