Results
| PMID | 24173391 |
| Gene Name | MIR183 |
| Condition | Endometriosis |
| Association |
Associated |
| Age | Controls: 38.9±4.8 yrs, Patients: 36.6±5.1 yrs |
| Sex | Female |
| Other associated phenotypes |
Endometriosis |
|
Int J Mol Med. 2014 Jan;33(1):59-67. doi: 10.3892/ijmm.2013.1536. Epub 2013 Oct Shi, Xiao-Yan| Gu, Lin| Chen, Jie| Guo, Xi-Rong| Shi, Ying-Li State Key Laboratory of Reproductive Medicine, Department of Gynecology, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China. Endometriosis is a common gynecological disease, yet its pathogenesis remains poorly understood. Recent studies have demonstrated that the aberrant expression of certain microRNAs (miRNAs) may correlate with the development and progression of endometriosis. In this study, we profiled several differentially expressed miRNAs in the normal, eutopic and ectopic endometrium by miRNA microarray screening analysis, among which, miR-183 was found to be downregulated in the ectopic and eutopic tissues, and the result was further confirmed by real-time PCR (qPCR). Functional analysis indicated that miR-183 plays a promotional role in endometrial stromal cell (ESC) apoptosis and has a negative regulatory impact on the invasive ability of cells, although it has no effect on ESC proliferation. Ovarian steroids (17beta-estradiol and progesterone) and inflammatory factors (tumor necrosis factor-alpha and interleukin-6) decreased the expression of miR-183 in the ESCs. This regulatory function may further manifest the growth and invasive potential of ESCs by altering the expression of miR-183. These findings suggest that the downregulation of miR-183 expression is involved in the development and progression of endometriosis. Mesh Terms: Apoptosis/drug effects| Cell Survival| *Down-Regulation| Endometriosis/genetics/*pathology| Endometrium/*cytology/metabolism| Estradiol/metabolism| Female| Humans| Interleukin-6/metabolism| MicroRNAs/genetics/*metabolism| Microarray Analysis| P |
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