Results
| PMID | 20940247 |
| Gene Name | LOXL1 |
| Condition | Endometriosis |
| Association |
Associated |
| Sex | Female |
| Associated genes | HTRA1, LOXL1 |
| Other associated phenotypes |
Endometriosis |
|
Reprod Sci. 2010 Nov;17(11):1016-23. doi: 10.1177/1933719110377662. Dentillo, Daniel Blassioli| Meola, Juliana| Rosa e Silva, Julio Cesar| Giuliatti, Silvana| Silva Junior, Wilson Araujo Jr| Ferriani, Rui Alberto| Martelli, Lucia Department of Genetics, School of Medicine of Ribeirao Preto, University of Sao Paulo, Avenida Bandeirantes, Ribeirao Preto, Sao Paulo, Brazil. danieldentillo@yahoo.com.br Endometriosis is a gynecologic disease characterized by the presence of endometrial tissue outside the uterine cavity. Although 15% of the female population in reproductive age is affected by endometriosis, its pathogenesis remains unclear. According to the most accepted pathogenesis hypothesis, endometrial fragments from the menstrual phase are transported through the uterine tubes to the peritoneal cavity, where they undergo implantation and growth, invading adjacent tissues. However, the establishment of the disease requires that endometrial cells present molecular characteristics favoring the onset and progression of ectopic implantation. In this investigation, we analyzed the differential gene expression profiles of peritoneal and ovarian endometriotic lesions compared to the endometrial tissue of nonaffected women using rapid subtraction hybridization (RaSH). In our study, this method was applied to samples of endometriotic lesions from affected women and to biopsies of endometrium of healthy women without endometriosis, where we could identify 126 deregulated genes. To evaluate the expression of genes found by RaSH method, we measured LOXL1, HTRA1, and SPARC genes by real-time polymerase chain reaction. Significant different expression was obtained for HTRA1 and LOXL1, upregulated in the ectopic endometrium, suggesting that these genes are involved in the physiopathology of endometriosis and may favor the viability of endometrial cells at ectopic sites. Mesh Terms: Amino Acid Oxidoreductases/genetics/*metabolism| Endometriosis/*metabolism| Endometrium/metabolism| Female| Gene Expression Regulation| Humans| Ovarian Diseases/metabolism| Peritoneal Diseases/metabolism| Serine Endopeptidases/genetics/*metabolism |
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