RHOC: a key gene for endometriosis.

Considerable efforts have been invested in elucidating the potential mechanisms involved in the physiopathology of endometriosis. The aims of our study were to investigate whether RHOC expression is differentially altered in the endometrium and in endometriotic lesions. A total of 40 patients diagnosed with endometriosis and 15 healthy fertile women were selected for the study. Paired biopsies of endometrial tissue (eutopic endometrium) and endometriotic lesions (ectopic endometrium) were obtained from the patients with endometriosis. Endometrium from women without endometriosis was used as a control. Expression of the RHOC gene was analyzed by real-time polymerase chain reaction in autologous endometrial tissues of women with endometriosis and in the endometrium of control women. Increased RHOC expression was detected in endometriotic lesions compared to the eutopic endometrium of women with endometriosis and control women. RHOC changes may be among the key elements involved in the origin and the maintenance of endometriosis.

Deregulation of LOXL1 and HTRA1 gene expression in endometriosis.

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.

Differentially expressed genes in eutopic and ectopic endometrium of women with endometriosis.

OBJECTIVE: To elucidate the potential mechanisms involved in the physiopathology of endometriosis. We analyzed the differential gene expression profiles of eutopic and ectopic tissues from women with endometriosis. DESIGN: Prospective laboratory study. SETTING: University hospital. PATIENT(S): Seventeen patients in whom endometriosis was diagnosed and 11 healthy fertile women. INTERVENTION(S): Endometrial biopsy specimens from the endometrium of healthy women without endometriosis and from the eutopic and ectopic endometrium tissues of patients with endometriosis were obtained in the early proliferative phase of the menstrual cycle. MAIN OUTCOME MEASURE(S): Six paired samples of eutopic and ectopic tissue were analyzed by subtractive hybridization. To evaluate the expression of genes found by rapid subtraction hybridization methods, we measured CTGF, SPARC, MYC, MMP, and IGFBP1 genes by real-time polymerase chain reaction in all samples. RESULT(S): This study identified 291 deregulated genes in the endometriotic lesions. Significant expression differences were obtained for SPARC, MYC, and IGFBP1 in the peritoneal lesions and for MMP3 in the ovarian endometriomas. Additionally, significant differences were obtained for SPARC and IGFBP1 between the peritoneal and ovarian lesions. No significant differences were found for the studied genes between the control and the eutopic endometrium. CONCLUSION(S): This study identified 291 genes with differential expression in endometriotic lesions. The deregulation of the SPARC, MYC, MMP3, and IGFBPI genes may be responsible for the loss of cellular homeostasis in endometriotic lesions.

Glycodelin expression in the endometrium of healthy women and in the eutopic and ectopic endometrium of women with endometriosis.

OBJECTIVE: To analyze the expression of the glycodelin gene to better understand the molecular environment of endometriotic lesions and to elucidate the potential mechanisms that underlie the complex physiopathology of endometriosis. DESIGN: Prospective laboratory study. SETTING: University hospital. PATIENT(S): Eleven healthy fertile women and 17 patients with endometriosis in the early proliferative phase of the menstrual cycle. INTERVENTION(S): Endometrial biopsy specimens were obtained from the endometrium of healthy women without endometriosis (controls) and from eutopic and ectopic endometrium tissues (pelvic and ovarian endometriotic implants) of endometriosis patients. MAIN OUTCOME MEASURE(S): The glycodelin relative expression level by real-time polymerase chain reaction (PCR) analysis. RESULT(S): The glycodelin down-regulation found in the endometriotic lesions was 332.26 and 123.17-fold lower, respectively, when compared with the eutopic tissue and the control endometrium. CONCLUSION(S): Glycodelin may be one of the molecules that contributes to the loss of cellular homeostasis in endometriotic lesions.