International Journal of
Reproductive Biomedicine
Wed, May 14, 2025
[Archive]
Volume 19, Issue 5 (Suppl- 2021)
IJRM 2021, 19(5): 247-247 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Sarshomar S, Chitsazian F, Ghaffari F, Shahhoseini M. P-80 Evaluation of the ALX1 and PDHX genes expression in endometriotic tissues of women with endometriosis in comparison with the normal endometrium. IJRM 2021; 19 (5) :247-247
URL: http://ijrm.ir/article-1-2886-en.html
URL: http://ijrm.ir/article-1-2886-en.html
1- Department of Basic Sciences and New Biological Technologies, Science and Culture University, Tehran, Iran. Department of Genetics, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran.
2- Department of Genetics, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran.
3- Department of Endocrinology and Female Infertility, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran.
4- Department of Genetics, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran. Reproductive Epidemiology Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran. ,m.shahhoseini@royaninstitute.org
2- Department of Genetics, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran.
3- Department of Endocrinology and Female Infertility, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran.
4- Department of Genetics, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran. Reproductive Epidemiology Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran. ,
Abstract: (247 Views)
Background: Endometriosis (EMs) is a benign, estrogen‐dependent disease and the leading cause of infertility in women of reproductive age. This disease is characterized by the presence of endometrial glandular tissue and stroma outside the uterus. EMs is considered as a multifactor disease affected by genetic, hormonal and environmental factors. Among genetic factors, aristaless-like homeobox1 (ALX1) and pyruvate dehydrogenase protein X (PDHX) genes are considered in this study. Studies show that upregulation of the ALX1 gene cause cell proliferation, migration, and invasion in cancer cells. PDHX is involved in cellular metabolism and acts as a tumor suppressor gene while maintaining normal homeostasis. Till now, the specific roles of the ALX1 and PDHX in EMs remain unclear.
Objective: In this study, we investigated the expression of the ALX1 and PDHX in endometriotic tissues of women with EMs in comparison to control endometrial samples.
Materials and Methods: In this case control study, ten eutopic and ectopic endometrium tissues (EMs group) as well as ten normal endometrium (as a control group) were collected. Ectopic biopsies were obtained using diagnostic laparoscopy, while the endometrial control samples and eutopic samples were collected via pipelle. RNA extraction and cDNA synthesis were done then the expression of ALX1 and PDHX genes evaluated by quantitative real-time polymerase chain reaction, using designed primers for the candidate gene. Data analysis performed using One-way ANOVA analysis (SPSS software) considered the significant level of p < 0.05.
Results: Results showed a significant decrease in the expression levels of the ALX1 in eutopic endometrial samples from patients compared to normal endometrium (p = 0.007). Although the expression of ALX1 increased in ectopic endometrium tissues of women with endometriosis compared with eutopic endometrium tissues, this increase was not statistically significant (p > 0.05). However, PDHX mRNA expression in both eutopic and ectopic groups was significantly reduced than in the control group (p = 0.017 and p = 0.021, respectively), although the PDHX mRNA decrease was not statistically significant between the endometriosis group (p > 0.05).
Conclusion: It is suggested that deregulation of ALX1 and PDHX genes could be involved in the pathogenesis of endometriosis.
Objective: In this study, we investigated the expression of the ALX1 and PDHX in endometriotic tissues of women with EMs in comparison to control endometrial samples.
Materials and Methods: In this case control study, ten eutopic and ectopic endometrium tissues (EMs group) as well as ten normal endometrium (as a control group) were collected. Ectopic biopsies were obtained using diagnostic laparoscopy, while the endometrial control samples and eutopic samples were collected via pipelle. RNA extraction and cDNA synthesis were done then the expression of ALX1 and PDHX genes evaluated by quantitative real-time polymerase chain reaction, using designed primers for the candidate gene. Data analysis performed using One-way ANOVA analysis (SPSS software) considered the significant level of p < 0.05.
Results: Results showed a significant decrease in the expression levels of the ALX1 in eutopic endometrial samples from patients compared to normal endometrium (p = 0.007). Although the expression of ALX1 increased in ectopic endometrium tissues of women with endometriosis compared with eutopic endometrium tissues, this increase was not statistically significant (p > 0.05). However, PDHX mRNA expression in both eutopic and ectopic groups was significantly reduced than in the control group (p = 0.017 and p = 0.021, respectively), although the PDHX mRNA decrease was not statistically significant between the endometriosis group (p > 0.05).
Conclusion: It is suggested that deregulation of ALX1 and PDHX genes could be involved in the pathogenesis of endometriosis.
Type of Study: Congress Abstract |
Subject:
Fertility & Infertility
Send email to the article author
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
