Human menstrual blood stem cells-derived exosomes inhibit endometriosis through apoptosis induction
Human menstrual blood stem cells-derived exosomes inhibit endometriosis through apoptosis induction
Seyedeh Saeideh Sahraei,1Faezeh Davoodi asl,2Naser Kalhor,3Hoda Fazaeli,4Mohsen Sheykhhasan,5Azar Sheikholeslami,6,*
1. 1. Department of Reproductive Biology, the Academic Centre for Education, Culture and Research, Qom Branch, Qom, Iran 2. 2. Department of Mesenchymal Stem Cells, the Academic Centre for Education, Culture and Research, Qom Branch, Qom, Iran 3. 2. Department of Mesenchymal Stem Cells, the Academic Centre for Education, Culture and Research, Qom Branch, Qom, Iran 4. 2. Department of Mesenchymal Stem Cells, the Academic Centre for Education, Culture and Research, Qom Branch, Qom, Iran 5. 2. Department of Mesenchymal Stem Cells, the Academic Centre for Education, Culture and Research, Qom Branch, Qom, Iran 6. 2. Department of Mesenchymal Stem Cells, the Academic Centre for Education, Culture and Research, Qom Branch, Qom, Iran
Introduction: Evidence suggests that retrograde menstrual blood which contains mesenchymal stem cells with differential gene expression compared to healthy women may play a role in endometriosis creation. Apoptosis suppression is one of the most important pathological processes of endometriosis. Also, exosomes have been found to play physiological roles as mediators of intercellular cell signaling between neighboring cells and even amongst distant tissues, and they may act independently but synergistically with soluble growth factors and hormones. The aim of the present study was to evaluate the effect of menstrual blood stem cells-derived exosomes (MenSCs-Exo) on apoptosis of endometriosis cells.
Methods: After confirm exosome extracted from healthy women’s MenSCs (NE-MenSCs) culture supernatant, endometriosis cell (E-MenSCs) were treated with MenSCs-Exo. Apoptosis was analyzed by flowcytometry assay with annexin V-PI kit before and after treatment compared with NE-MenSCs, and the expression level of apoptosis genes (BAX and BCL2) were evaluated by real-time PCR.
Results: MenSCs-Exo surface markers (CD63 and CD81) were verified by flow cytometry and their size by DLS. MenSCs-Exo induced apoptosis in E-MenSCs by increasing annexinb V and propidium iodide (PI) (P < 0.01). Also, induction of apoptosis can be due to regulation of apoptosis related genes expression, including BAX (P<0.05) and BCL-2 (P<0.01). Moreover, the BAX/BCL-2 ratio was significantly higher (R=1.995; p=0.04) in treated E-MenSCs with MenSCs-Exo compared to E-MenSCs.
Conclusion: The results of the present study suggest that MenSCs-Ex can inhibit endometriosis progression at a mild-to-moderate level through induction of apoptosis. However, further studies on endometriosis cell signaling are necessary to achieve more accurate results.