卵巢早衰
生物
卵泡发生
卵巢
旁分泌信号
干细胞
间充质干细胞
抗苗勒氏激素
内分泌学
内科学
卵泡膜
移植
男科
激素
细胞生物学
受体
医学
胚胎发生
胚胎
生物化学
作者
Khadijeh Bahrehbar,Sarah Gholami,Zahra Nazari,Mostafa Khanjarpoor Malakhond
标识
DOI:10.1016/j.bbrc.2022.10.014
摘要
Premature ovarian failure (POF) is characterized by amenorrhea, hypoestrogenism, elevated gonadotropin levels, and infertility. Although some of previous studies reported that Mesenchymal stem cells (MSC) transplantation could rescue the ovary function of POF animal models through the paracrine pathways, these mechanisms require further investigation. Here, we aimed to investigate the possible mechanisms of therapeutic effects of human embryonic stem cells derived MSC (ES-MSC) in a mice model of chemotherapy-induced POF. For this purpose, Cyclophosphamide (Cy) was injected intraperitoneally into female mice to induce POF. 10 days after Cy injection, we evaluated follicle count, follicle-stimulating hormone (FSH) and estradiol (E2) hormone concentrations, and TUNEL assay. Then, ES-MSC was transplanted into mice and the expression of Anti-müllerian hormone (AMH) and apoptosis was evaluated in ovary. Results indicated that ES-MSC reduced apoptosis in the follicles and increased the expression of AMH protein in the ovary of POF mice. So, ES-MSC may inhibit the apoptosis of ovarian granulosa cells. Then, to investigate the potential mechanisms of therapeutic effects of ES-MSC and their fate in the ovary, MSC were labeled with green fluorescent protein (GFP) before transplantation. Immunofluorescence staining indicated that although GFP-labeled ES-MSC was located in the ovarian stroma, they did not express granulosa cell markers: AMH and Follicle-stimulating hormone receptor (FSHR), theca cell marker: luteinizing hormone receptor (LHR), and oocyte marker: Growth/differentiation factor 9 (GDF9). Therefore, ES-MSC may not differentiate into ovarian cells directly and they might restore ovarian function in chemotherapy-induced POF mice by paracrine mechanisms.
科研通智能强力驱动
Strongly Powered by AbleSci AI