Intravenous human endothelial progenitor cell administration into aged mice enhances embryo development and oocyte quality by reducing inflammation, endoplasmic reticulum stress and apoptosis

The Journal of Veterinary Medical Science

Hyun Ju OH¹  Geon A KIM²  Yeonjae LEE³  Hyun Jin KIM⁴ 

[1] Biostar Stem Cell Research Institute, R Bio Co., Ltd., Seoul 08506, Republic of Korea;Department of Theriogenology and Biotechnology, College of Veterinary Medicine, Seoul National University, Seoul, 08826, Republic of Korea;Hankuk Academy of Foreign Studies, Yongin-si, Gyeonggi-do 17035, Republic of Korea;Seoul National University, Seoul 08826, Republic of Korea

关键词: endoplasmic reticulum stress;    human endothelial progenitor cells;    inflammation;    ovarian aging;   

DOI  :  10.1292/jvms.18-0242

学科分类：兽医学

来源: Japanese Society of Veterinary Science

【 摘 要 】

Stem cell therapy has been proposed to restore the function and structure of injured tissues. In the present study, we investigated the ability of human endothelial progenitor cells (hEPCs) to attenuate ovarian aging and dysfunction. Female ICR mice aged 4 and 6 months were injected with cultured hEPCs. Cultured hEPCs were injected intravenously twice with 5 × 104 cells with a 4 day interval. After pregnant mare serum gonadotropin and human chorionic gonadotropin stimulation, oocytes and ovaries of aged mice were collected, cumulus-free oocytes were activated by SrCl2 and gene expression levels related to inflammation, apoptosis, follicle development and endoplasmic reticulum (ER) stress in ovaries were compared. Administration of hEPCs attenuated the level of inflammatory cytokines and adverse apoptotic factor, as well as reducing ER stress in the ovaries. Increased cleavage and blastocyst formation rates and cell numbers in blastocysts from hEPCs-treated aged mice vs. same aged control mice demonstrated a protective function of hEPCs against reproductive aging. Based on these data, we suggest that treatment with hEPCs attenuates reproductive aging and dysfunction potentially via regulation of inflammation, apoptosis and ER stress.

【 授权许可】

Unknown