{"title":"高血压缺血条件下内皮祖细胞外泌体与内皮细胞通讯受损","authors":"Shuzhen Chen, Venkata Polaki, J. Bihl, Jinju Wang","doi":"10.3389/fstro.2022.1015463","DOIUrl":null,"url":null,"abstract":"We have previously demonstrated that endothelial progenitor cell (EPC) derived exosomes (EPC-EXs) can protect endothelial cells (ECs) against hypoxia injury. Given that EX function varies upon the cellular status and EPC function is declined in hypertension, we speculate the function of EPC-EXs is altered in hypertension-ischemia conditions. Here, we studied the EPC-EX mediated communications of EPCs with ECs in hypertension-ischemia conditions. EPC-EXs were prepared from the bone marrow EPCs of wild-type (WT) and hypertensive renin transgene (R+) mice (WT-EPC-EXs and R-EPC-EXs, respectively). To mimic hypertension-ischemia injury, ECs were challenged with angiotensin II (Ang II; 10−6 M) plus hypoxia (1% O2 for 6 h) and reoxygenation (21% O2 for 24 h). To determine the function of EPC-EXs, ECs were co-cultured with EXs during the reoxygenation period. EX uptake efficiency, EC viability, and angiogenic function were assessed. We found that: (1) The incorporation efficiency of R-EPC-EXs by ECs was significantly decreased compared to the WT-EPC-EXs. (2) Ang II plus hypoxia reoxygenation-injured ECs displayed decreased cell viability, increased cell apoptosis, and compromised angiogenic ability, which were alleviated by R-EPC-EXs. (3) WT-EPC-EXs elicited better effects than R-EPC-EXs on protecting ECs from hypertension plus hypoxia injury. In conclusion, our data have demonstrated that EPC-EXs mediated communication of EPCs and ECs is compromised in hypertension-ischemia conditions, suggesting that impairment of EPC exosomal communication might contribute to the exaggerated cerebral ischemia injury in hypertension-associated ischemic stroke.","PeriodicalId":73108,"journal":{"name":"Frontiers in stroke","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Compromised endothelial progenitor cell exosomal communication with endothelial cells in hypertension ischemia conditions\",\"authors\":\"Shuzhen Chen, Venkata Polaki, J. Bihl, Jinju Wang\",\"doi\":\"10.3389/fstro.2022.1015463\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"We have previously demonstrated that endothelial progenitor cell (EPC) derived exosomes (EPC-EXs) can protect endothelial cells (ECs) against hypoxia injury. Given that EX function varies upon the cellular status and EPC function is declined in hypertension, we speculate the function of EPC-EXs is altered in hypertension-ischemia conditions. Here, we studied the EPC-EX mediated communications of EPCs with ECs in hypertension-ischemia conditions. EPC-EXs were prepared from the bone marrow EPCs of wild-type (WT) and hypertensive renin transgene (R+) mice (WT-EPC-EXs and R-EPC-EXs, respectively). To mimic hypertension-ischemia injury, ECs were challenged with angiotensin II (Ang II; 10−6 M) plus hypoxia (1% O2 for 6 h) and reoxygenation (21% O2 for 24 h). To determine the function of EPC-EXs, ECs were co-cultured with EXs during the reoxygenation period. EX uptake efficiency, EC viability, and angiogenic function were assessed. We found that: (1) The incorporation efficiency of R-EPC-EXs by ECs was significantly decreased compared to the WT-EPC-EXs. (2) Ang II plus hypoxia reoxygenation-injured ECs displayed decreased cell viability, increased cell apoptosis, and compromised angiogenic ability, which were alleviated by R-EPC-EXs. (3) WT-EPC-EXs elicited better effects than R-EPC-EXs on protecting ECs from hypertension plus hypoxia injury. In conclusion, our data have demonstrated that EPC-EXs mediated communication of EPCs and ECs is compromised in hypertension-ischemia conditions, suggesting that impairment of EPC exosomal communication might contribute to the exaggerated cerebral ischemia injury in hypertension-associated ischemic stroke.\",\"PeriodicalId\":73108,\"journal\":{\"name\":\"Frontiers in stroke\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2022-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Frontiers in stroke\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3389/fstro.2022.1015463\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in stroke","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3389/fstro.2022.1015463","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Compromised endothelial progenitor cell exosomal communication with endothelial cells in hypertension ischemia conditions
We have previously demonstrated that endothelial progenitor cell (EPC) derived exosomes (EPC-EXs) can protect endothelial cells (ECs) against hypoxia injury. Given that EX function varies upon the cellular status and EPC function is declined in hypertension, we speculate the function of EPC-EXs is altered in hypertension-ischemia conditions. Here, we studied the EPC-EX mediated communications of EPCs with ECs in hypertension-ischemia conditions. EPC-EXs were prepared from the bone marrow EPCs of wild-type (WT) and hypertensive renin transgene (R+) mice (WT-EPC-EXs and R-EPC-EXs, respectively). To mimic hypertension-ischemia injury, ECs were challenged with angiotensin II (Ang II; 10−6 M) plus hypoxia (1% O2 for 6 h) and reoxygenation (21% O2 for 24 h). To determine the function of EPC-EXs, ECs were co-cultured with EXs during the reoxygenation period. EX uptake efficiency, EC viability, and angiogenic function were assessed. We found that: (1) The incorporation efficiency of R-EPC-EXs by ECs was significantly decreased compared to the WT-EPC-EXs. (2) Ang II plus hypoxia reoxygenation-injured ECs displayed decreased cell viability, increased cell apoptosis, and compromised angiogenic ability, which were alleviated by R-EPC-EXs. (3) WT-EPC-EXs elicited better effects than R-EPC-EXs on protecting ECs from hypertension plus hypoxia injury. In conclusion, our data have demonstrated that EPC-EXs mediated communication of EPCs and ECs is compromised in hypertension-ischemia conditions, suggesting that impairment of EPC exosomal communication might contribute to the exaggerated cerebral ischemia injury in hypertension-associated ischemic stroke.