Endothelial-derived extracellular vesicles associated with electronic cigarette use impair cerebral microvascular cell function.
Endothelial-derived extracellular vesicles associated with electronic cigarette use impair cerebral microvascular cell function.
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与电子烟使用相关的内皮源性细胞外囊泡会损害脑微血管细胞功能。
DOI：
10.1152/japplphysiol.00243.2023
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发表时间：
2023
期刊：
影响因子：
--
通讯作者：
Garcia,ViniciusP
中科院分区：
文献类型：
--
作者：
Cardenas,HannahL;Evanoff,NicholasG;Fandl,HannahK;Berry,AuburnR;Wegerson,KendraN;Ostrander,EmilyI;Greiner,JaredJ;Dufresne,SheenaR;Kotlyar,Michael;Dengel,DonaldR;DeSouza,ChristopherA;Garcia,ViniciusP
本研究旨在探讨电子烟使用者循环内皮细胞来源的微囊泡(EMVS)对人脑微血管内皮细胞(HCMECs)、一氧化氮(NO)和内皮素(ET)-1产生及组织型纤溶酶原激活物(t-PA)释放的影响。采用流式细胞仪对27例19~25岁青年(10例非吸烟者(6例男性/4岁)、10例电子烟使用者(6例男性/4岁女性)和7例吸烟者(4例男性/3岁女性)的循环EMV(CD144-PE)进行检测。电子烟使用者和吸烟者的EMVS诱导hCMEC表达p-eNOS(495；28.4±4.6vs.29.1±2.8vs.22.9±3.8AU)、Big ET-1(138.8±19.0vs.141.7±19.1vs.90.3±18.8AU)和内皮素转换酶(107.6±10.1vs.86.5±13.2AU)，p-eNOS表达显著降低(Ser1177；7.4±1.7比6.5±0.5比9.7±1.6 AU)。经电子烟(5.7±0.8)µm ol/L；吸烟组(6.3±0.7)µm o l/L；吸烟组(32.1±3.9pg/m L)刺激的内皮细胞产生的NO显著低于非吸烟组(7.6±1.2)µm o l/L；电子烟使用者和吸烟者经EMVS处理后的凝血酶反应T-PA显著低于非吸烟者的EMVS(38.9±4.3至48.4±7.9pg/mL)。在电子烟使用者和吸烟者经EMVS处理的hCMECs中，NO、ET-1或t-PA蛋白的表达或产生没有显著差异。与电子烟使用相关的循环EMVS对脑微血管内皮细胞产生不利影响，并可能导致已报道的电子烟使用后的脑血管功能障碍。在本研究中，我们确定了从电子烟使用者中分离的循环内皮细胞衍生微泡(EMVS)对人脑微血管内皮细胞(HCMECs)、一氧化氮(NO)和内皮素(ET)-1产生以及组织型纤溶酶原激活物(t-PA)释放的影响。电子烟使用者的EMVS减少了脑微血管内皮细胞NO的产生，增加了ET-1的产生，并损害了内皮t-PA的释放。EMV是与使用电子烟相关的中风风险增加的潜在中介因素。
The aim of this study was to determine the effect of circulating endothelial cell-derived microvesicles (EMVs) isolated from e-cigarette users on human cerebral microvascular endothelial cells (hCMECs) nitric oxide (NO) and endothelin (ET)-1 production and tissue-type plasminogen activator (t-PA) release. Circulating EMVs (CD144-PE) were isolated (flow cytometry) from 27 young adults (19–25 yr): 10 nonsmokers (6 M/4 F), 10 e-cigarette users (6 M/4 F), and 7 tobacco cigarette smokers (4 M/3 F). hCMECs were cultured and treated with isolated EMVs for 24 h. EMVs from e-cigarette users and cigarette smokers induced significantly higher expression of p-eNOS (Thr495; 28.4±4.6 vs. 29.1±2.8 vs. 22.9±3.8 AU), Big ET-1 (138.8±19.0 vs. 141.7±19.1 vs. 90.3±18.8 AU) and endothelin converting enzyme (107.6±10.1 and 113.5±11.8 vs. 86.5±13.2 AU), and significantly lower expression of p-eNOS (Ser1177; 7.4±1.7 vs. 6.5±0.5 vs. 9.7±1.6 AU) in hCMECs than EMVs from nonsmokers. NO production was significantly lower and ET-1 production was significantly higher in hCMECs treated with EMVs from e-cigarette (5.7±0.8 µmol/L; 33.1±2.9 pg/mL) and cigarette smokers (6.3±0.7 µmol/L; 32.1±3.9 pg/mL) than EMVs from nonsmokers (7.6±1.2 µmol/L; 27.9±3.1 pg/mL). t-PA release in response to thrombin was significantly lower in hCMECs treated with EMVs from e-cigarette users (from 38.8±6.3 to 37.4±8.3 pg/mL) and cigarette smokers (31.5±5.5 to 34.6±8.4 pg/mL) than EMVs from nonsmokers (38.9±4.3 to 48.4±7.9 pg/mL). There were no significant differences in NO, ET-1, or t-PA protein expression or production in hCMECs treated with EMVs from e-cigarette users and smokers. Circulating EMVs associated with e-cigarette use adversely affects brain microvascular endothelial cells and may contribute to reported cerebrovascular dysfunction with e-cigarette use.NEW & NOTEWORTHY In the present study, we determined the effect of circulating endothelial cell-derived microvesicles (EMVs) isolated from e-cigarette users on human cerebral microvascular endothelial cells (hCMECs) nitric oxide (NO) and endothelin (ET)-1 production and tissue-type plasminogen activator (t-PA) release. EMVs from e-cigarette users reduced brain microvascular endothelial cell NO production, enhanced ET-1 production, and impaired endothelial t-PA release. EMVs are a potential mediating factor in the increased risk of stroke associated with e-cigarette use.
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