未经证实:先兆子痫(PE)与心血管疾病的终生风险增加有关。高密度脂蛋白(HDL)的主要保护功能之一是其在胆固醇反向转运中的作用。患有PE的妇女在怀孕期间HDL介导的胆固醇流出能力(CEC)降低。产后这种情况是否持续未知。
UNASSIGNED:在正常血压(n=44)或PE(n=42)妊娠的妇女产后6个月确定基底和转运蛋白特异性CEC。还在23名正常血压和20名PE妇女中测量了CEC,这些妇女在产后24个月收集了样本。基础,主要使用稳定表达人ABCA1或ABCG1的中国仓鼠卵巢细胞测定ATP结合盒转运蛋白A1(ABCA1)-和-G1(ABCG1)-特异性CEC,并且还使用J774小鼠巨噬细胞系进行评估。
UNASSIGNED:在产后6个月患有PE的女性中,ABCA1特异性CEC显着降低(0.57±0.1vs0.53±0.08;p<0.05),而基础和ABCG1特异性外排没有显着差异。PE后6个月,J774细胞的cAMP特异性CEC也较低(0.85±0.21vs0.75±0.25,p<0.05)。虽然apoA-I,apoE,与对照组相比,患有PE的女性的纤溶酶原和PON-1水平没有显着差异,ABCA1外排确实与apoA-1相关,HDL-C和apoE水平正常后,以及PE妊娠后apoA-1和HDL-C水平。ABCA1特异性外排在产后6至24个月的所有女性中减少,妊娠血压正常的女性为11±1.6%,PE女性为9±1.3%。调整apoA-I水平后,随着时间的推移,两组在产后6个月和血压正常的女性之间的ABCA1特异性外排没有显着差异,但在6至24个月之间,PE女性仍然存在显着差异。
UnASSIGNED:ABCA1介导的CEC在PE妊娠后6个月受损,此后在正常血压和PE妊娠中均下降。ABCA1介导的外排在妊娠后是动态的,但不太可能解释PE女性长期增加的CVD风险。
UNASSIGNED: Preeclampsia (PE) is associated with life-long increased risk of cardiovascular disease. One of the main protective functions of high-density lipoprotein (HDL) is its role in reverse cholesterol transport. HDL-mediated cholesterol efflux capacity (CEC) is decreased during pregnancy in women with PE. Whether this persists postpartum is unknown.
UNASSIGNED: Basal and transporter-specific CEC were determined 6 months postpartum in women who had a normotensive (n = 44) or a PE (n = 42) pregnancy. CEC was also measured in 23 normotensive and 20 PE women for whom samples were collected 24 months postpartum. Basal, ATP-binding cassette transporter-A1 (ABCA1)- and -G1 (ABCG1)-specific CEC were primarily determined using Chinese hamster ovary cells stably expressing human ABCA1 or ABCG1, and were also assessed using a J774 mouse macrophage cell line.
UNASSIGNED: ABCA1-specific CEC was significantly lower in women who had PE 6 months postpartum (0.57 ± 0.1 vs 0.53 ± 0.08; p < 0.05), whilst basal and ABCG1-specific efflux were not significantly different. cAMP-specific CEC in J774 cells was also lower 6 months after PE (0.85 ± 0.21 vs 0.75 ± 0.25, p < 0.05). Although apoA-I, apoE, plasminogen and PON-1 levels were not significantly different in women who had PE compared with controls, ABCA1 efflux did correlate with apoA-l, HDL-C and apoE levels after a normal, and with apoA-l and HDL-C levels after a PE pregnancy. ABCA1-specific efflux decreased in all women between 6 and 24 months postpartum, by 11 ± 1.6% in women who had a normotensive pregnancy and 9 ± 1.3% in women who had PE. After adjustment for apoA-I levels, there was no significant difference in ABCA1-specific efflux between the groups at 6 months postpartum and in normotensive women over time, but remained significantly different between 6 and 24 months in women who had PE.
UNASSIGNED: ABCA1-mediated CEC is impaired 6 months postpartum after a PE pregnancy and decreases thereafter in both normotensive and PE pregnancies. ABCA1-mediated efflux is dynamic after pregnancy but is unlikely to explain the long-term increased CVD risk in women with PE.