Pressure-induced maturation of endothelial cells on newborn mouse carotid arteries.
Pressure-induced maturation of endothelial cells on newborn mouse carotid arteries.
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压力诱导新生小鼠颈动脉内皮细胞的成熟。
DOI：
10.1152/ajpheart.00099.2013
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发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Flavahan,NicholasA
中科院分区：
文献类型：
--
作者：
Flavahan,Sheila;Mozayan,MansoorM;Lindgren,Isa;Flavahan,NicholasA
实验研究了出生后内皮细胞功能的成熟。分离新生(出生后第1天，P1)至P21小鼠的颈动脉，在跨壁压(Ptm)为20 mm Hg(P1血压，BP)的情况下进行肌图检查。乙酰胆碱对P1无效，但对P7动脉有强烈的扩张作用，而NO供体DEA-NOate在P1和P7引起类似的扩张。抑制一氧化氮合酶(L-NAME)或磷脂酰肌醇-3-激酶(PI3K)(Wortmannin，LY294002)可消除P7时对乙酰胆碱的扩张。内皮型一氧化氮合酶(ENOS)在P7较P1动脉表达减少，但乙酰胆碱使P7的PO4-eNOS-Ser1177表达增加，但对P1动脉无影响。因此，内皮成熟可能反映了PI3K、Akt和eNOS信号的增加。全身性血压在出生后早期显著升高。将P1动脉暴露于短暂增加的PTM(50毫米汞柱，60min)后，乙酰胆碱引起强烈的扩张和PO4-eNOS-Ser1177的增加。PI3K或NOS抑制可取消压力诱导的乙酰胆碱扩张的挽救作用。一过性增加的PTM不影响P7动脉的扩张，也不影响P1动脉对NO供体的扩张。内皮细胞黏附连接的宽度(VE-钙粘附素免疫荧光)从P1到P7显著增加，在暴露于一过性PTM的P1动脉中增加。VE-钙粘附素的功能阻断抗体减少了压力诱导的P1处乙酰胆碱反应的挽救，以及P7动脉对乙酰胆碱的扩张。因此，新生儿内皮扩张器功能的成熟可能是通过出生后血压升高来诱导的。此外，这可能是由VE-钙粘附素在粘附性连接处的信号所介导。这一成熟途径的中断可能导致发育和成人血管疾病。
Experiments investigated maturation of endothelial function in the postnatal period. Carotid arteries isolated from newborn (postnatalday 1, P1) to P21 mice were assessed in myographs at transmural pressure (PTM) of 20 mmHg (P1 blood pressure, BP). Acetylcholine was ineffective in P1 but powerfully dilated P7 arteries, whereas NO-donor DEA-NONOate caused similar dilation at P1 and P7. Dilation to acetylcholine at P7 was abolished by inhibition of NO synthase (NOS) (l-NAME) or of phosphoinositide-3-kinase (PI3K) (wortmannin, LY294002). Endothelial NOS (eNOS) expression decreased in P7 compared with P1 arteries, although acetylcholine increased PO4-eNOS-Ser1177in P7 but not in P1 arteries. Endothelial maturation may therefore reflect increased signaling through PI3K, Akt, and eNOS. Systemic BP increases dramatically in the early postnatal period. After exposing P1 arteries to transient increased PTM(50 mmHg, 60 min), acetylcholine caused powerful dilation and increased PO4-eNOS-Ser1177. Pressure-induced rescue of acetylcholine dilation was abolished by PI3K or NOS inhibition. Transient increased PTMdid not affect dilation at P7, or dilation to NO-donor in P1 arteries. Width of endothelial adherens junctions (VE-cadherin immunofluorescence) increased significantly from P1 to P7, and in P1 arteries exposed to transient increased PTM. A function-blocking antibody to VE-cadherin reduced the pressure-induced rescue of acetylcholine responses at P1, and the dilation to acetylcholine in P7 arteries. Therefore, maturation of newborn endothelium dilator function may be induced by increasing BP in the postnatal period. Furthermore, this may be mediated by VE-cadherin signaling at adherens junctions. Interruption of this maturation pathway may contribute to developmental and adult vascular diseases.
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DOI：
10.1152/ajpregu.00427.2004
发表时间：
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期刊：
American journal of physiology. Regulatory, integrative and comparative physiology
影响因子：
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