Overexpression of CD39 protects in a mouse model of preeclampsia
Overexpression of CD39 protects in a mouse model of preeclampsia
复制标题
CD39 过度表达可保护先兆子痫小鼠模型
作者：
J. McRae;P. Russell;Joanne S. J. Chia;K. Dwyer
CD39 (NTPDase1) 是一种重要的免疫和血管核酸外切酶，可将促炎和促血栓形成的核苷酸（5'-三磷酸腺苷 (ATP) 和二磷酸腺苷）水解为腺苷。在人类中，CD39 是胎盘滋养层组织中的主要核酸外切酶，可调节 ATP 依赖性滋养层功能。 CD39 是调节性 T 细胞 (Treg) 的重要组成部分，对于免疫耐受和正常妊娠的维持至关重要。我们研究了 CD39 过度表达对先兆子痫小鼠模型的影响。在原始 BALB/c 雌性（野生型（WT）或 CD39 转基因（CD39TG））和 C57BL/6 雄性小鼠之间进行交配。在怀孕第 10 天和第 12 天，注射 BALB/c Th1 极化细胞。在整个怀孕期间测量收缩压（SBP）。小鼠在怀孕第15天被处死。 Th1极化细胞转移后，怀孕WT小鼠的SBP增加（118±3mmHg至142±5mmHg）。尽管肾脏超微结构变化明显，但并不伴有明显的蛋白尿。妊娠 CD39TG 小鼠的 SBP 保持不变（115±±2mmHg 至 114±±3mmHg），没有肾脏病变的证据。我们得出的结论是，母体来源的 Th1 极化细胞转移后可以在小鼠中诱导妊娠高血压，并且 CD39 的过度表达在此模型中具有保护作用。
CD39 (NTPDase1), a critical immune and vascular ecto‐nucleotidase, hydrolyses pro‐inflammatory and pro‐thrombotic nucleotides (adenosine‐5′‐triphosphate (ATP) and adenosine diphosphate) to adenosine. In humans, CD39 is the dominant ecto‐nucleotidase in placental trophoblastic tissues and modulates ATP‐dependent trophoblastic functions. CD39 is an integral component of regulatory T cells (Treg), which are central to immunological tolerance and maintenance of normal pregnancy. We examined the impact of CD39 overexpression in a mouse model of preeclampsia. Matings were performed between virginal BALB/c female (wild‐type (WT) or CD39 transgenic (CD39TG)) and C57BL/6 male mice. On days 10 and 12 of pregnancy BALB/c Th1‐polarized cells were injected. Systolic blood pressure (SBP) was measured throughout pregnancy. Mice were sacrificed at day 15 of pregnancy. Following transfer of Th1‐polarized cells, SBP of pregnant WT mice increased (118 ± 3 mmHg to 142 ± 5 mmHg). Although ultrastructural changes were evident in the kidney this was not accompanied by significant proteinuria. SBP remained unchanged (115 ± 2 mmHg to 114 ± 3 mmHg) in pregnant CD39TG mice without evidence of renal lesions. We conclude that gestational hypertension can be induced in mice following transfer of maternally derived Th1‐polarized cells and that overexpression of CD39 is protective in this model.
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DOI：
10.1152/ajpregu.00049.2012
发表时间：
2012-07
期刊：
American journal of physiology. Regulatory, integrative and comparative physiology
影响因子：
--
作者：
K. Wallace;Sarah Novotny;J. Heath;Janae Moseley;J. Martin;M. Owens;B. LaMarca
通讯作者：
K. Wallace;Sarah Novotny;J. Heath;Janae Moseley;J. Martin;M. Owens;B. LaMarca
影响因子：
9.8
作者：
Buchbinder, A;Sibai, BM;Thurnau, G
通讯作者：
Thurnau, G
先兆子痫中人胎盘腺苷受体的表达升高，缺氧会增加 A2A 受体的表达。
影响因子：
3.8
作者：
vonVersen-Höynck,F;Rajakumar,A;Bainbridge,SA;Gallaher,MJ;Roberts,JM;Powers,RW
通讯作者：
Powers,RW
P2Y1 受体和 NTPDase1/CD39 在人胎盘小凹内的共定位。
DOI：
--
发表时间：
2004
期刊：
European journal of histochemistry : EJH
影响因子：
--
作者：
Kittel,A;Csapó,ZS;Csizmadia,E;Jackson,SW;Robson,SC
通讯作者：
Robson,SC