Soluble VEGF Receptor (sVEGFR1/sFlt-1)可溶性血管内皮生长因子受体1是反映血管内皮功能的可靠指标

妊娠高血压或先兆子癫是一种妊娠相关高血压疾病， 并严重影响胎儿发育和存活率， 以及妊娠妇女的安全，目前发病机理尚不清楚。胎盘组织缺血缺氧在这一病理过程发生发展中具有重要作用。 有研究报告， 先兆子癫患者胎盘组织缺血缺氧、血管内皮细胞功能异常， 造成血液循环中可溶性血管内皮生长因子受体1明显升高。可溶性血管内皮生长因子受体1的高度表达、合成和释放所致的血液中含量升高可以作为一种有效的临床检测手段，为研究先兆子癫的早期预警提供依据。北京爱迪博生物推出人可溶性血管内皮生长因子受体1酶联试剂盒，可以检测血清或血浆中可溶性血管内皮生长因子受体1水平。

血管内皮生长因子试剂盒

Synonyms

• fms-related tyrosine kinase 1
• Vascular endothelial growth factor receptor 1 precursor

试剂盒名称 人可溶性血管内皮生长因子受体1酶联试剂盒 产品号 SK00114-02 规格 96 T 检测范围 150-10000 pg/mL 样本体积. 100 ul 样本类型 血清, EDTA 血浆, 唾液 正常值 < 300 pg/mL 先兆子癫 6700 +- 1500 pg/mL 检测操作时间 4 hours 批内差异 <6.5% 批间差异 <10% 说明书   试剂盒名称 人可溶性血管内皮生长因子受体1酶联试剂盒 目录号码 SK00114-01 规格 96 T 监测范围 31.2-2000 pg/mL 样本体积 100 ul ( 10 x dilution required) 样本类型 Serum, EDTA Plasma, Saliva 正常值 75-179 pg/mlL Preeclampsia   检测操作时间 4 hours 批内差异 <4.5% 批内差异 <7% 试剂盒名称 小鼠可溶性血管内皮生长因子受体1酶联试剂盒 目录号码 SK00114-03 规格 96 T 监测范围 156-10000 pg/mL 样本体积 100 ul 样本类型 Serum, EDTA Plasma, Saliva 正常值   Preeclampsia   检测操作时间 4 hours 批内差异 <4.5% 批内差异 <5% 试剂盒名称 人可溶性血管内皮生长因子受体2酶联试剂盒 产品号 SK00123-02 规格 96 T 检测范围 31-2000 pg/mL 样本稀释 10倍 样本体积. 100 ul 样本类型 血清, EDTA 血浆, 唾液 正常值 6500 -15000 pg/mL 检测操作时间 4 hours 批内差异 <4% 批间差异 <8% 试剂盒名称 人可溶性血管内皮生长因子受体2酶联试剂盒 产品号 SK00123-01 规格 96 T 检测范围 78-5000 pg/mL 样本稀释 5倍 样本体积. 100 ul 样本类型 血清, EDTA 血浆, 唾液 正常值 6500 -15000 pg/mL 检测操作时间 4 hours 批内差异 <3.8% 批间差异 <4.9% 试剂盒名称 人可溶性血管内皮生长因子受体3酶联试剂盒 产品号 SK00124-02 规格 96 T 检测范围 0.156-10 ng/mL 样本稀释   样本体积. 100 ul 样本类型 血清, EDTA 血浆, 唾液 检测操作时间 4 hours 批内差异 <6% 批间差异 <9% 试剂盒名称 小鼠可溶性血管内皮生长因子受体3酶联试剂盒 产品号 SK00124-03 规格 96 T 检测范围 62.5 - 2000 pg/mL 样本稀释   样本体积. 100 ul 样本类型 血清, EDTA 血浆, 唾液 检测操作时间 4 hours 批内差异 <5% 批间差异 <7%

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A possible placental factor for preeclampsia: sFlt-1

Despite its clinical importance, the mechanism of preeclampsia is unclear; however, many believe placental pathology might be related to maternal systemic disease. If this is true, a factor which mediates information from the placenta to the maternal circulation can be hypothesized. Among a variety of such reported factors, soluble fms-like tyrosine kinase-1 (sFlt1) will be the focus of this review. The hypoxic placenta, which is commonly found in preeclampsia, produces sFlt1; furthermore, animal experiments suggest its over-expression leads to preeclampsia-like symptoms.

Kita N, Mitsushita J. Curr Med Chem. 2008;15(7):711-5.

Autoantibody from women with preeclampsia induces soluble Fms-like tyrosine kinase-1 production via angiotensin type 1 receptor and calcineurin/nuclear factor of activated T-cells signaling

Preeclampsia is a pregnancy-specific hypertensive syndrome that causes substantial maternal and fetal morbidity and mortality. Recent evidence indicates that maternal endothelial dysfunction in preeclampsia results from increased soluble Fms-like tyrosine kinase-1 (sFlt-1), a circulating antiangiogenic protein. Factors responsible for excessive production of sFlt-1 in preeclampsia have not been identified. We tested the hypothesis that angiotensin II type 1 (AT(1)) receptor activating autoantibodies, which occur in women with preeclampsia, contribute to increased production of sFlt-1. IgG from women with preeclampsia stimulates the synthesis and secretion of sFlt-1 via AT(1) receptor activation in pregnant mice, human placental villous explants, and human trophoblast cells. Using FK506 or short-interfering RNA targeted to the calcineurin catalytic subunit mRNA, we determined that calcineurin/nuclear factor of activated T-cells signaling functions downstream of the AT(1) receptor to induce sFlt-1 synthesis and secretion by AT(1)-receptor activating autoantibodies. AT(1)-receptor activating autoantibody-induced sFlt-1 secretion resulted in inhibition of endothelial cell migration and capillary tube formation in vitro. Overall, our studies demonstrate that an autoantibody from women with preeclampsia induces sFlt-1 production via angiotensin receptor activation and downstream calcineurin/nuclear factor of activated T-cells signaling. These autoantibodies represent potentially important targets for diagnosis and therapeutic intervention.

Zhou CC, et al. Hypertension. 2008 Apr;51(4):1010-9. Epub 2008 Feb 7.