[Role of tumor necrosis factor -alpha in the pathogenesis of pregnancy-induced hypertension].
Xu Wang, Jinying Yang, Qibing Xie
Abstract
Xu Wang, Jinying Yang, Qibing Xie
Abstract
OBJECTIVE: To investigate the role of tumor necrosis factor-alpha (TNFalpha) in the pathogenesis of pregnancy induced hypertension (PIH) by damaging endothelial cells. METHODS: 41 patients with PIH and 17 healthy pregnant women were studied. The concentration of TNFalpha in maternal plasma was measured by sensitive radioimmunoassay. The morphology of endothelial cells of placental blood vessels was observed. Endothelial cells were incubated in the presence of TNFalpha (400 U/ml) and sera (30% vol/vol) from PIH women and normal pregnant women to observe their growth and shape. RESULTS: Maternal plasma TNFalpha level in PIH was 2.29 microgram/L +/- 0.51 microgram/L, higher than that in normal pregnancy (the latter was 1.73 microgram/L +/- 0.25 microgram/L, t = 5.60, P < 0.01). The endothelial cells of placental blood vessels in PIH revealed morphologic damages. Both sera of PIH women and TNFalpha were cytotoxic to endothelial cells in culture, including inhibition of the proliferation and morphologic changes of the cells. CONCLUSION: Damage of the endothelial cells of placental blood vessels is associated with the abnormal increase in the maternal blood TNFalpha. Sera of PIH women can damage the endothelial cells in culture and this effect is also associated with TNFalpha.
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OBJECTIVE: To investigate the role of tumor necrosis factor-alpha (TNFalpha) in the pathogenesis of pregnancy induced hypertension (PIH) by damaging endothelial cells. METHODS: 41 patients with PIH and 17 healthy pregnant women were studied. The concentration of TNFalpha in maternal plasma was measured by sensitive radioimmunoassay. The morphology of endothelial cells of placental blood vessels was observed. Endothelial cells were incubated in the presence of TNFalpha (400 U/ml) and sera (30% vol/vol) from PIH women and normal pregnant women to observe their growth and shape. RESULTS: Maternal plasma TNFalpha level in PIH was 2.29 microgram/L +/- 0.51 microgram/L, higher than that in normal pregnancy (the latter was 1.73 microgram/L +/- 0.25 microgram/L, t = 5.60, P < 0.01). The endothelial cells of placental blood vessels in PIH revealed morphologic damages. Both sera of PIH women and TNFalpha were cytotoxic to endothelial cells in culture, including inhibition of the proliferation and morphologic changes of the cells. CONCLUSION: Damage of the endothelial cells of placental blood vessels is associated with the abnormal increase in the maternal blood TNFalpha. Sera of PIH women can damage the endothelial cells in culture and this effect is also associated with TNFalpha.
Key concepts: Pathogenesis, Tumor necrosis factor alpha, Microgram, Endocrinology, Endothelial stem cell, Internal medicine, Medicine, Necrosis