Abstract
We examined the interaction of polymorphisms in the genes heme oxygenase-1 (HMOX1) and nitric oxide synthase (NOS3) in patients with preeclampsia (PE) as well as the responsiveness to methyldopa and to total antihypertensive therapy. The genes HMOX1 (rs2071746, A/T) and NOS3 (rs1799983, G/T) were genotyped using TaqMan allele discrimination assays (Applied Biosystems, Foster City, CA, USA ), and the levels of enzyme heme oxygenase-1 (HO-1) were measured using enzyme-linked immunosorbent assay (ELISA). We found interactions between genotypes of the HMOX-1 and NOS3 genes and responsiveness to methyldopa and that PE genotyped as AT presents lower levels of protein HO-1 compared with AA. We found interactions between the HMOX-1 and NOS3 genes and responsiveness to methyldopa and that the HMOX1 polymorphism affects the levels of enzyme HO-1 in responsiveness to methyldopa and to total antihypertensive therapy. These data suggest impact of the combination of these two polymorphisms on antihypertensive responsiveness in PE.
Highlights
Preeclampsia (PE) is a syndrome characterized by hypertension associated with proteinuria or other systemic signs and is considered one of the major causal factors for maternal and fetal morbidity worldwide.[1]
We found interactions between the HMOX-1 and nitric oxide synthase 3 (NOS3) genes and responsiveness to methyldopa and that the heme oxygenase-1 (HMOX1) polymorphism affects the levels of enzyme heme oxygenase-1 (HO-1) in responsiveness to methyldopa and to total antihypertensive therapy
We investigated if interactions among NFE2L2, HMOX1, and NOS3 polymorphisms were associated with PE and with the responsiveness to antihypertensive therapy in pregnant patients with PE
Summary
Preeclampsia (PE) is a syndrome characterized by hypertension associated with proteinuria or other systemic signs and is considered one of the major causal factors for maternal and fetal morbidity worldwide.[1] Several studies have explored the role of an unbalance between antioxidant and oxidant agents in the pathophysiology of PE, as reviewed elsewhere.[2] despite these efforts, a small number of clinical studies have investigated the heme oxygenase-1 (HO-1), a pivotal enzyme that protects cells against oxidative stress.[3,4,5,6,7,8] Heme oxygenase-1 cleaves heme-producing bilirubin and carbon monoxide (CO), promoting cell protection by its antiapoptotic, antioxidant and antiinflammatory properties. The rs2071746 (A/T) was associated with protective factor for patients with stroke carriers of the A allele, and it was associated with higher expression of HMOX1.13,14
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