Placental endothelial nitric oxide synthase expression and role of oxidative stress in susceptibility to preeclampsia in Pakistani women

Shaheen, Ghazala; Jahan, Sarwat; Ain, Qurat Ul; Ullah, Asad; Afsar, Tayyaba; Almajwal, Ali; Alam, Iftikhar; Razak, Suhail

doi:10.1002/mgg3.1019

Cited by 21 publications

(11 citation statements)

References 60 publications

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“…The reduced bioavailability of NO results from the decrease in NO production and/or an increase in reactive oxygen species (ROS) production, leading to an imbalance between NO and O 2 •− , the formation of ONOO - and the inhibition of eNOS activity [ 157 , 158 ] ( Table 1 ). Oxidative stress may affect NO synthesis substrates and eNOS activity or expression [ 159 ].…”

Section: Placental Enos Dysfunction and Oxidative Stress In Pe Pathogmentioning

confidence: 99%

Role of oxidative stress in the dysfunction of the placental endothelial nitric oxide synthase in preeclampsia

et al. 2021

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Preeclampsia (PE) is a multifactorial pregnancy disease, characterized by new-onset gestational hypertension with (or without) proteinuria or end-organ failure, exclusively observed in humans. It is a leading cause of maternal morbidity affecting 3–7% of pregnant women worldwide. PE pathophysiology could result from abnormal placentation due to a defective trophoblastic invasion and an impaired remodeling of uterine spiral arteries, leading to a poor adaptation of utero-placental circulation. This would be associated with hypoxia/reoxygenation phenomena, oxygen gradient fluctuations, altered antioxidant capacity, oxidative stress, and reduced nitric oxide (NO) bioavailability. This results in part from the reaction of NO with the radical anion superoxide (O 2 •− ), which produces peroxynitrite ONOO - , a powerful pro-oxidant and inflammatory agent. Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S -glutathionylation). The uncoupling of eNOS triggers a switch of its activity from a NO-producing enzyme to a NADPH oxidase-like system generating O 2 •− , thereby potentiating ROS production and oxidative stress. Moreover, in PE placentas, eNOS could be post-translationally modified by lipid peroxidation-derived aldehydes such as 4-oxononenal (ONE) a highly bioreactive agent, able to inhibit eNOS activity and NO production. This review summarizes the dysfunction of placental eNOS evoked by oxidative stress and lipid peroxidation products, and the potential consequences on PE pathogenesis.

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Section: Placental Enos Dysfunction and Oxidative Stress In Pe Pathogmentioning

confidence: 99%

Role of oxidative stress in the dysfunction of the placental endothelial nitric oxide synthase in preeclampsia

et al. 2021

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“…In Shaheen et al (), the address reflected for the corresponding author, Suhail Razak, in the Correspondence section was incorrect. The correct information is shown below.…”

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confidence: 99%

Placental endothelial nitric oxide synthase expression and role of oxidative stress in susceptibility to preeclampsia in Pakistani women

Shaheen¹,

Jahan²,

Ain³

et al. 2020

Molec Gen & Gen Med

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“…In women with preeclampsia, the rate of complications can reach 22% [ 4 ]. Preeclampsia is the main cause of preterm birth, intrauterine growth restriction, and perinatal mortality [ 11 ]. Thus, in healthy women, the probability of preterm birth is 7.2%, in pregnant women with hypertension, it increases to 12.5%, in women with preeclampsia, it reaches 39.2% [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

“…However, conducted analysis already allows us to speak about certain patterns in the occurrence of preeclampsia [ 8 ]. Since this disease occurs at the placenta formation and is eliminated when it is separated, it is logical to assume that the pathogenesis, or at least some of its events, should be associated with this organ [ 11 ]. The main pathogenetic events can be divided into two stages.…”

Section: Introductionmentioning

confidence: 99%

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Erythropoietin Mimetic Peptide (pHBSP) Corrects Endothelial Dysfunction in a Rat Model of Preeclampsia

Korokin

Гуреев

Гудырев

et al. 2020

IJMS

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Preeclampsia is a severe disease of late pregnancy. Etiological factors and a pathogenetic pattern of events still require significant clarification, but it is now recognized that a large role is played by placentation disorders and emerging endothelial dysfunction. The administration of short-chain peptides mimicking the spatial structure of the B erythropoietin chain may become one of the directions of searching for new drugs for preeclampsia prevention and therapy. Simulation of ADMA-like preeclampsia in Wistar rats was performed by the administration of a non-selective NOS blocker L-NAME from the 14th to 20th day of pregnancy. The administration of the pHBSP at the doses of 10 µg/kg and 250 µg/kg corrected the established morphofunctional disorders. The greatest effect was observed at a dose of 250 µg/kg. There was a decrease in systolic and diastolic blood pressure by 31.2 and 32.8%, respectively (p < 0.0001), a decrease in the coefficient of endothelial dysfunction by 48.6% (p = 0.0006), placental microcirculation increased by 82.8% (p < 0.0001), the NOx concentration was increased by 42,6% (p = 0.0003), the greater omentum edema decreased by 11.7% (p = 0.0005) and proteinuria decreased by 76.1% (p < 0.0002). In addition, there was an improvement in the morphological pattern of the fetoplacental complex and the ratio of BAX to Bcl-2 expression which characterizes the apoptotic orientation of the cells.

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Placental endothelial nitric oxide synthase expression and role of oxidative stress in susceptibility to preeclampsia in Pakistani women

Cited by 21 publications

References 60 publications

Role of oxidative stress in the dysfunction of the placental endothelial nitric oxide synthase in preeclampsia

Role of oxidative stress in the dysfunction of the placental endothelial nitric oxide synthase in preeclampsia

Placental endothelial nitric oxide synthase expression and role of oxidative stress in susceptibility to preeclampsia in Pakistani women

Erythropoietin Mimetic Peptide (pHBSP) Corrects Endothelial Dysfunction in a Rat Model of Preeclampsia

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