Positive correlations between circulating adiponectin and MMP2 in preeclampsia pregnant

Eleuterio, Nibia Mariana; Palei, Ana C.; Machado, Jackeline de Souza Rangel; Tanus‐Santos, Jose E.; Cavalli, Ricardo de Carvalho; Sandrim, Valéria C.

doi:10.1016/j.preghy.2015.03.001

Cited by 39 publications

(29 citation statements)

References 35 publications

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“…Measurements of TIMP-1 and -2 in the circulation and umbilical serum have shown increases or no change in PE versus Norm-Preg women (Montagnana et al, 2009; Deng et al, 2015; Eleuterio et al, 2015), while other studies have shown increases in TIMP-1 and -3 in PE patients (Zhu et al, 2014). The role of MMPs and TIMPs in modulating vascular function and the endothelial dysfunction associated with PE should be further examined in future studies.…”

Section: Placental Ischemia As An Initiating Event In Preeclampsiamentioning

confidence: 91%

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Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Possomato-Vieira

Khalil

2016

Advances in Pharmacology

191

117

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Preeclampsia is a pregnancy-related disorder characterized by hypertension, and could lead to maternal and fetal morbidity and mortality. Although the causative factors and pathophysiological mechanisms are unclear, endothelial dysfunction is a major hallmark of preeclampsia. Clinical tests and experimental research have suggested that generalized endotheliosis in the systemic, renal, cerebral and hepatic circulation could decrease endothelium-derived vasodilators such as nitric oxide, prostacyclin and hyperpolarization factor and increase vasoconstrictors such as endothelin-1 and thromboxane A2, leading to increased vasoconstriction, hypertension and other manifestation of preeclampsia. In search for the upstream mechanisms that could cause endothelial dysfunction, certain genetic, demographic and environmental risk factors have been suggested to cause abnormal expression of uteroplacental integrins, cytokines and matrix metalloproteinases, leading to decreased maternal tolerance, apoptosis of invasive trophoblast cells, inadequate spiral arteries remodeling, reduced uterine perfusion pressure (RUPP), and placental ischemia/hypoxia. RUPP may cause imbalance between the anti-angiogenic factors soluble fms-like tyrosine kinase-1 and soluble endoglin and the pro-angiogenic factors vascular endothelial growth factor and placental growth factor, or stimulate the release of other circulating bioactive factors such as inflammatory cytokines, hypoxia-inducible factor-1, reactive oxygen species, and angiotensin AT1 receptor agonistic autoantibodies. These circulating factors could then target endothelial cells and cause generalized endothelial dysfunction. Therapeutic options are currently limited, but understanding the factors involved in endothelial dysfunction could help design new approaches for prediction and management of preeclampsia.

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Section: Placental Ischemia As An Initiating Event In Preeclampsiamentioning

confidence: 91%

“…2). Some studies showed an increase in circulating MMP-2 and -9 in PE versus Norm-Preg women (Eleuterio et al, 2015) (Table 3). Other studies showed a decrease in serum MMP-9 in PE (Montagnana et al, 2009).…”

Section: Placental Ischemia As An Initiating Event In Preeclampsiamentioning

confidence: 99%

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Possomato-Vieira

Khalil

2016

Advances in Pharmacology

191

117

View full text Add to dashboard Cite

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“…In first trimester trophoblasts, suppression of MMP-9 expression inhibits the trophoblast invasive capability, supporting a role of MMP-9 in trophoblast invasion [54]. However, while some studies showed a decrease in serum MMP-9 in preeclampsia [16], other studies showed an increase in circulating MMP-2 and −9 in preeclamptic vs. normal Preg women [24]. This is likely because plasma MMPs represent global MMP secretion from various maternal tissues, making it important to measure the localized changes in specific MMPs in different maternal tissues.…”

Section: Discussionmentioning

confidence: 99%

“…Also, TIMPs are important endogenous modulators of MMPs activity [16, 18, 25, 88, 89]. Some studies have shown increases or no change in TIMP-1 and −2 in the circulation and umbilical cord serum of preeclamptic vs normal Preg women [16, 24, 90]. Other studies have shown increases in TIMP-1 and −3 in preeclamptic patients [91].…”

Section: Discussionmentioning

confidence: 99%

“…We have previously shown that MMP-2 and MMP-9 are upregulated in the uterus and aorta of Preg rats, and suggested a role of gelatinases in pregnancy-related uterine and vascular remodeling [22, 23]. However, measurements of MMP levels in preeclampsia have not been consistent, with some studies showing an increase in circulating levels of MMP-2 and MMP-9 [24], while other studies show a decrease in MMP-9 in preeclamptic vs normal Preg women [16]. Because plasma MMPs may represent the global MMP production from various maternal tissues, we have previously measured the levels of MMP-2 and MMP-9 in maternal tissues and found that they are reduced in uterus, placenta and aorta of RUPP vs Preg rats, and suggested that downregulation of gelatinases would cause excess collagen deposition, and interfere with spiral arteries remodeling [17].…”

Section: Introductionmentioning

confidence: 99%

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Decreased homodimerization and increased TIMP-1 complexation of uteroplacental and uterine arterial matrix metalloproteinase-9 during hypertension-in-pregnancy

Chen

Ren

Zhu

et al. 2017

Biochemical Pharmacology

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Preeclampsia is a complication of pregnancy manifested as hypertension-in-pregnancy (HTN-Preg) and often intrauterine growth restriction (IUGR). Placental ischemia could be an initiating event, but the molecular mechanisms are unclear. To test the hypothesis that dimerization of matrix metalloproteinases (MMPs) plays a role in HTN-Preg and IUGR, the levels/activity of MMP-9, tissue inhibitor of metalloproteinase (TIMP-1), and their dimerization forms were measured in the placenta, uterus, and uterine artery of normal pregnant (Preg) rats and a rat model of reduced uteroplacental perfusion pressure (RUPP). Consistent with our previous report, blood pressure (BP) was higher, pup weight was lower, and gelatin zymography showed different gelatinolytic activity for pro-MMP-9, MMP-9, pro-MMP-2 and MMP-2 in RUPP vs Preg rats. Careful examination of the zymograms showed additional bands at 200 and 135 kDa. Western blots with MMP-9 antibody suggested that the 200 kDa band was a MMP-9 homodimer. Western blots with TIMP-1 antibody as well as reverse zymography suggested that the 135 kDa band was a MMP-9/TIMP-1 complex. The protein levels and gelatinase activity of MMP-9 homodimer were decreased while MMP-9/TIMP-1 complex was increased in placenta, uterus and uterine artery of RUPP vs Preg rats. The epidermal growth factor (EGF) receptor blocker erlotinib and protein kinase C (PKC) inhibitor bisindolylmaleimide decreased MMP-9 homodimer and increased MMP-9/TIMP-1 complex in placenta, uterus and uterine artery of Preg rats. EGF and the PKC activator phorbol-12,13-dibutyrate (PDBu) reversed the decreases in MMP-9 homodimer and the increases in MMP-9/TIMP-1 complex in tissues of RUPP rats. Thus, the increased BP and decreased pup weight in placental ischemia model of HTN-Preg are associated with a decrease in MMP-9 homodimer and an increase in MMP-9/TIMP-1 complex in placenta, uterus, and uterine artery, which together would cause a net decrease in MMP-9 activity and reduce uteroplacental and vascular remodeling in the setting of HTN-Preg and IUGR. Enhancing EGFR/PKC signaling may reverse the MMP-9 unfavorable dimerization patterns and thereby promote uteroplacental and vascular remodeling in preeclampsia.

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Pregnancy-induced hypertension, preterm birth, and cord blood adipokine levels

et al. 2020

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Maternal hypertension may alter physiological parameters, dysregulating the release of hormones such as adipokines, thus influencing the fetal growth course. This study investigated whether hypertensive disorders of pregnancy alter cord blood adipokine levels and correlate these with anthropometric parameters in preterm infants. This is a prospective cohort study with pregnant women < 37-week gestation with and without hypertension and their offspring. Cord blood leptin, adiponectin, and ghrelin were analyzed by LUMINEX®. These adipokines were compared between the groups exposed or not to gestational hypertension using non-parametric statistical tests. The hypertensive pregnancies had significantly higher cord blood leptin (1.00 (IQR 0.67-1.20 ng/mL)) and adiponectin (18.52 (IQR 17.52-25.13 μg/mL)) levels than those without hypertension (0.07 (IQR 0.06-0.08 ng/mL) and 8.13 (IQR 6.50-8.68 μg/mL), respectively, p < 0.0001). The adipokine levels were higher in AGA and SGA infants in the exposed group for both moderate and late preterm. SGA had significantly higher ghrelin levels than the AGA infants. Ghrelin levels were negatively correlated with birth weight (r = − 0.613, p < 0.001), birth length (r = − 0.510, p < 0.001), head circumference (− 0.346, p < 0.002), and gestational age (r = − 0.612, p < 0.001).Conclusions: Our findings demonstrate an increase in adipokine levels in the cord blood of preterm newborn infants exposed to maternal hypertension. What is Known:• Clinical evidence suggests that concentration of the serum adipokines may be affected by risk of hypertension in both adults and pregnant women.• Maternal profile as hypertension alters intrauterine environment and could affect the function of fetal metabolism, impairing fetal growth.

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Positive correlations between circulating adiponectin and MMP2 in preeclampsia pregnant

Cited by 39 publications

References 35 publications

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Decreased homodimerization and increased TIMP-1 complexation of uteroplacental and uterine arterial matrix metalloproteinase-9 during hypertension-in-pregnancy

Pregnancy-induced hypertension, preterm birth, and cord blood adipokine levels

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