Increased ADAM10 expression in preeclamptic placentas is associated with decreased expression of hydrogen sulfide production enzymes

Hu, Tianxiao; Wang, G.; Zhu, ZhangChun; Huang, Ying; Gu, Hang; Ni, Xin

doi:10.1016/j.placenta.2015.05.007

Cited by 22 publications

(25 citation statements)

References 15 publications

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“…Furthermore, in a study of pre-eclampsia and ADAM10, Hu et al [33] revealed that the expression of ADAM10 in the placenta of patients with pre-eclampsia was significantly increased, which potentially resulted from the decrease in hydrogen sulfide (H 2 S) in the placenta. ADAM19 had also been reported to play an important role in the invasion of trophoblast cells [34].…”

Section: Discussionmentioning

confidence: 99%

miR-126a-3p induces proliferation, migration and invasion of trophoblast cells in pre-eclampsia-like rats by inhibiting A Disintegrin and Metalloprotease 9

et al. 2019

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The present study aimed to investigate the underlying mechanism of miR-126a-3p in the proliferation, migration and invasion of trophoblast cells in pre-eclampsia-like rats by targeting A Disintegrin and Metalloprotease 9 (ADAM9). First, the interaction between miR-126a-3p and ADAM9 was confirmed via biochemical assays. Placental tissues and trophoblast cells were then obtained. RNA in situ hybridization was performed in order to detect miR-126a-3p expression in the placenta. Subsequently, a series of biological assays, including reverse transcription-quantitative PCR (RT-qPCR), Western blotting, MTT assay, apoptosis assay, cell cycle assay, wound healing assay and transwell assay were adopted in order to determine the cell proliferation, cell cycle distribution, apoptotic rate, and migration and invasion of trophoblast cells in each group. The results revealed that miR-126a-3p was down-regulated in the placenta of pre-eclampsia-like rats. In vivo experiments’ results indicated that miR-126a-3p could inhibit ADAM9 expression, and induce cyclin D1, Matrix metalloproteinase (MMP) 2 (MMP-2), MMP-9 expression. MTT, apoptosis and cell cycle assay results revealed that trophoblast cells transfected with miR-126a-3p mimic or si-ADAM9 exhibited higher proliferative activity and a lower apoptotic rate compared with the blank group (all P<0.05). The wound healing assay and transwell assay results confirmed that, compared with the blank group, the migration and invasion ability of trophoblast cells in the miR-126a-3p mimic group and small interfering RNA (siRNA)-ADAM9 group were significantly increased (all P<0.05). Conversely, miR-126a-3p inhibitor treatment revealed the opposite effect (all P<0.05). In conclusion, the present study demonstrated that miR-126a-3p could enhance proliferation, migration and invasion, but decrease the apoptosis rate of trophoblast cells in pre-eclampsia-like rats through targeting ADAM9.

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Section: Discussionmentioning

confidence: 99%

miR-126a-3p induces proliferation, migration and invasion of trophoblast cells in pre-eclampsia-like rats by inhibiting A Disintegrin and Metalloprotease 9

et al. 2019

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“…Our previous study has demonstrated that H 2 S significantly suppresses sFlt-1 release from placental cells and this effect is associated with inhibition of the shedding process of Flt-1 [7]. H 2 S can be produced in a wide spectrum of tissues through the activity of the synthase enzymes including CSE, CBS, and 3-MST [9].…”

Section: Discussionmentioning

confidence: 99%

“…However, whether or not adipose tissue is the major source of elevated sFlt-1 levels in T2DM patients with peripheral arterial disease remains unknown. Several studies have demonstrated that sFlt-1 can be shedded from the ectodomain of transmembrane Flt-1 by A disintegrin and metalloproteinase 10 (ADAM10) and ADAM17 [6, 7]. In Raikwar et al's study [8], overexpression of ADAM17 increasing Flt-1 cleavage while knockdown of ADAM17 reducing Flt-1 cleavage suggested that ADAM17 was responsible for ectodomain shedding of Flt1.…”

Section: Introductionmentioning

confidence: 99%

Hydrogen Sulfide Inhibits High Glucose-Induced sFlt-1 Production via Decreasing ADAM17 Expression in 3T3-L1 Adipocytes

Wang

et al. 2017

International Journal of Endocrinology

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Hydrogen sulfide (H 2 S) has recently been identified as an endogenous gaseous signaling molecule. The aim of the present study was to investigate the effect of H 2 S on high glucose-(HG-) induced ADAM17 expression and sFlt-1 production in 3T3-L1 adipocytes. Firstly, we found that HG DMEM upregulated the expression of ADAM17 and production of sFlt-1 in 3T3-L1 adipocytes. Knocking down ADAM17 attenuated the effect of high glucose on sFlt-1 production in adipocytes. HG decreased the expression of CSE and 3-MST, as well as the endogenous H 2 S production. Furthermore, knocking down CSE and 3-MST significantly increased ADAM17 expression and sFlt-1 production. The addition of exogenous H 2 S through the administration of sodium hydrosulfide (NaHS) inhibited HG-induced upregulation of ADAM17 expression and sFlt-1 production. In conclusion, decreased expression of CSE and 3-MST and the subsequent decrease in H 2 S production contribute to high glucose-induced sFlt-1 production via activating ADAM17 in adipocytes. Exogenous H 2 S donor NaHS has a potential therapeutic value for diabetic vascular complications.

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“…These observations have provided direct evidence of the role of endogenous H 2 S in the maintenance of vascular health. Human placental CSE and CBS expression and H 2 S production are reduced in PE [338,417]. The inhibition of placenta CSE/H 2 S production by PAG results in PE-like symptoms in mice due to impaired placental angiogenesis [338]; H 2 S supplementation using NaSH or GYY4237 reverses sFlt-1-induced hypertension and proteinuria in rats [338,418].…”

Section: Pathophysiological Evidencementioning

confidence: 99%

Estrogen Receptors and Estrogen-Induced Uterine Vasodilation in Pregnancy

Bai

et al. 2020

IJMS

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Normal pregnancy is associated with dramatic increases in uterine blood flow to facilitate the bidirectional maternal–fetal exchanges of respiratory gases and to provide sole nutrient support for fetal growth and survival. The mechanism(s) underlying pregnancy-associated uterine vasodilation remain incompletely understood, but this is associated with elevated estrogens, which stimulate specific estrogen receptor (ER)-dependent vasodilator production in the uterine artery (UA). The classical ERs (ERα and ERβ) and the plasma-bound G protein-coupled ER (GPR30/GPER) are expressed in UA endothelial cells and smooth muscle cells, mediating the vasodilatory effects of estrogens through genomic and/or nongenomic pathways that are likely epigenetically modified. The activation of these three ERs by estrogens enhances the endothelial production of nitric oxide (NO), which has been shown to play a key role in uterine vasodilation during pregnancy. However, the local blockade of NO biosynthesis only partially attenuates estrogen-induced and pregnancy-associated uterine vasodilation, suggesting that mechanisms other than NO exist to mediate uterine vasodilation. In this review, we summarize the literature on the role of NO in ER-mediated mechanisms controlling estrogen-induced and pregnancy-associated uterine vasodilation and our recent work on a “new” UA vasodilator hydrogen sulfide (H2S) that has dramatically changed our view of how estrogens regulate uterine vasodilation in pregnancy.

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Increased ADAM10 expression in preeclamptic placentas is associated with decreased expression of hydrogen sulfide production enzymes

Cited by 22 publications

References 15 publications

miR-126a-3p induces proliferation, migration and invasion of trophoblast cells in pre-eclampsia-like rats by inhibiting A Disintegrin and Metalloprotease 9

miR-126a-3p induces proliferation, migration and invasion of trophoblast cells in pre-eclampsia-like rats by inhibiting A Disintegrin and Metalloprotease 9

Hydrogen Sulfide Inhibits High Glucose-Induced sFlt-1 Production via Decreasing ADAM17 Expression in 3T3-L1 Adipocytes

Estrogen Receptors and Estrogen-Induced Uterine Vasodilation in Pregnancy

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