NLRP3 inflammasome activation in gestational diabetes mellitus placentas is associated with hydrogen sulfide synthetase deficiency

Wu, Wei; Tan, Qingying; Xi, Fangfang; Ruan, Yun; Wang, Jing; Luo, Qiong; Dou, Xiaobing; Hu, Tianxiao

doi:10.3892/etm.2021.11017

Cited by 10 publications

(3 citation statements)

References 56 publications

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“…Thus, we propose the possibility that miR-17-5p could NLRP3 inflammasome participates in the regulation of interleukin (IL)-1β and IL-18, 30 which have been considered as important inflammatory cytokines in the development of insulin resistance during GDM. 31 Wu et al found the excessive activation of NLRP3 inflammasome in GDM placental tissues, 32 which was consistent with our results. Besides, NLRP3 inflammasome activation can impair insulin sensitivity by promoting macrophage-T cell activation in adipose tissues.…”

Section: Dovepresssupporting

confidence: 93%

miR-17-5p Promotes Glucose Uptake of HTR8/SVneo Trophoblast Cells by Inhibiting TXNIP/NLRP3 Inflammasome Pathway

Jiang¹,

Wei²,

Zhang³

et al. 2022

DMSO

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Gestational diabetes mellitus (GDM) is one of the common metabolic disorders of pregnancy and results in poor pregnancy outcomes for both mother and fetus. MiR-17-5p is considered as the strongest predictor of metabolic syndrome status, but the relationship between GDM and miR-17-5p remains unclear. TXNIP, which leads to activation of NLRP3, is considered as a potential target of miR-17-5p, and the miR-17-5p/TXNIP/NLRP3 axis has been shown to play a major role in the occurrence and development of many metabolic diseases but has not been validated in GDM. Methods: MiR-17-5p was detected by RT-qPCR. The expression of TXNIP and NLRP3 in placenta was detected by immunofluorescence, RT-qPCR and Western blot. To explore the effect of miR-17-5p on TXNIP and NLRP3 and glucose uptake of HTR8/SVneo cells, miR-17-5p mimic and miR-17-5p inhibitor were transfected to achieve overexpression and inhibition. The interaction between miR-17-5p and TXNIP was confirmed by dual-luciferase reporter assay. Besides, glucose consumption of trophoblast cells was detected by glucose assay kit. Results: MiR-17-5p expression was down-regulated, while the expression of TXNIP and NLRP3 was up-regulated in GDM placental tissues. MiR-17-5p targeted TXNIP and inhibited its expression. MiR-17-5p also regulated NLRP3 expression and glucose uptake of HTR8/SVneo cells, which could be reversed by overexpression of TXNIP, suggesting that miR-17-5p improved glucose uptake of HTR8/SVneo cells by TXNIP/NLRP3 axis. The results were consistent with the above findings in high-glucose treated HTR8/SVneo cells. Conclusion:Our results suggested that miR-17-5p ameliorates the glucose uptake of HTR8/SVneo cells by TXNIP/NLRP3 axis, which may provide a new idea for offspring health of GDM patients.

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Section: Dovepresssupporting

confidence: 93%

miR-17-5p Promotes Glucose Uptake of HTR8/SVneo Trophoblast Cells by Inhibiting TXNIP/NLRP3 Inflammasome Pathway

Jiang¹,

Wei²,

Zhang³

et al. 2022

DMSO

View full text Add to dashboard Cite

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“…Future works should explore the expression levels of IL-12 in patients with CVD and evaluate the pathophysiological consequences of IL-18 overexpression. In particular, due to the association of this cytokine with the NLRP3 inflammasome-a system commonly increased in pathological pregnancies [50,51]-further efforts might be directed to explore this component in women with CVD.…”

Section: Discussionmentioning

confidence: 99%

Histopathological Clues of Enhanced Inflammation in the Placental Tissue of Women with Chronic Venous Disease in Lower Limbs during Pregnancy

Sánchez-Gil,

Fraile-Martinez,

García-Montero

et al. 2024

JPM

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It is estimated that approximately one in three women develop chronic venous disease (CVD) during pregnancy, a broad spectrum of morphofunctional disorders affecting the venous system in different regions of the body, including the lower limbs. A growing body of evidence supports the diverse maternofetal consequences derived from this condition, with the placenta being an organ particularly affected. Among other consequences, having CVD during pregnancy has been associated with systemic inflammation and altered cytokines and chemokine profiles in the maternal and fetal serum related to this condition. In the present work, we aimed to analyze if these inflammatory changes also occurred in the placental tissue of women with CVD, exploring by immunohistochemistry and real-time PCR (RT-qPCR) gene and protein expression of critical inflammatory markers like allograft inflammatory factor 1 (AIF-1), interleukin 10 (IL-10), IL-12A, and IL-18. Our results demonstrate an enhanced tissue expression of AIF-1, IL-12A, and IL-18, accompanied by a decrease in IL-10 in the placentas of women who had undergone CVD during pregnancy. Overall, our results suggest a possible pathophysiological role of inflammation in the placental tissue of women with CVD during pregnancy, although the precise consequences of this feature remain to be deeply analyzed.

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“…The placenta is crucial in the pathogenesis of gestational diabetes mellitus (GDM) [169]. In GDM, deficiency of H 2 S-producing enzymes in the placenta results in excessive activation of the NLRP3 inflammasome, an important inflammatory cytokine involved in the initiation of maternal insulin resistance [111]. Therefore, H 2 S may be involved in the pathogenesis of GDM by controlling NLPR3 inflammasome activation in the placenta.…”

Section: H 2 S Improves Placental Oxidative Damagementioning

confidence: 99%

Therapeutic Potential of Hydrogen Sulfide in Reproductive System Disorders

Sun,

Mao,

Xie

et al. 2024

Biomolecules

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Hydrogen sulfide (H2S), previously regarded as a toxic exhaust and atmospheric pollutant, has emerged as the third gaseous signaling molecule following nitric oxide (NO) and carbon monoxide (CO). Recent research has revealed significant biological effects of H2S in a variety of systems, such as the nervous, cardiovascular, and digestive systems. Additionally, H2S has been found to impact reproductive system function and may have therapeutic implications for reproductive disorders. This paper explores the relationship between H2S and male reproductive disorders, specifically erectile dysfunction, prostate cancer, male infertility, and testicular damage. Additionally, it examines the impact of H2S regulation on the pathophysiology of the female reproductive system, including improvements in preterm birth, endometriosis, pre-eclampsia, fetal growth restriction, unexplained recurrent spontaneous abortion, placental oxidative damage, embryo implantation, recovery of myometrium post-delivery, and ovulation. The study delves into the regulatory functions of H2S within the reproductive systems of both genders, including its impact on the NO/cGMP pathway, the activation of K+ channels, and the relaxation mechanism of the spongy smooth muscle through the ROCK pathway, aiming to broaden the scope of potential therapeutic strategies for treating reproductive system disorders in clinical settings.

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NLRP3 inflammasome activation in gestational diabetes mellitus placentas is associated with hydrogen sulfide synthetase deficiency

Cited by 10 publications

References 56 publications

miR-17-5p Promotes Glucose Uptake of HTR8/SVneo Trophoblast Cells by Inhibiting TXNIP/NLRP3 Inflammasome Pathway

miR-17-5p Promotes Glucose Uptake of HTR8/SVneo Trophoblast Cells by Inhibiting TXNIP/NLRP3 Inflammasome Pathway

Histopathological Clues of Enhanced Inflammation in the Placental Tissue of Women with Chronic Venous Disease in Lower Limbs during Pregnancy

Therapeutic Potential of Hydrogen Sulfide in Reproductive System Disorders

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