CsA Promotes XIST Expression to Regulate Human Trophoblast Cells Proliferation and Invasion Through miR-144/Titin Axis

Yu, Nanhui; Liang, Ying; Zhu, Hong; Mo, Hong-ying; Pei, Haiping

doi:10.1002/jcb.25867

Cited by 11 publications

(9 citation statements)

References 24 publications

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“…41,42,20 A recent report also showed that CsA exerts specific effects on the inhibition of miR-144 expression to regulate proliferation and the invasion of the human cytotrophoblast and therefore acts as an adjuvant in the vitality of trophoblast cells. 43 Although we have not studied proliferation, the analysis of cellular metabolism by MTT did not show metabolic changes, suggesting that there should be no significant cell death associated with CsA treatment, thereby reinforcing the data from the literature.…”

Section: Discussionsupporting

confidence: 81%

The Impact of Immunosuppressive Drugs on Human Placental Explants

et al. 2019

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The use of immunosuppressive drugs guarantees the vitality of the graft and allows gestation in spite of intercurrences such as prematurity and intrauterine growth restriction. However, little is known about the direct effects of immunosuppressive drugs on placental cells. We investigated the effects of immunosuppressive drugs in the chorionic villous explants from human term placentas of healthy gestations. Human placental explants from term gestations (37-39 week gestational age, n = 12) were exposed to cyclosporine A (CSA, 0, 62.5, 125, 1250 ng/mL) or azathioprine (AZA, 0, 5, 10, 100 ng/mL) separately or, in combination for up to 48 hours. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays showed a significant decrease in the explant metabolic activity between AZA and the control group (24 hours, 100 ng/mL, 48 hours, all concentrations, P < .005). Cyclosporin A (CsA) reduced cell activity when associated with AZA (48 hours, P < .005). Fibrinoid deposits increased in AZA-treated explants alone (5 ng/mL, 48 hours; 10 ng/mL, 24-48 hours; P < .005) or when associated with CsA (10 AZA/125 CsA, P < .05), whereas in CsA treatment alone, there was an augment in syncytial knots (24-48 hours, P < .005). The sFLT1 gene (24 hours, P < .05) and protein ( P < .005) expression increased in AZA and CsA-treatments separately or in combination ( P < .05). Placental growth factor increased in AZA (24 hours, 10 ng/mL) and CsA (125 ng/mL; P < .05). In conclusion, our data indicate that AZA primarily acts on the villous metabolism, perturbing placental homeostasis. Since these drugs may alter the balance of angiogenic factors in its selection for clinical application, their impact on the behavior of placental villous should be considered.

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Section: Discussionsupporting

confidence: 81%

The Impact of Immunosuppressive Drugs on Human Placental Explants

et al. 2019

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“…FOS and 3 other members, FOSB, FOSL1 and FOSL2, belong to the Fos gene family, which encode leucine zipper proteins that dimerize with JUN family proteins. The dimers can form a transcription factor complex with activator protein-1 (AP-1) [48][49][50]. Proteins encoded by Fos genes play an important role in cell differentiation, transformation, proliferation and apoptosis [51][52][53].…”

Section: Agingmentioning

confidence: 99%

LncRNA XIST promotes myocardial infarction by regulating FOS through targeting miR-101a-3p

Lin

Wang

et al. 2020

Aging

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The purpose of this study was to reveal the hypothesis that lncRNA X inactive specific transcript (XIST) can participate in the regulation of cardiomyocyte apoptosis in neonatal mice cardiomyocytes (NMCMs) and myocardial infarction (MI) through targeting miR-101a-3p. NMCMs were isolated from neonatal C57BL/6 mice and anoxia was induced in hypoxic chamber. MTT assay and flow cytometry were used to determine proliferation and apoptosis respectively. The target relationship among XIST, miR-101a-3p and FOS was revealed by bioinformatic analysis, luciferase reporter assay, pull-down assay and RNA immunoprecipitation assay. The expression of XIST, miR-101a-3p, FOS and apoptosis-related proteins was determined by qRT-PCR or western blot. MI model was constructed to reveal the role of XIST. We found that XIST was up-regulated in NMCMs under anoxia condition. Moreover, XIST increased FOS expression by sponging miR-101a-3p in anoxia cells. Silencing XIST expression improved cell viability and suppressed apoptosis in vitro and inhibited myocardial infarction by reducing the level of c-FOS and apoptosis-related proteins in vivo. Our findings suggest that XIST is involved in MI, modulation of its level can be used as a new strategy or potential target in the treatment of myocardial infarction.

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“…Certain of these nuclear isoforms of connectins have been implicated as cell cycle promoters 11 , 17 – 19 . The N-terminal short fragment of connectin was expressed in the nucleus of human osteoblastic cells, and promoted proliferation by activating the Wnt/β-catenin pathway 17 .…”

Section: Introductionmentioning

confidence: 99%

Nuclear connectin novex-3 promotes proliferation of hypoxic foetal cardiomyocytes

Hashimoto

Kodama

Sugino

et al. 2018

Sci Rep

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Loss of cardiomyocyte proliferative capacity after birth is a major obstacle for therapeutic heart regeneration in adult mammals. We and others have recently shown the importance of hypoxic in utero environments for active foetal cardiomyocyte proliferation. Here, we report the unexpected expression of novex-3, the short splice variant of the giant sarcomeric protein connectin (titin), in the cardiomyocyte nucleus specifically during the hypoxic foetal stage in mice. This nuclear localisation appeared to be regulated by the N-terminal region of novex-3, which contains the nuclear localisation signal. Importantly, the nuclear expression of novex-3 in hypoxic foetal cardiomyocytes was repressed at the postnatal stage following the onset of breathing and the resulting elevation of oxygen tension, whereas the sarcomeric expression remained unchanged. Novex-3 knockdown in foetal cardiomyocytes repressed cell cycle-promoting genes and proliferation, whereas novex-3 overexpression enhanced proliferation. Mechanical analysis by atomic force microscopy and microneedle-based tensile tests demonstrated that novex-3 expression in hypoxic foetal cardiomyocytes contributes to the elasticity/compliance of the nucleus at interphase and facilitates proliferation, by promoting phosphorylation-induced disassembly of multimer structures of nuclear lamins. We propose that novex-3 has a previously unrecognised role in promoting cardiomyocyte proliferation specifically at the hypoxic foetal stage.

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CsA Promotes XIST Expression to Regulate Human Trophoblast Cells Proliferation and Invasion Through miR-144/Titin Axis

Cited by 11 publications

References 24 publications

The Impact of Immunosuppressive Drugs on Human Placental Explants

The Impact of Immunosuppressive Drugs on Human Placental Explants

LncRNA XIST promotes myocardial infarction by regulating FOS through targeting miR-101a-3p

Nuclear connectin novex-3 promotes proliferation of hypoxic foetal cardiomyocytes

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