Carbon disulfide induces embryo loss by perturbing the expression of the mTOR signalling pathway in uterine tissue in mice

Huang, Fengyan; Sun, Yuan; Gao, Han; Wu, Hanbin; Wang, Zhiping

doi:10.1016/j.cbi.2018.12.001

Cited by 7 publications

(6 citation statements)

References 29 publications

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“…However, only high levels of iodine were able to upregulate the expression of vascular endothelial growth factor (VEGF)-A in W3 cells (21), MAPK in TPC-1 cells (22), and AKT in TFC (thyroid follicular cells) (23). AKT and MAPK are involved in the PI3K/AKT/mTOR and MAPK signaling pathways, respectively (24,25); both activate downstream VEGF (26,27), which is responsible for angiogenic activation and immune microenvironment disorders in carcinomas (27,28), contributing to proliferation and metastasis (29)(30)(31)(32)(33)(34)(35). It was therefore hypothesized that only high concentrations of iodine can trigger the activation of the PI3K/AKT/mTOR and MAPK pathways and alter VEGF-mediated angiogenesis and immune reactions, thereby promoting the proliferation and metastasis of PTC.…”

Section: Discussionmentioning

confidence: 99%

Association between excessive chronic iodine exposure and the occurrence of papillary thyroid carcinoma

et al. 2020

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The aim of the present study was to elucidate the association between excessive chronic iodine exposure and the risk of developing papillary thyroid carcinoma (PTC). The demographic information and pathological characteristics of patients with thyroid nodules were retrieved from medical records at The Second Hospital of Shandong University. A fasting urine specimen was collected, and creatinine and urinary iodine concentration (UIC) were determined. The water iodine data from the domicile districts of these patients were collated from published reports. The results revealed that almost half of the patients with PTC (44.3%) also exhibited a high UIC (≥300 µg/l). Multivariate analysis revealed that the adjusted odds ratio for high UIC was 3.987 (95% CI: 1.355-11.736) and the adjusted area under the receiver operating characteristic curve was 0.776 (95% CI: 0.687-0.864), which was associated with PTC risk in patients with thyroid nodules. Integrated ecological assessment of chronic iodine exposures demonstrated that >80% (81.4%) of the patients with PTC who also exhibited a high UIC were from historically non-iodine-deficient regions, and 66.7% of patients with PTC who resided in historically iodine-excessive regions were characterized by high UICs. Importantly, a high UIC was significantly associated with capsular invasion and extrathyroid metastasis (P<0.05). Moreover, self-matching results indicated that, in patients with PTC, there were no significant differences in UIC grading between the pre-and postoperative specimens. In conclusion, excessive chronic iodine exposure is significantly associated with the risk of PTC, which contributes to increased capsular invasion and extrathyroid metastases. However, further research is required to validate these findings and to elucidate the potential molecular mechanisms involved.

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Section: Discussionmentioning

confidence: 99%

Association between excessive chronic iodine exposure and the occurrence of papillary thyroid carcinoma

et al. 2020

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“…Chen et al, 2009). Moreover, mTOR, an important factor for embryo loss induced by carbon disulfide, could be downregulated by p-AKT and p-AMPK (Huang et al, 2018). In this study, we explored the AMPK/mTOR signal pathway and found that AMPK was inhibited and mTOR was activated in the aberrant decidualization induced by folate deficiency.…”

Section: Discussionmentioning

confidence: 90%

“…Meanwhile, recent studies found that mTOR is very important for early pregnancy (X. Chen et al, 2009;Huang et al, 2018;J. Kim et al, 2010;Rosario, Nathanielsz, et al, 2017;Zeng et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

AMPK/mTOR downregulated autophagy enhances aberrant endometrial decidualization in folate‐deficient pregnant mice

Zhang

Gao

Zhang

et al. 2021

Journal Cellular Physiology

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Existing evidence suggests that adverse pregnancy outcomes are closely related to dietary factors. Folate plays an important role in neural tube formation and fetal growth, folate deficiency is a major risk factor of birth defects. Our early studies showed that folate deficiency could impair enddecidualization, however, the mechanism is still unclear. Dysfunctional autophagy is associated with many diseases.Here, we aimed to evaluate the adverse effect of folate deficiency on endometrial decidualization, with a particular focus on endometrial cell autophagy. Mice were fed with no folate diet in vivo and the mouse endometrial stromal cell was cultured in a folate-free medium in vitro. The decrease of the number of endometrial autophagosomes and the protein expressions of autophagy in the folate-deficient group indicated that autophagosome formation, autophagosome-lysosome fusion, and lysosomal degradation were inhibited. Autophagic flux examination using mCherry-GFP-LC3 transfection showed that the fusion of autophagosomes with lysosomes was inhibited by folate deficiency. Autophagy inducer rapamycin could reverse the impairment of folate deficiency on endometrial decidualization. Moreover, folate deficiency could reduce autophagy by disrupting AMPK/mTOR signaling, resulting in aberrant endometrial decidualization and adverse pregnancy outcomes. Further coimmunoprecipitation examination showed that decidual marker protein Hoxa10 could interact with autophagic marker protein Cathepsin L, and the interaction was notably reduced by folate deficiency. In conclusion, AMPK/mTOR downregulated autophagy was essential for aberrant endometrial decidualization in early pregnant mice, which could result in adverse pregnancy outcomes. This provided some new clues for understanding the causal mechanisms of birth defects induced by folate deficiency.

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“…The synthesis of cholesterol and oestrogen are dependent on a series of enzymes which are directly regulated by the mTOR (mechanistic target of rapamycin) signalling pathway. As a precursor of arginine, NCG has been shown to activate the mTOR signalling pathway in numerous studies [74][75][76]; it is possible that NCG affects cholesterol and oestrogen synthesis through this pathway as well. Overall, we found that NCG supplementation increases the numbers of large follicles (>5 mm in diameter), angiogenesis, and cholesterol metabolism (including cholesterol biosynthesis and its conversion into oestrogen) in yak ovaries.…”

Section: Discussionmentioning

confidence: 99%

N-Carbamylglutamate Promotes Follicular Development by Modulating Cholesterol Metabolism in Yak Ovaries

Zhou

Yue³

et al. 2021

Agriculture

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This study aimed to investigate the effects of N-carbamylglutamate (NCG) supplementation on the follicular development of yaks to identify potential mechanisms essential for fertility in yaks. Twelve multiparous anoestrous female yaks were randomly assigned to two groups—Control (fed with a basal diet, n = 6) and NCG (basal diet supplemented with 6.0 g day−1 NCG, n = 6). Yaks in the NCG group had higher numbers of large follicles (>5 mm in diameter) than those in the Control group. An RNA-sequencing analysis of yak ovaries revealed a total of 765 genes were differentially expressed between experimental groups, of which 181 genes were upregulated and 584 genes were downregulated following NCG supplementation. The results of a transcriptome functional analysis, qRT-PCR validation, and immunohistochemistry revealed that NCG supplementation increased angiogenesis and de novo synthesis of cholesterol in yak ovaries. NCG was also found to upregulate the gene expression of steroidogenic enzymes. Based on this, it was concluded that NCG supplementation promotes the follicular development of yaks mainly by affecting cholesterol metabolism to initiate steroidogenesis in ovaries. The results provide evidence for understanding the mechanisms responsible for NCG promoting follicular development of female yaks, which may contribute to the development and application of NCG in animal reproduction.

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Carbon disulfide induces embryo loss by perturbing the expression of the mTOR signalling pathway in uterine tissue in mice

Cited by 7 publications

References 29 publications

Association between excessive chronic iodine exposure and the occurrence of papillary thyroid carcinoma

Association between excessive chronic iodine exposure and the occurrence of papillary thyroid carcinoma

AMPK/mTOR downregulated autophagy enhances aberrant endometrial decidualization in folate‐deficient pregnant mice

N-Carbamylglutamate Promotes Follicular Development by Modulating Cholesterol Metabolism in Yak Ovaries

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