Glycine ameliorates MBP-induced meiotic abnormalities and apoptosis by regulating mitochondrial-endoplasmic reticulum interactions in porcine oocytes

Gao, Lepeng; Zhang, Chang; Yu, Sicong; Liu, Shuang; Wang, Guoxia; Lan, Hainan; Zheng, Xin; Li, Suo

doi:10.1016/j.envpol.2022.119756

Cited by 15 publications

(10 citation statements)

References 36 publications

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“…Numerous in vivo and in vitro studies have shown that MPs cause oxidative stress, apoptosis, inflammation, mitochondrial and lysosomal dysfunction, autophagy, and genotoxicity in various tissues (gut, intestine, liver) and cell types (human keratinocytes, human intestinal epithelial cells, gastric epithelial cells, human umbilical vein endothelial cells) [ 35 , 63 , 70 , 71 , 72 ]. Abnormal colocalization of mitochondria and endoplasmic reticulum has been also found in porcine oocytes exposed to Monobutyl phthalate (phthalates are a group of chemicals associated with PVC products as plasticizers in medical tubing, soft plastic toys, food packaging and in many personal care products) [ 73 ].…”

Section: Resultsmentioning

confidence: 99%

Deeply in Plasticenta: Presence of Microplastics in the Intracellular Compartment of Human Placentas

Ragusa

Matta

Cristiano

et al. 2022

IJERPH

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Microplastics (MPs) are defined as plastic particles smaller than 5 mm. They have been found almost everywhere they have been searched for and recent discoveries have also demonstrated their presence in human placenta, blood, meconium, and breastmilk, but their location and toxicity to humans have not been reported to date. The aim of this study was twofold: 1. To locate MPs within the intra/extracellular compartment in human placenta. 2. To understand whether their presence and location are associated with possible structural changes of cell organelles. Using variable pressure scanning electron microscopy and transmission electron microscopy, MPs have been localized in ten human placentas. In this study, we demonstrated for the first time the presence and localization in the cellular compartment of fragments compatible with MPs in the human placenta and we hypothesized a possible correlation between their presence and important ultrastructural alterations of some intracytoplasmic organelles (mitochondria and endoplasmic reticulum). These alterations have never been reported in normal healthy term pregnancies until today. They could be the result of a prolonged attempt to remove and destroy the plastic particles inside the placental tissue. The presence of virtually indestructible particles in term human placenta could contribute to the activation of pathological traits, such as oxidative stress, apoptosis, and inflammation, characteristic of metabolic disorders underlying obesity, diabetes, and metabolic syndrome and partially accounting for the recent epidemic of non-communicable diseases.

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Section: Resultsmentioning

confidence: 99%

Deeply in Plasticenta: Presence of Microplastics in the Intracellular Compartment of Human Placentas

Ragusa

Matta

Cristiano

et al. 2022

IJERPH

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“…TESPA1 is a protein-bridging subunit that binds and activates ip3r1 to control the release of Ca 2+ from the ER ( Parys and Vervliet, 2020 ), which is the main site of intracellular Ca 2+ storage. When exogenous compounds enter cells, abnormal Ca 2+ metabolism in the ER leads to ERS and thus apoptosis, which has been reported to be a feature of DCM and other heart diseases ( Gao et al, 2022 ; Martinez-Amaro et al, 2023 ).The protein encoded by the THBS4 gene belongs to the platelet-responsive protein family. Members of the platelet-responsive protein family are adhesion glycoproteins that mediate intercellular and intercellular matrix interactions.…”

Section: Discussionmentioning

confidence: 99%

Endoplasmic reticulum stress-related gene expression causes the progression of dilated cardiomyopathy by inducing apoptosis

Chen,

Yang,

et al. 2024

Front. Genet.

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Background: Previous studies have shown that endoplasmic reticulum stress (ERS) -induced apoptosis is involved in the pathogenesis of dilated cardiomyopathy (DCM). However, the molecular mechanism involved has not been fully characterized.Results: In total, eight genes were obtained at the intersection of 1,068 differentially expressed genes (DEGs) from differential expression analysis between DCM and healthy control (HC) samples, 320 module genes from weighted gene co-expression network analysis (WGCNA), and 2,009 endoplasmic reticulum stress (ERGs). These eight genes were found to be associated with immunity and angiogenesis. Four of these genes were related to apoptosis. The upregulation of MX1 may represent an autocompensatory response to DCM caused by a virus that inhibits viral RNA and DNA synthesis, while acting as an autoimmune antigen and inducing apoptosis. The upregulation of TESPA1 would lead to the dysfunction of calcium release from the endoplasmic reticulum. The upregulation of THBS4 would affect macrophage differentiation and apoptosis, consistent with inflammation and fibrosis of cardiomyocytes in DCM. The downregulation of MYH6 would lead to dysfunction of the sarcomere, further explaining cardiac remodeling in DCM. Moreover, the expression of genes affecting the immune micro-environment was significantly altered, including TGF-β family member. Analysis of the co-expression and competitive endogenous RNA (ceRNA) network identified XIST, which competitively binds seven target microRNAs (miRNAs) and regulates MX1 and THBS4 expression. Finally, bisphenol A and valproic acid were found to target MX1, MYH6, and THBS4.Conclusion: We have identified four ERS-related genes (MX1, MYH6, TESPA1, and THBS4) that are dysregulated in DCM and related to apoptosis. This finding should help deepen understanding of the role of endoplasmic reticulum stress-induced apoptosis in the development of DCM.

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“…In contrast, mitochondrial fusion acts as a restorative mechanism to restore a part of mitochondria from reversible damage. Inhibition of mitochondrial fission by depletion of Drp1 caused the failure of follicular maturation and aberrant mitochondria function in oocyte [ 36 – 38 ]. Additionally, MFN1/2 was also demonstrated to be required for maintaining ovarian follicular reserve and oocyte growth [ 39 , 40 ].…”

Section: Discussionmentioning

confidence: 99%

Zinc deficiency deteriorates ovarian follicle development and function by inhibiting mitochondrial function

Liu,

Li,

Lan

et al. 2024

J Ovarian Res

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Zinc (Zn) is a crucial trace element essential for human growth and development, particularly for reproductive health. Previous research has shown a decrease in serum zinc concentration with age and individuals with conditions such as polycystic ovary syndrome (PCOS) and diabetes mellitus. However, the specific effects of zinc deficiency on the female reproductive system, especially ovarian function, are not fully understood. In our study, we observed a significant reduction in the total number of follicles and mature follicles in the zinc deficiency group. This reduction correlated with decreased level of anti-Mullerian hormone (AMH) and abnormal gene expression affecting hormone secretion regulation. Furthermore, we found that zinc deficiency disrupted mitochondrial dynamics, leading to oxidative stress in the ovaries, which further inhibited autophagy and increased ovarian apoptosis. These changes ultimately resulted in the failure of germinal vesicle breakdown (GVBD) and reduced oocyte quality. Meanwhile, administration of zinc glycine effectively alleviated the oocyte meiotic arrest caused by dietary zinc deficiency. In conclusion, our findings demonstrated that dietary zinc deficiency can affect hormone secretion and follicle maturation by impairing mitochondrial function and autophagy.

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Glycine ameliorates MBP-induced meiotic abnormalities and apoptosis by regulating mitochondrial-endoplasmic reticulum interactions in porcine oocytes

Cited by 15 publications

References 36 publications

Deeply in Plasticenta: Presence of Microplastics in the Intracellular Compartment of Human Placentas

Deeply in Plasticenta: Presence of Microplastics in the Intracellular Compartment of Human Placentas

Endoplasmic reticulum stress-related gene expression causes the progression of dilated cardiomyopathy by inducing apoptosis

Zinc deficiency deteriorates ovarian follicle development and function by inhibiting mitochondrial function

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