Boron Attenuates Heat Stress–Induced Apoptosis by Inhibiting Endoplasmic Reticulum Stress in Mouse Granulosa Cells

Xiong, Yi; Jin, Erhui; Yin, Qirun; Che, Chuanyan; He, Shang

doi:10.1007/s12011-020-02180-1

Cited by 14 publications

(3 citation statements)

References 49 publications

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“…Caspase-3 was a protein implicated in apoptosis and its suppression led to inhibited apoptosis. 35 Caspase-8 played a role in receptor-mediated extrinsic pathway, while caspase-9 was involved in the mitochondrial intrinsic pathway, and both caspase-8 and caspase-9 were implicated in apoptosis following caspase-3 activation. 36 Meanwhile, some proteins from the Bcl-2 family were also involved in apoptosis, such as Bcl-2 and Bax.…”

Section: Discussionmentioning

confidence: 99%

Etanercept Protected Against Cigarette Smoke Extract-Induced Inflammation and Apoptosis of Human Pulmonary Artery Endothelial Cells via Regulating TNFR1

Xue¹,

Xie²,

Xu³

et al. 2021

COPD

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Purpose: Etanercept (ETN), a tumor necrosis factor-α (TNF-α) inhibitor, has been applied in the treatment of many diseases. However, whether it has effects on chronic obstructive pulmonary disease (COPD) and its interaction with tumor necrosis factor receptor 1 (TNFR1) remained unknown. Methods: Histopathological analysis of lung tissues from non-smokers and smokers with or without COPD was conducted using hematoxylin-eosin (H&E) staining, Van Gieson (VG) staining, and terminal transferase-mediated biotin dUTP nick end labeling (TUNEL). TNF-α content was measured using Immunohistochemistry. Correlation analysis among apoptosis rate, smoke index, the FEV1/FVC ratio, and TNF-α-positive cells was performed. After ETN treatment and transfection of overexpressed or silenced TNFR1, levels of inflammatory cytokines, apoptosis and related genes expressions in cigarette smoke extract (CSE)-treated human pulmonary artery endothelial cells (HPAECs) were detected using enzyme-linked immunosorbent assay (ELISA), Hoechst 33342 staining, flow cytometry, quantitative realtime PCR (qRT-PCR) and Western blot. Results: Pulmonary arterial remodeling and increased apoptotic and TNF-α + HPAECs were found in lung tissue of smokers with or without COPD, with higher degrees in smokers with COPD. The numbers of apoptotic and TNF-α + HPAECs were positively correlated with smoke index, while the FEV1/FVC ratio was negatively correlated with apoptotic HPAECs. In HPAECs, ETN downregulated the expressions of proteins related to CSE-induced apoptosis and the TNF receptor family, decreased CSE-induced cell apoptosis and inflammatory cytokine levels, and inhibited TNFR1 expression and p65 phosphorylation. Overexpressed TNFR1 reversed the effects of ETN on CSE-treated HPAECs, whereas silencing TNFR1 did the opposite. Conclusion: ETN protected HPAECs against CSE-induced inflammation and apoptosis via downregulating TNFR1, thus providing a potential therapy for smoking-induced COPD.

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Section: Discussionmentioning

confidence: 99%

Etanercept Protected Against Cigarette Smoke Extract-Induced Inflammation and Apoptosis of Human Pulmonary Artery Endothelial Cells via Regulating TNFR1

Xue¹,

Xie²,

Xu³

et al. 2021

COPD

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“…Bax is a proapoptotic protein which could prevent the suppressive effect of Bcl‐2 on apoptosis by forming heterodimers with Bcl‐2, whereas Bcl‐2 was identified as an antiapoptotic protein in many cells (Tirapelli et al, 2017; Wang et al, 2011). Protein C Caspase‐3 belongs to the endo‐protease family and was reported to have a regulatory effect on inflammation and apoptosis signaling networks, and inhibiting C Caspase‐3 activation led to inhibited apoptosis (Xiong et al, 2020). It was also suggested that miR‐139‐5p could upregulate Bcl‐2 expression and downregulate Bax and C Caspase‐3 expressions in ultraviolet B (UVB)‐induced keratinocyte cells (Yu et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

miR‐139‐5p upregulation alleviated spontaneous recurrent epileptiform discharge‐induced oxidative stress and apoptosis in rat hippocampal neurons via regulating the Notch pathway

Zhao

Yang

Wang

et al. 2020

Cell Biology International

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Epilepsy was characterized by the occurrence of spontaneous recurrent epileptiform discharges (SREDs) in neurons. Previous studies suggested that microRNA (miR)−139‐5p and the Notch pathway were implicated in epilepsy; however, their interaction remained vague. Rat primary hippocampal neurons were isolated and identified by immunofluorescence staining. The cells were then used for SREDs model construction and further subjected to flow cytometry for apoptosis detection. Contents of lactate dehydrogenase (LDH), malondialdehyde (MDA), super oxidase dismutase (SOD) contents, and reactive oxygen species (ROS), and the level of mitochondrial membrane potential (MMP) were determined using commercial kits. Target gene and potential binding sites of miR‐139‐5p were predicted with TargetScan and confirmed by dual‐luciferase reporter assay. Expressions of miR‐139‐5p, Notch pathway‐related proteins and apoptosis‐related proteins were measured by quantitative real‐time polymerase chain reaction and western blot as needed. The results showed that the hippocampal neurons were microtubule‐associated protein 2 (MAP2)‐positive. miR‐139‐5p was downregulated in SREDs model cells. SREDs promoted apoptosis and increased the contents of LDH, MDA, and ROS and the level of MMP while reducing miR‐139‐5p expression and SOD content in cells, which was reversed by miR‐139‐5p overexpression. Notch‐1 was recognized as the target gene of miR‐139‐5p, and its expression was negatively regulated by miR‐139‐5p. Besides, Notch‐1 overexpression reversed the effects of miR‐139‐5p upregulation on the expressions of Notch pathway‐related proteins and apoptosis‐related proteins, cell apoptosis, oxidative stress and MMP in SREDs‐treated cells. Our results indicated that miR‐139‐5p upregulation alleviated SREDs‐induced oxidative stress and cell apoptosis via regulating the Notch pathway, which provides new insights into the role of miRNA in the occurrence and development of epilepsy.

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“…Activation of both JNK and CHOP attenuates the function of anti-apoptotic protein Bcl-2, while enhancing the activity of pro-apoptotic proteins such as Bim, Bax and PUMA, leading to mitochondrial dysfunction and Cyt c release. ER stress activates IRE1 to recruit and activate necrotic tumor receptor-associated factor 2 (TRAF2), which further activates JNK and leads to apoptosis ( 60 , 61 ). CHOP can regulate the expression of Bcl-2, GADD34 and TRB3 ( 62 ).…”

Section: Mechanism Of Apoptosismentioning

confidence: 99%

The role of interaction between autophagy and apoptosis in tumorigenesis (Review)

Xi¹,

Wang²,

Wang³

et al. 2022

Oncol Rep

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Autophagy is a highly conserved process that maintains cellular homeostasis during evolution. Autophagy can occur in the form of macroautophagy, microautophagy or molecular chaperone autophagy, among which macroautophagy is the most common. Apoptosis exists in all kinds of cell organisms, and is a kind of programmed cell death which is regulated by pro-apoptotic factors and anti-apoptotic signals.The main biological feature of apoptosis is the activation of caspase. Apoptosis is induced by a variety of cell signals, such as endoplasmic reticulum stress, induction of toxic substances, stimulation of pathogenic microorganisms and DNA damage. Inextricable links are found between autophagy and apoptosis. Studies have found that numerous of the autophagy molecules and autophagy signaling pathways involved in the process of autophagy are related to apoptosis. In addition to regulating autophagy, the autophagy signaling pathway also regulates apoptosis. The interaction between the two can achieve a dynamic balance to certain extent, which maintains the basic physiological functions of cells and reduces the damage to the body under stress. Disease occurs when the balance between autophagy and apoptosis is disrupted. Tumors form due to the ability of cells to avoid apoptosis. Autophagy is closely related to apoptosis, there must be a close connection between the three. In the present review, the mechanism between autophagy and apoptosis and the impact of their interaction on tumorigenesis shall be discussed.

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Boron Attenuates Heat Stress–Induced Apoptosis by Inhibiting Endoplasmic Reticulum Stress in Mouse Granulosa Cells

Cited by 14 publications

References 49 publications

Etanercept Protected Against Cigarette Smoke Extract-Induced Inflammation and Apoptosis of Human Pulmonary Artery Endothelial Cells via Regulating TNFR1

Etanercept Protected Against Cigarette Smoke Extract-Induced Inflammation and Apoptosis of Human Pulmonary Artery Endothelial Cells via Regulating TNFR1

miR‐139‐5p upregulation alleviated spontaneous recurrent epileptiform discharge‐induced oxidative stress and apoptosis in rat hippocampal neurons via regulating the Notch pathway

The role of interaction between autophagy and apoptosis in tumorigenesis (Review)

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