The role of necroptosis in neurosurgical diseases

Liu, T.; Bao, Yang; Wang, Y.; Jiang, Jiyao

doi:10.1590/1414-431x20144310

Cited by 25 publications

(18 citation statements)

References 79 publications

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“…il-1β, il-6 and TnF-α are crucial cytokines in vivo (37)(38)(39). a previous study reported that the initiation of apoptosis was due to the activation of the homologous il-1β-converting enzyme protease family; it converts the newly synthesized precursor of il-1β into active il-1β, and results in the breakdown of matrix proteins that maintain the structure and function of cells, in addition to mediating apoptosis by activating other members of the family (37).…”

Section: Discussionmentioning

confidence: 99%

Identification of microRNA‑363‑3p as an essential regulator of chondrocyte apoptosis in osteoarthritis by targeting NRF1 through the p53‑signaling pathway

Zhang

Wang

et al. 2020

Mol Med Report

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osteoarthritis (oa) is a degenerative joint disease that affects the physical, and mental health of middle-aged and elderly people. The aims of the present study were to determine the biological function and molecular mechanisms of mir-363-3p in chondrocyte apoptosis. exploration of the molecular mechanisms of oa may be helpful in the understand of the causes, and facilitating the prevention and treatment of oa. in the present study, the expression of nuclear respiratory factor1 (nrF1) was downregulated in the articular cartilage of oa rats in vivo and lipopolysaccharide (lPS)-treated chondrocytes in vitro. Micrornas (mirna) are regulators of gene expression in the progression of oa. TargetScan software was used to predict that nrF1 was a potential target for mirna (miR)-363, and this was confirmed in subsequent experiments. The expression of mir-363-3p was negatively correlated with the expression of NRF1, and its expression was significantly upregulated in oa model rats and in lPS-induced chondrocytes compared with the expression in the respective controls. in addition, the overexpression of mir-363-3p increased the levels of interleukin (il)-1β, il-6 and tumor necrosis factor-α in vivo, and was demonstrated to promote chondrocyte injury and apoptosis by Safranin o staining and Tunel. Moreover, the inhibition of mir-363-3p expression increased the expression of nrF1 and protected chondrocytes from apoptosis in vitro and in vivo, whereas the overexpression of mir-363-3p downregulated nrF1 expression and promoted lPS-induced chondrocyte apoptosis through the p53 pathway in vitro. The results of this study suggested that mir-363-3p-mediated inhibition of nrF1may be associated with chondrocyte apoptosis in oa.

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Section: Discussionmentioning

confidence: 99%

Identification of microRNA‑363‑3p as an essential regulator of chondrocyte apoptosis in osteoarthritis by targeting NRF1 through the p53‑signaling pathway

Zhang

Wang

et al. 2020

Mol Med Report

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“…A recent study also shows that the ROS-activated MAPK pathway attributes to the HG-induced cardiac cell injury [33]. However, the intracellular mechanisms responsible for the hyperglycemia-induced cardiac injury and inflammation are complicated, several signal molecules, including TLR4 [22, 23] and RIP3 [21, 25] have been shown to participate in the cardiac injury caused by hyperglycemia. But what is the relationship between ROS, TLR4 and RIP3 is still unclear in the HG-treated cardiac cells.…”

Section: Discussionmentioning

confidence: 99%

“…For example, RIP3 expression is increased in ischemic hearts and RIP3 deficiency protects mice hearts against ischemic injury [49]. Furthermore, the expression of RIP3 is enhanced in diabetic rat hearts [25] and the HG-treated cardiac cells [21], suggesting involvement of RIP3 in the hyperglycemia-induced cardiac injury. Of note, the activation of TLR4 has been reported to induce necroptosis, and ROS can also elicit necroptosis in cardiomyocytes [21] and other types of cells [50, 51].…”

Section: Discussionmentioning

confidence: 99%

“…RIP3-mediated necroptosis has now been recognized to be a common cell death pathway implicated in cytokine-, virus-, and genotoxic stress-induced cell death. Liu et al and our team have shown that the expression level of RIP3 is up-regulated in diabetic rat hearts [25] and the HG-treated cardiac cells [21]. Increasing evidence indicates that necroptosis is activated by several pathways, such as tumor necrosis factor-α (TNF-α) [26, 27], TLRs [28, 29] and ROS [21, 30].…”

Section: Introductionmentioning

confidence: 99%

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The Opening of ATP-Sensitive K+ Channels Protects H9c2 Cardiac Cells Against the High Glucose-Induced Injury and Inflammation by Inhibiting the ROS-TLR4-Necroptosis Pathway

Liang

Chen²,

Zheng

et al. 2017

Cell Physiol Biochem

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Background/Aims: Hyperglycemia activates multiple signaling molecules, including reactive oxygen species (ROS), toll-like receptor 4 (TLR4), receptor-interacting protein 3 (RIP3, a kinase promoting necroptosis), which mediate hyperglycemia-induced cardiac injury. This study explored whether inhibition of ROS-TLR4-necroptosis pathway contributed to the protection of ATP-sensitive K⁺ (K_ATP) channel opening against high glucose-induced cardiac injury and inflammation. Methods: H9c2 cardiac cells were treated with 35 mM glucose (HG) to establish a model of HG-induced insults. The expression of RIP3 and TLR4 were tested by western blot. Generation of ROS, cell viability, mitochondrial membrane potential (MMP) and secretion of inflammatory cytokines were measured as injury indexes. Results: HG increased the expression of TLR4 and RIP3. Necrostatin-1 (Nec-1, an inhibitor of necroptosis) or TAK-242 (an inhibitor of TLR4) co-treatment attenuated HG-induced up-regulation of RIP3. Diazoxide (DZ, a mitochondrial K_ATP channel opener) or pinacidil (Pin, a non-selective K_ATP channel opener) or N-acetyl-L-cysteine (NAC, a ROS scavenger) pre-treatment blocked the up-regulation of TLR4 and RIP3. Furthermore, pre-treatment with DZ or Pin or NAC, or co-treatment with TAK-242 or Nec-1 attenuated HG-induced a decrease in cell viability, and increases in ROS generation, MMP loss and inflammatory cytokines secretion. However, 5-hydroxy decanoic acid (5-HD, a mitochondrial K_ATP channel blocker) or glibenclamide (Gli, a non-selective K_ATP channel blocker) pre-treatment did not aggravate HG-induced injury and inflammation. Conclusion: K_ATP channel opening protects H9c2 cells against HG-induced injury and inflammation by inhibiting ROS-TLR4-necroptosis pathway.

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“…There are two recognized forms of neuron death after brain I/R: necrosis and delayed neuronal death (DND) . Long durations of stroke (~6–8 h) and cardiac arrest (>30 min) cause irreversible lysis of neurons and result in necrotic brain tissue .…”

Section: Brain I/r Phenomenologymentioning

confidence: 99%

Regulation of mRNA following brain ischemia and reperfusion

DeGracia

2017

WIREs RNA

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There is growing appreciation that mRNA regulation plays important roles in disease and injury. mRNA regulation and ribonomics occur in brain ischemia and reperfusion (I/R) following stroke and cardiac arrest and resuscitation. It was recognized over 40 years ago that translation arrest (TA) accompanies brain I/R and is now recognized as part of the intrinsic stress responses triggered in neurons. However, neuron death correlates to a prolonged TA in cells fated to undergo delayed neuronal death (DND). Dysfunction of mRNA regulatory processes in cells fated to DND prevents them from translating stress-induced mRNAs such as heat shock proteins. The morphological and biochemical studies of mRNA regulation in postischemic neurons are discussed in the context of the large variety of molecular damage induced by ischemic injury. Open issues and areas of future investigation are highlighted. A sober look at the molecular complexity of ischemia-induced neuronal injury suggests that a network framework will assist in making sense of this complexity. The ribonomic network sits between the gene network and the various protein and metabolic networks. Thus, targeting the ribonomic network may prove more effective at neuroprotection than targeting specific molecular pathways, for which all efforts have failed to the present time to stop DND in stroke and after cardiac arrest. WIREs RNA 2017, 8:e1415. doi: 10.1002/wrna.1415 For further resources related to this article, please visit the WIREs website.

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The role of necroptosis in neurosurgical diseases

Cited by 25 publications

References 79 publications

Identification of microRNA‑363‑3p as an essential regulator of chondrocyte apoptosis in osteoarthritis by targeting NRF1 through the p53‑signaling pathway

Identification of microRNA‑363‑3p as an essential regulator of chondrocyte apoptosis in osteoarthritis by targeting NRF1 through the p53‑signaling pathway

The Opening of ATP-Sensitive K+ Channels Protects H9c2 Cardiac Cells Against the High Glucose-Induced Injury and Inflammation by Inhibiting the ROS-TLR4-Necroptosis Pathway

Regulation of mRNA following brain ischemia and reperfusion

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