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Article ; Online: Hypoxic Preconditioning Attenuates Neuroinflammation via Inhibiting NF-κB/NLRP3 Axis Mediated by p-MLKL after Transient Global Cerebral Ischemia.

Lu, Xiaomei / Zhan, Lixuan / Chai, Guorong / Chen, Meiyan / Sun, Weiwen / Xu, En

2023 Volume 61, Issue 2, Page(s) 1080–1099

Abstract: Hypoxic preconditioning (HPC) has been reported to alleviate neuronal damage and microglial activation in hippocampal CA1 after transient global cerebral ischemia (tGCI). However, the molecular mechanism is unclear. Recent studies identified that nuclear ...

Abstract	Hypoxic preconditioning (HPC) has been reported to alleviate neuronal damage and microglial activation in hippocampal CA1 after transient global cerebral ischemia (tGCI). However, the molecular mechanism is unclear. Recent studies identified that nuclear factor-kappa-B (NF-κB)/oligomerization domain-like receptors protein (NLRP) 3 inflammasome pathway is mainly involved in the activation of microglia and that phosphorylated (p)-mixed lineage kinase domain-like (MLKL) is related to the regulation of NF-κB/NLRP3 axis. Hence, in this study, we set out to investigate whether HPC attenuates neuronal damage and microglial activation through inhibiting NF-κB/NLRP3 axis mediated by p-MLKL after tGCI in CA1 of male rats. We found that HPC decreased NLRP3 inflammasome in microglia and inhibited M1 polarization of microglia in CA1 after tGCI. Mechanistically, HPC inhibited the activation of NF-κB signaling pathway and reduced the mRNA and protein levels of NLRP3 inflammasome after tGCI. Additionally, the knockdown of p-MLKL by short hairpin RNA (shRNA) administration inhibited the activation of the NF-κB signaling pathway and reduced the formation of NLRP3 inflammasome, thus attenuating M1 polarization of microglia and decreasing the release of interleukin 1 beta (IL-1β) and necrosis factor alpha (TNF-α) in CA1 post ischemia. We consider that p-MLKL in microglia may be derived from necroptotic neurons after tGCI. In conclusion, the new finding in this study is that HPC-induced neuroprotection against tGCI through inhibiting NF-κB/NLRP3 pathway mediated by p-MLKL.
MeSH term(s)	Rats ; Male ; Animals ; NF-kappa B ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Inflammasomes/metabolism ; Neuroinflammatory Diseases ; Ischemic Attack, Transient ; Hypoxia/metabolism ; Protein Kinases
Chemical Substances	NF-kappa B ; NLR Family, Pyrin Domain-Containing 3 Protein ; Inflammasomes ; MLKL protein, rat (EC 2.7.-) ; Protein Kinases (EC 2.7.-)
Language	English
Publishing date	2023-09-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-023-03628-w
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Zs.A 2411: Show issues

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Article ; Online: Hypoxic postconditioning restores mitophagy against transient global cerebral ischemia via Parkin-induced posttranslational modification of TBK1.

Wen, Haixia / Zuo, Yunyan / Li, Luxi / Zhan, Lixuan / Xue, Jiahui / Sun, Weiwen / Xu, En

Neurobiology of disease

2023 Volume 179, Page(s) 106043

Abstract: Hypoxic postconditioning (HPC) has been reported to enhance Parkin-catalyzed mitochondrial ubiquitination to restore mitophagy in hippocampal CA1 against transient global cerebral ischemia (tGCI). However, the molecular mechanism leading ubiquitinated ... ...

Abstract	Hypoxic postconditioning (HPC) has been reported to enhance Parkin-catalyzed mitochondrial ubiquitination to restore mitophagy in hippocampal CA1 against transient global cerebral ischemia (tGCI). However, the molecular mechanism leading ubiquitinated mitochondria to final clearance during HPC-mediated mitophagy after tGCI is unclear. This study aims to investigate whether HPC restores mitophagy after tGCI through Parkin-induced K63-linked poly-ubiquitination (K63-Ub) to activate tumor necrosis factor associated factor family member associated nuclear factor κB activator -binding kinase 1 (TBK1) in CA1 of male rats. We found that HPC maintained TBK1 expression, promoted p62 and TBK1 phosphorylation in mitochondria, and enhanced their recruitments to mitochondria in CA1 after tGCI. However, these effects were partially abolished by TBK1 inhibitor BX795. K63-Ub of mitochondrial TBK1 was disturbed at 26 h of reperfusion after tGCI, which was reversed by HPC. The maintenance of K63-Ub of mitochondrial TBK1 induced by HPC was counteracted under Parkin knockdown with AAV-mediated Prkn small-interfering RNA, accompanied by the suppression on TBK1 activation and the reduction of mitochondrial p62 phosphorylation. This innovative study indicated that HPC maintained K63-Ub of TBK1 in a Parkin-dependent manner to promote TBK1 phosphorylation, and then phosphorylated TBK1 activated p62 to restore mitophagy, thereby alleviating neuronal damage in CA1 after tGCI.
MeSH term(s)	Animals ; Male ; Rats ; Ischemic Attack, Transient ; Mitophagy ; Protein Processing, Post-Translational ; Rats, Wistar ; Ubiquitin-Protein Ligases/genetics
Chemical Substances	Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Tbk1 protein, rat (EC 2.7.11.1) ; parkin protein (EC 2.3.2.27)
Language	English
Publishing date	2023-02-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2023.106043
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Zs.A 4444: Show issues

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Article ; Online: Stabilization of nuclear β-catenin by inhibiting KDM2A mediates cerebral ischemic tolerance.

Zuo, Yunyan / Zhan, Lixuan / Wen, Haixia / Xue, Jiahui / Tan, Yafu / Sun, Weiwen / Xu, En

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2023 Volume 37, Issue 3, Page(s) e22796

Abstract: Hypoxic postconditioning (HPC) with 8% oxygen increases nuclear accumulation of β-catenin through activating the classical Wnt pathway, thereby alleviating transient global cerebral ischemia (tGCI)-induced neuronal damage in the hippocampal CA1 subregion ...

Abstract	Hypoxic postconditioning (HPC) with 8% oxygen increases nuclear accumulation of β-catenin through activating the classical Wnt pathway, thereby alleviating transient global cerebral ischemia (tGCI)-induced neuronal damage in the hippocampal CA1 subregion of adult rats. However, little is understood about the regulatory mechanism of nuclear β-catenin in HPC-mediated cerebral ischemic tolerance. Although lysine(K)-specific demethylase 2A (KDM2A) has been known as a crucial regulator of nuclear β-catenin destabilization, whether it plays an important role through modulating nuclear β-catenin in cerebral ischemic tolerance induced by HPC remains unknown. In this study, we explored the molecular mechanism of stabilizing nuclear β-catenin by inhibiting KDM2A-mediated demethylation in the HPC-offered neuroprotection against tGCI. In addition, we confirmed that nuclear methylated-β-catenin in CA1 decreased and nuclear β-catenin turnover increased after tGCI, which were reversed by HPC. The administration with methyltransferase inhibitor AdOx abrogated HPC-induced methylation and stabilization of nuclear β-catenin in CA1, as well as the neuroprotection against tGCI. Notably, HPC downregulated the expression of KDM2A in CA1 and reduced the interaction between KDM2A and β-catenin in the nucleus after tGCI. The knockdown of KDM2A with small-interfering RNA could upregulate nuclear methylated-β-catenin and stabilize β-catenin, thereby increasing survivin in CA1 and improving the cognitive function of rats after tGCI. Opposite results were observed by the administration of KDM2A-carried adenovirus vector. Furthermore, we demonstrated that KDM2A mediates the demethylation of nuclear β-catenin through jumonji C (JmjC) domain of KDM2A in HEK-293T and SH-SY5Y cells. Our data support that the inhibition of KDM2A-mediated demethylation of nuclear β-catenin contributes to HPC-induced neuroprotection against tGCI.
MeSH term(s)	Rats ; Humans ; Animals ; Rats, Wistar ; beta Catenin/metabolism ; Neuroblastoma ; Ischemic Attack, Transient ; Hippocampus/metabolism ; F-Box Proteins/metabolism ; Jumonji Domain-Containing Histone Demethylases/genetics ; Jumonji Domain-Containing Histone Demethylases/metabolism
Chemical Substances	beta Catenin ; KDM2A protein, human (EC 1.14.11.27) ; F-Box Proteins ; Jumonji Domain-Containing Histone Demethylases (EC 1.14.11.-)
Language	English
Publishing date	2023-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202201657
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Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 296: Show issues

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Article: Epigenetic Regulations of Microglia/Macrophage Polarization in Ischemic Stroke.

Qiu, Meiqian / Xu, En / Zhan, Lixuan

Frontiers in molecular neuroscience

2021 Volume 14, Page(s) 697416

Abstract: Ischemic stroke is one of the leading causes of death and disability worldwide. Microglia/macrophages (MMs)-mediated neuroinflammation contributes significantly to the pathological process of ischemic brain injury. Microglia, serving as resident innate ... ...

Abstract	Ischemic stroke is one of the leading causes of death and disability worldwide. Microglia/macrophages (MMs)-mediated neuroinflammation contributes significantly to the pathological process of ischemic brain injury. Microglia, serving as resident innate immune cells in the central nervous system, undergo pro-inflammatory phenotype or anti-inflammatory phenotype in response to the microenvironmental changes after cerebral ischemia. Emerging evidence suggests that epigenetics modifications, reversible modifications of the phenotype without changing the DNA sequence, could play a pivotal role in regulation of MM polarization. However, the knowledge of the mechanism of epigenetic regulations of MM polarization after cerebral ischemia is still limited. In this review, we present the recent advances in the mechanisms of epigenetics involved in regulating MM polarization, including histone modification, non-coding RNA, and DNA methylation. In addition, we discuss the potential of epigenetic-mediated MM polarization as diagnostic and therapeutic targets for ischemic stroke. It is valuable to identify the underlying mechanisms between epigenetics and MM polarization, which may provide a promising treatment strategy for neuronal damage after cerebral ischemia.
Language	English
Publishing date	2021-10-11
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2021.697416
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Article ; Online: Inhibition of MLKL-dependent necroptosis via downregulating interleukin-1R1 contributes to neuroprotection of hypoxic preconditioning in transient global cerebral ischemic rats.

Zhan, Lixuan / Lu, Xiaomei / Xu, Wensheng / Sun, Weiwen / Xu, En

Journal of neuroinflammation

2021 Volume 18, Issue 1, Page(s) 97

Abstract: Background: Our previous study indicated that hypoxic preconditioning reduced receptor interacting protein (RIP) 3-mediated necroptotic neuronal death in hippocampal CA1 of adult rats after transient global cerebral ischemia (tGCI). Although mixed ... ...

Abstract	Background: Our previous study indicated that hypoxic preconditioning reduced receptor interacting protein (RIP) 3-mediated necroptotic neuronal death in hippocampal CA1 of adult rats after transient global cerebral ischemia (tGCI). Although mixed lineage kinase domain-like (MLKL) has emerged as a crucial molecule for necroptosis induction downstream of RIP3, how MLKL executes necroptosis is not yet well understood. In this study, we aim to elucidate the molecular mechanism underlying hypoxic preconditioning that inactivates MLKL-dependent neuronal necroptosis after tGCI. Methods: Transient global cerebral ischemia was induced by the four-vessel occlusion method. Twenty-four hours before ischemia, rats were exposed to systemic hypoxia with 8% O Results: Hypoxic preconditioning decreased the phosphorylation of MLKL both in neurons and microglia of CA1 after tGCI. The knockdown of MLKL with siRNA decreased the expression of p-MLKL and exerted neuroprotective effects after tGCI, whereas treatment with lentiviral delivery of MLKL showed opposite results. Mechanistically, hypoxic preconditioning or MLKL siRNA attenuated the RIP3-p-MLKL interaction, reduced the plasma membrane translocation of p-MLKL, and blocked Ca Conclusions: These data support that the inhibition of MLKL-dependent neuronal necroptosis through downregulating IL-1R1 contributes to neuroprotection of hypoxic preconditioning against tGCI.
MeSH term(s)	Animals ; Brain/metabolism ; Brain/pathology ; Brain/physiopathology ; CA1 Region, Hippocampal/metabolism ; Down-Regulation ; Gene Knockdown Techniques ; Hypoxia/metabolism ; Ischemic Attack, Transient/metabolism ; Ischemic Preconditioning ; Male ; Necroptosis ; Neuroprotection ; Neuroprotective Agents ; Phosphorylation ; Protein Kinases/metabolism ; Rats ; Rats, Wistar ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Receptors, Interleukin-1 Type I/metabolism
Chemical Substances	Neuroprotective Agents ; Receptors, Interleukin-1 Type I ; MLKL protein, rat (EC 2.7.-) ; Protein Kinases (EC 2.7.-) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2021-04-20
Publishing country	England
Document type	Journal Article
ISSN	1742-2094
ISSN (online)	1742-2094
DOI	10.1186/s12974-021-02141-y
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Article ; Online: Nurses' knowledge and attitudes towards palliative care and death: a learning intervention.

Hao, Yanping / Zhan, Lixuan / Huang, Meiling / Cui, Xianying / Zhou, Ying / Xu, En

BMC palliative care

2021 Volume 20, Issue 1, Page(s) 50

Abstract: Background: In many countries, nurses are ill-prepared to provide care to patients with terminal illnesses. Limited education and training affect their ability to deliver proper palliative care. Only a few studies have explored appropriate and effective ...

Abstract	Background: In many countries, nurses are ill-prepared to provide care to patients with terminal illnesses. Limited education and training affect their ability to deliver proper palliative care. Only a few studies have explored appropriate and effective training methods of palliative care in China. Therefore, we aimed to provide evidence for a palliative care training system by appraising the effects of a mixed-method intervention on participants' knowledge of palliative care and attitudes towards dying patients and death. Methods: An e-learning intervention approach was adopted for 97 nurses from oncology departments across five hospitals, using a mobile terminal combined with a virtual forum and face-to-face interactions. We conducted a pre- and post-training evaluation through the Palliative Care Quiz of Nursing (PCQN), Frommelt Attitude Toward Care of the Dying Scale Form B (FATCOD-B), and Death Attitude Profile-Revised (DAP-R). Results: After a three-week intervention, there was a significant increase in the PCQN and FATCOD-B scores as compared to the baseline. For PCQN, the total score increased from 10.3 ± 1.9 to 11.1 ± 2.2 (p = .011) and the score for management of pain and other symptoms increased from 7.7 ± 1.7 to 8.4 ± 1.7 (p = .003). FATCOD-B scores increased noticeably from 100.6 ± 7.9 to 102.9 ± 8.9 (p = .019). The DAP-R scores showed no obvious difference between pre- and post-intervention results. Conclusions: The mixed-method intervention was effective in improving participants' knowledge and attitudes about palliative care. The implementation of training for nurses at appropriate intervals during both education and professional life is required, especially regarding the improvement in participants' attitudes towards death. Therefore, palliative care training in China should receive more attention.
MeSH term(s)	Attitude of Health Personnel ; Attitude to Death ; Clinical Competence ; Humans ; Palliative Care ; Surveys and Questionnaires ; Terminal Care
Language	English
Publishing date	2021-03-25
Publishing country	England
Document type	Journal Article
ISSN	1472-684X
ISSN (online)	1472-684X
DOI	10.1186/s12904-021-00738-x
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Article ; Online: Attenuation of Piwil2 induced by hypoxic postconditioning prevents cerebral ischemic injury by inhibiting CREB2 promoter methylation.

Zhan, Lixuan / Chen, Meiyan / Pang, Taoyan / Li, Xinyu / Long, Long / Liang, Donghai / Peng, Linhui / Sun, Weiwen / Xu, En

Brain pathology (Zurich, Switzerland)

2022 Volume 33, Issue 1, Page(s) e13109

Abstract: Epigenetic modification contributes to the pathogenesis of cerebral ischemia. Piwil2 belongs to the PIWI proteins subfamily and has a key role in the regulation of gene transcription through epigenetics. However, the roles of Piwil2 in cerebral ischemia ... ...

Abstract	Epigenetic modification contributes to the pathogenesis of cerebral ischemia. Piwil2 belongs to the PIWI proteins subfamily and has a key role in the regulation of gene transcription through epigenetics. However, the roles of Piwil2 in cerebral ischemia have not been investigated. In this study, we aim to elucidate the roles and the underlying molecular mechanisms of Piwil2 in ischemic tolerance induced by hypoxic postconditioning (HPC) against transient global cerebral ischemia (tGCI). We found that the expression of Piwil2 in CA1 was downregulated by HPC after tGCI. Silencing Piwil2 with antisense oligodeoxynucleotide (AS-ODN) in CA1 after tGCI decreased the expression of apoptosis-related proteins and exerted neuroprotective effects. Opposite results were observed after overexpression of Piwil2 induced by administration of Piwil2-carried lentivirus. Furthermore, we revealed differentially expressed Piwil2-interacting piRNAs in CA1 between HPC and tGCI groups by RNA binding protein immunoprecipitation (RIP) assay. Moreover, downregulating Piwil2 induced by HPC or AS-ODN after tGCI caused a marked reduction of DNA methyltransferase 3A (DNMT3A), which in turn abolished the tGCI-induced increase in the DNA methylation of cyclic AMP response element-binding 2 (CREB2), thus increasing mRNA and protein of CREB2. Finally, downregulating Piwil2 restored dendritic complexity and length, prevented the loss of dentritic spines, thereby improving cognitive function after tGCI. These data firstly reveal that Piwil2 plays an important part in HPC-mediated neuroprotection against cerebral ischemia through epigenetic regulation of CREB2.
MeSH term(s)	Animals ; Rats ; Brain Ischemia/pathology ; CA1 Region, Hippocampal/pathology ; Cerebral Infarction/pathology ; Epigenesis, Genetic ; Ischemic Attack, Transient/metabolism ; Ischemic Attack, Transient/pathology ; Ischemic Attack, Transient/prevention & control ; Methylation ; Rats, Wistar ; RNA-Binding Proteins/metabolism
Chemical Substances	Piwil2 protein, rat ; RNA-Binding Proteins
Language	English
Publishing date	2022-07-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1051484-3
ISSN	1750-3639 ; 1015-6305
ISSN (online)	1750-3639
ISSN	1015-6305
DOI	10.1111/bpa.13109
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Zs.A 3585: Show issues

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Article ; Online: Neuroprotective Effects of Rhodiola Sacra on Transient Global Cerebral Ischemia Through Activating AMPK/Nrf2 Pathway in Rats.

Li, Kongping / Jiang, Jiaqi / Shi, Zhe / Zhan, Lixuan / Peng, Linhui / Sun, Weiwen / Tang, Yanyan / Zuo, Xialin / Xu, En

Antioxidants & redox signaling

2022 Volume 36, Issue 7-9, Page(s) 567–591

Abstract: Aims: ...

Abstract	Aims:
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Animals ; Brain Ischemia/drug therapy ; Brain Ischemia/metabolism ; CA1 Region, Hippocampal/metabolism ; Ischemic Attack, Transient/metabolism ; Male ; Molecular Docking Simulation ; NF-E2-Related Factor 2/metabolism ; Neuroprotective Agents/metabolism ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Rats ; Rats, Wistar ; Rhodiola/metabolism ; Sacrum/metabolism
Chemical Substances	NF-E2-Related Factor 2 ; Neuroprotective Agents ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2022-01-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2020.8224
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Zs.A 5488: Show issues

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Article ; Online: Transplantation of hESCs-Derived Neural Progenitor Cells Alleviates Secondary Damage of Thalamus After Focal Cerebral Infarction in Rats.

Li, Kongping / Peng, Linhui / Xing, Qi / Zuo, Xialin / Huang, Wenhao / Zhan, Lixuan / Li, Heying / Sun, Weiwen / Zhong, Xiaofen / Zhu, Tieshi / Pan, Guangjin / Xu, En

Stem cells translational medicine

2023 Volume 12, Issue 8, Page(s) 553–568

Abstract: Human embryonic stem cells-derived neural progenitor cells (hESCs-NPCs) transplantation holds great potential to treat stroke. We previously reported that delayed secondary degeneration occurs in the ventroposterior nucleus (VPN) of ipsilateral thalamus ... ...

Abstract	Human embryonic stem cells-derived neural progenitor cells (hESCs-NPCs) transplantation holds great potential to treat stroke. We previously reported that delayed secondary degeneration occurs in the ventroposterior nucleus (VPN) of ipsilateral thalamus after distal branch of middle cerebral artery occlusion (dMCAO) in adult male Sprague-Dawley (SD) rats. In this study, we investigate whether hESCs-NPCs would benefit the neural recovery of the secondary damage in the VPN after focal cerebral infarction. Permanent dMCAO was performed with electrocoagulation. Rats were randomized into Sham, dMCAO groups with or without hESCs-NPCs treatment. HESCs-NPCs were engrafted into the peri-infarct regions of rats at 48 h after dMCAO. The transplanted hESCs-NPCs survive and partially differentiate into mature neurons after dMCAO. Notably, hESCs-NPCs transplantation attenuated secondary damage of ipsilateral VPN and improved neurological functions of rats after dMCAO. Moreover, hESCs-NPCs transplantation significantly enhanced the expression of BDNF and TrkB and their interaction in ipsilateral VPN after dMCAO, which was reversed by the knockdown of TrkB. Transplantated hESCs-NPCs reconstituted thalamocortical connection and promoted the formation of synapses in ipsilateral VPN post-dMCAO. These results suggest that hESCs-NPCs transplantation attenuates secondary damage of ipsilateral thalamus after cortical infarction, possibly through activating BDNF/TrkB pathway, enhancing thalamocortical projection, and promoting synaptic formation. It provides a promising therapeutic strategy for secondary degeneration in the ipsilateral thalamus post-dMCAO.
MeSH term(s)	Humans ; Embryonic Stem Cells/transplantation ; Animals ; Rats ; Rats, Sprague-Dawley ; Infarction, Middle Cerebral Artery/metabolism ; Infarction, Middle Cerebral Artery/pathology ; Infarction, Middle Cerebral Artery/therapy ; Neural Stem Cells/transplantation ; Cell Differentiation ; Cell Movement ; Signal Transduction ; Neuroprotection ; Thalamus/metabolism
Language	English
Publishing date	2023-07-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2642270-0
ISSN	2157-6580 ; 2157-6580
ISSN (online)	2157-6580
ISSN	2157-6580
DOI	10.1093/stcltm/szad037
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Article ; Online: Hypoxic postconditioning promotes mitophagy against transient global cerebral ischemia via PINK1/Parkin-induced mitochondrial ubiquitination in adult rats.

Wen, Haixia / Li, Luxi / Zhan, Lixuan / Zuo, Yunyan / Li, Kongping / Qiu, Meiqian / Li, Heying / Sun, Weiwen / Xu, En

Cell death & disease

2021 Volume 12, Issue 7, Page(s) 630

Abstract: Mitophagy alleviates neuronal damage after cerebral ischemia by selectively removing dysfunctional mitochondria. Phosphatase and tensin homolog (PTEN) induced putative kinase 1 (PINK1)/Parkin-mediated mitophagy is the most well-known type of mitophagy. ... ...

Abstract	Mitophagy alleviates neuronal damage after cerebral ischemia by selectively removing dysfunctional mitochondria. Phosphatase and tensin homolog (PTEN) induced putative kinase 1 (PINK1)/Parkin-mediated mitophagy is the most well-known type of mitophagy. However, little is known about the role of PINK1/Parkin-mediated mitophagy in ischemic tolerance induced by hypoxic postconditioning (HPC) with 8% O
MeSH term(s)	Animals ; CA1 Region, Hippocampal/enzymology ; CA1 Region, Hippocampal/ultrastructure ; Disease Models, Animal ; Hypoxia/enzymology ; Hypoxia/genetics ; Hypoxia/pathology ; Ischemic Attack, Transient/enzymology ; Ischemic Attack, Transient/genetics ; Ischemic Attack, Transient/pathology ; Male ; Mitochondria/enzymology ; Mitochondria/genetics ; Mitochondria/ultrastructure ; Mitophagy ; Neurons/enzymology ; Neurons/ultrastructure ; Protein Kinases/genetics ; Protein Kinases/metabolism ; Protein Transport ; Rats, Wistar ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination ; Rats
Chemical Substances	Ubiquitin-Protein Ligases (EC 2.3.2.27) ; parkin protein (EC 2.3.2.27) ; Protein Kinases (EC 2.7.-) ; PTEN-induced putative kinase (EC 2.7.11.1)
Language	English
Publishing date	2021-06-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-021-03900-8
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