Heat shock protein 22 modulates NRF1/TFAM-dependent mitochondrial biogenesis and DRP1-sparked mitochondrial apoptosis through AMPK-PGC1α signaling pathway to alleviate the early brain injury of subarachnoid hemorrhage in rats

Fan, Haiyan; Ding, Rui; Li, Wenchao; Xin, Zhang; Li, Ran; Wei, Boyang; Su, Shixing; Jin, Fa; Wei, Chengcong; He, Xiaofu; Li, Xifeng; Duan, Chuanzhi

doi:10.1016/j.redox.2021.101856

Cited by 102 publications

(56 citation statements)

References 56 publications

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“…Mice were euthanized at 24 hours after surgery for IF staining, which was conducted as previously described ( 3 , 19 ). Brain sections with 8-μm thickness were incubated with 5% bovine serum albumin (BSA) and 0.3% Triton X-100 for 2 h at room temperature.…”

Section: Methodsmentioning

confidence: 99%

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TREM1 Regulates Neuroinflammatory Injury by Modulate Proinflammatory Subtype Transition of Microglia and Formation of Neutrophil Extracellular Traps via Interaction With SYK in Experimental Subarachnoid Hemorrhage

Zeng

et al. 2021

Front. Immunol.

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Neuroinflammation is a key process in the pathogenesis of subarachnoid hemorrhage (SAH) and contributes to poor outcome in patients. The purpose of this study is to explore the effect of triggering receptor expressed on myeloid cells 1 (TREM1) in the SAH, as well as its potential mechanism. In our study, plasma levels of soluble TREM1 was increased significantly after SAH and correlated to SAH severity and serum C-reactiveprotein. TREM1 inhibitory peptide LP17 alleviated the neurological deficits, attenuated brain water content, and reduced neuronal damage after SAH. Meanwhile, TREM1 inhibitory peptide decreased neuroinflammation (evidenced by the decreased levels of markers including IL-6, IL-1β, TNF-α) by attenuating proinflammatory subtype transition of microglia (evidenced by the decreased levels of markers including CD68, CD16, CD86) and decreasing the formation of neutrophil extracellular traps (evidenced by the decreased levels of markers including CitH3, MPO, and NE). Further mechanistic study identified that TREM1 can activate downstream proinflammatory pathways through interacting with spleen tyrosine kinase (SYK). In conclusion, inhibition of TREM1 alleviates neuroinflammation by attenuating proinflammatory subtype transition of microglia and decreasing the formation of neutrophil extracellular traps through interacting with SYK after SAH. TREM1 may be a a promising therapeutic target for SAH.

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Section: Methodsmentioning

confidence: 99%

“…Subarachnoid hemorrhage (SAH) is a major cause of devastating outcomes after neurosurgery practice, leading to severe neurological deficits for survivors (1,2). Early brain injury (EBI) has been thought to be a major factor affecting the prognosis after SAH (3,4). Neuroinflammation has been considered to be a vital role in EBI (5,6).…”

Section: Introductionmentioning

confidence: 99%

TREM1 Regulates Neuroinflammatory Injury by Modulate Proinflammatory Subtype Transition of Microglia and Formation of Neutrophil Extracellular Traps via Interaction With SYK in Experimental Subarachnoid Hemorrhage

Zeng

et al. 2021

Front. Immunol.

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“…Accumulating evidence manifested that damaged mitochondria-mediated oxidative stress is closely related to the mechanism of EBI after SAH [ 37 , 38 ]. Specifically, mitochondrial dysfunction caused by SAH leads to the overplus of ROS, resulting in oxidative stress injury [ 7 ] and ultimately activation of the apoptotic signaling pathway [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

ACEA Attenuates Oxidative Stress by Promoting Mitophagy via CB1R/Nrf1/PINK1 Pathway after Subarachnoid Hemorrhage in Rats

Liu

Tian

et al. 2022

Oxidative Medicine and Cellular Longevity

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Background and Purpose. Oxidative stress plays a pivotal role in early brain injury (EBI) after subarachnoid hemorrhage (SAH). The CB1R agonist ACEA has been reported to have a neuroprotective effect in many central nervous system diseases. Our study was aimed at exploring the effect and mechanism of ACEA in an experimental SAH model. Method. Endovascular perforation was performed to establish a SAH model of rats. ACEA was administered intraperitoneally 1 h after SAH. The CB1R antagonist AM251 was injected intraperitoneally 1 h before SAH induction. Adenoassociated virus- (AAV-) Nrf1 shRNA was infused into the lateral ventricle 3 weeks before SAH induction. Neurological tests, immunofluorescence, DHE, TUNEL, Nissl staining, transmission electron microscopy (TEM), and Western blot were performed. Results. The expression of CB1R, Nrf1, PINK1, Parkin, and LC3II increased and peaked at 24 h after SAH. ACEA treatment exhibited the antioxidative stress and antiapoptosis effects after SAH. In addition, ACEA treatment increased the expression of Nrf1, PINK1, Parkin, LC3II, and Bcl-xl but repressed the expression of Romo-1, Bax, and cleaved caspase-3. Moreover, the TEM results demonstrated that ACEA promoted the formation of mitophagosome and maintained the normal mitochondrial morphology of neurons. The protective effect of ACEA was reversed by AM251 and Nrf1 shRNA, respectively. Conclusions. This study demonstrated that ACEA alleviated oxidative stress and neurological dysfunction by promoting mitophagy after SAH, at least in part via the CB1R/Nrf1/PINK1 signaling pathway.

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“…After SAH, exhibiting aberrant redox hemostasis, the production of oxidants mainly comes from the disruption of mitochondria ( Yan et al, 2015 ; Fan et al, 2021 ; Xu W. et al, 2021 ), extravascular hemolyzed blood ( Vecchione et al, 2009 ; Deng et al, 2018 ), and enzymatic sources of free radicals ( Sies et al, 2017 ; Yang et al, 2017 ; Sies and Jones, 2020 ). Intrinsic antioxidant activity can be exhausted by excessive free radicals, resulting in lipid peroxidation, protein breakdown, and DNA damage.…”

Section: Oxidative Stress In Subarachnoid Hemorrhagementioning

confidence: 99%

“…Moreover, an additional NRF family member, namely, Nrf1 ( Qian et al, 2019 ), responsible for ROS detoxification, participates in an effective treatment to moderate SAH-elicited EBI. Researchers concluded that HSP22 played a part in neuroprotective effects by regulating TFAM/Nrf1-triggered mitochondrial biogenesis with positive feedback, further attenuating OS and EBI ( Fan et al, 2021 ).…”

Section: Oxidative Stress In Early Brain Injurymentioning

confidence: 99%

An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage

Lin

Zhao

et al. 2021

Front. Aging Neurosci.

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The main reasons for disability and death in aneurysmal subarachnoid hemorrhage (aSAH) may be early brain injury (EBI) and delayed cerebral ischemia (DCI). Despite studies reporting and progressing when DCI is well-treated clinically, the prognosis is not well-improved. According to the present situation, we regard EBI as the main target of future studies, and one of the key phenotype-oxidative stresses may be called for attention in EBI after laboratory subarachnoid hemorrhage (SAH). We summarized the research progress and updated the literature that has been published about the relationship between experimental and clinical SAH-induced EBI and oxidative stress (OS) in PubMed from January 2016 to June 2021. Many signaling pathways are related to the mechanism of OS in EBI after SAH. Several antioxidative stress drugs were studied and showed a protective response against EBI after SAH. The systematical study of antioxidative stress in EBI after laboratory and clinical SAH may supply us with new therapies about SAH.

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Heat shock protein 22 modulates NRF1/TFAM-dependent mitochondrial biogenesis and DRP1-sparked mitochondrial apoptosis through AMPK-PGC1α signaling pathway to alleviate the early brain injury of subarachnoid hemorrhage in rats

Cited by 102 publications

References 56 publications

TREM1 Regulates Neuroinflammatory Injury by Modulate Proinflammatory Subtype Transition of Microglia and Formation of Neutrophil Extracellular Traps via Interaction With SYK in Experimental Subarachnoid Hemorrhage

TREM1 Regulates Neuroinflammatory Injury by Modulate Proinflammatory Subtype Transition of Microglia and Formation of Neutrophil Extracellular Traps via Interaction With SYK in Experimental Subarachnoid Hemorrhage

ACEA Attenuates Oxidative Stress by Promoting Mitophagy via CB1R/Nrf1/PINK1 Pathway after Subarachnoid Hemorrhage in Rats

An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage

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