Restoration of L-OPA1 alleviates acute ischemic stroke injury in rats via inhibiting neuronal apoptosis and preserving mitochondrial function

Lai, Yongxing; Lin, Peiqiang; Chen, Manli; Zhang, Yixian; Chen, Jianhao; Zheng, Mouwei; Ji, Liu; Du, Houwei; Chen, Ronghua; Pan, Xiaodong; Liu, Nan; Chen, Hongbin

doi:10.1016/j.redox.2020.101503

Cited by 106 publications

(78 citation statements)

References 67 publications

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“…The observed changes in the studied markers of mitochondrial dynamics could, on the one hand, increase energy shortages (in the case of increased dnm1l expression), but on the other hand, could be adaptive mechanisms limiting energy deficits (in the case of increased opa 1 expression). However, in the case of opa 1, the available data indicate that only a long isoform of this protein promotes mitochondrial fusion, whereas a short isoform intensifies fission instead; thus, the observed increase in opa1 expression did not necessarily lead to increased fusion [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Contribution of Hypothyroidism to Cognitive Impairment and Hippocampal Synaptic Plasticity Regulation in an Animal Model of Depression

Głombik

Detka

Bobula

et al. 2021

IJMS

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The role that thyroid hormone deficiency plays in depression and synaptic plasticity in adults has only begun to be elucidated. This paper analyzes the possible link between depression and hypothyroidism in cognitive function alterations, using Wistar–Kyoto (WKY—an animal model of depression) rats and control Wistar rats under standard and thyroid hormone deficiency conditions (propylthiouracil administration—PTU). A weakening of memory processes in the WKY rats is shown behaviorally, and in the reduction of long-term potentiation (LTP) in the dentate gyrus (DG) and CA1 hippocampal regions. PTU administration decreased LTP and increased basal excitatory transmission in the DG in Wistar rats. A decrease in short-term synaptic plasticity is shown by the paired-pulse ratio measurement, occurring during hypothyroidism in DG and CA1 in WKY rats. Differences between the strains may result from decreases in the p-CaMKII, p-AKT, and the level of acetylcholine, while in the case of the co-occurrence of depression and hypothyroidism, an increase in the p-ERK1-MAP seemed to be important. Obtained results show that thyroid hormones are less involved in the inhibition of glutamate release and/or excitability of the postsynaptic neurons in WKY rats, which may indicate a lower sensitivity of the hippocampus to the action of thyroid hormones in depression.

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Section: Discussionmentioning

confidence: 99%

Contribution of Hypothyroidism to Cognitive Impairment and Hippocampal Synaptic Plasticity Regulation in an Animal Model of Depression

Głombik

Detka

Bobula

et al. 2021

IJMS

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“…As previously reported, mitochondrial morphology is vital for sustaining mitochondrial dynamics after cerebral injury (Wei et al, 2019 ; Lai et al, 2020 ). In our current study, the results observed from TEM indicated that nascent mitochondria were increased, with less vacuole and less swelling mitochondria after irisin treatment.…”

Section: Discussionmentioning

confidence: 62%

Irisin Contributes to Neuroprotection by Promoting Mitochondrial Biogenesis After Experimental Subarachnoid Hemorrhage

Yin

Pang

et al. 2021

Front. Aging Neurosci.

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Subarachnoid hemorrhage (SAH) is a devastating form of stroke, which poses a series of intractable challenges to clinical practice. Imbalance of mitochondrial homeostasis has been thought to be the crucial pathomechanism in early brain injury (EBI) cascade after SAH. Irisin, a protein related to metabolism and mitochondrial homeostasis, has been reported to play pivotal roles in post-stroke neuroprotection. However, whether this myokine can exert neuroprotection effects after SAH remains unknown. In the present study, we explored the protective effects of irisin and the underlying mechanisms related to mitochondrial biogenesis in a SAH animal model. Endovascular perforation was used to induce SAH, and recombinant irisin was administered intracerebroventricularly. Neurobehavioral assessments, TdT-UTP nick end labeling (TUNEL) staining, dihydroethidium (DHE) staining, immunofluorescence, western blot, and transmission electron microscopy (TEM) were performed for post-SAH assessments. We demonstrated that irisin treatment improved neurobehavioral scores, reduced neuronal apoptosis, and alleviated oxidative stress in EBI after SAH. More importantly, the administration of exogenous irisin conserved the mitochondrial morphology and promoted mitochondrial biogenesis. The protective effects of irisin were partially reversed by the mitochondrial uncoupling protein-2 (UCP-2) inhibitor. Taken together, irisin may have neuroprotective effects against SAH via improving the mitochondrial biogenesis, at least in part, through UCP-2 related targets.

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“…Mfn2 is reported to exert an anti-apoptotic effect, and its expression decreases in the presence of ROS. Opa1 can attenuate infarct volume in ischemic stroke, and its expression is increased after exercise (Anzell et al, 2018 ; Kameoka et al, 2018 ; Wei et al, 2019 ; Lai et al, 2020 ).…”

Section: Mitochondrial Dynamics and Strokementioning

confidence: 99%

The Neuroprotective Effect of Irisin in Ischemic Stroke

Liu

Zhu

Guo

et al. 2020

Front. Aging Neurosci.

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Irisin is a PGC-1α-dependent myokine that causes increased energy expenditure by driving the development of white adipose tissue into brown fat-like tissue. Exercise can improve irisin levels and lead to its release into the blood. In ischemic stroke, neurons are always sensitive to energy supply; after a series of pathophysiological processes, reactive oxygen species that are detrimental to cell survival via mitochondrial dysfunction are generated in large quantities. As a protein associated with exercise, irisin can alleviate brain injury in the pathogenesis of ischemic stroke. It is thought that irisin can upregulate the levels of brain-derived neurotrophic factor (BDNF), which protects nerve cells from injury during ischemic stroke. Furthermore, the release of irisin into the blood via exercise influences the mitochondrial dynamics crucial to maintaining the normal function of nerve cells. Consequently, we intended to summarize the known effects of irisin during ischemic stroke.

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Restoration of L-OPA1 alleviates acute ischemic stroke injury in rats via inhibiting neuronal apoptosis and preserving mitochondrial function

Cited by 106 publications

References 67 publications

Contribution of Hypothyroidism to Cognitive Impairment and Hippocampal Synaptic Plasticity Regulation in an Animal Model of Depression

Contribution of Hypothyroidism to Cognitive Impairment and Hippocampal Synaptic Plasticity Regulation in an Animal Model of Depression

Irisin Contributes to Neuroprotection by Promoting Mitochondrial Biogenesis After Experimental Subarachnoid Hemorrhage

The Neuroprotective Effect of Irisin in Ischemic Stroke

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