Ischemic brain injury decreases dynamin-like protein 1 expression in a middle cerebral artery occlusion animal model and glutamate-exposed HT22 cells

Jang, Ahram; Koh, Phil-Ok

doi:10.5625/lar.2016.32.4.194

Cited by 7 publications

(9 citation statements)

References 24 publications

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“…Immunoblot analysis was carried out as a previously described method [ 48 ]. Samples from right cerebral cortexes were homogenized in lysis buffer [1 % Triton X-100 and 1 mM EDTA in PBS (pH 7.4)] using a tissue homogenizer and centrifuged at 16,000 g for 20 min at 4°C.…”

Section: Methodsmentioning

confidence: 99%

Quercetin attenuates the reduction of parvalbumin in middle cerebral artery occlusion animal model

et al. 2021

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Background Calcium is a critical factor involved in modulation of essential cellular functions. Parvalbumin is a calcium buffering protein that regulates intracellular calcium concentrations. It prevents rises in calcium concentrations and inhibits apoptotic processes during ischemic injury. Quercetin exerts potent antioxidant and anti-apoptotic effects during brain ischemia. We investigated whether quercetin can regulate parvalbumin expression in cerebral ischemia and glutamate toxicity-induced neuronal cell death. Adult male rats were treated with vehicle or quercetin (10 mg/kg) 30 min prior to middle cerebral artery occlusion (MCAO) and cerebral cortical tissues were collected 24 h after MCAO. We used various techniques including Western blot, reverse transcription-PCR, and immunohistochemical staining to elucidate the changes of parvalbumin expression. Results Quercetin ameliorated MCAO-induced neurological deficits and behavioral changes. Moreover, quercetin prevented MCAO-induced a decrease in parvalbumin expression. Conclusions These findings suggest that quercetin exerts a neuroprotective effect through regulation of parvalbumin expression.

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Section: Methodsmentioning

confidence: 99%

Quercetin attenuates the reduction of parvalbumin in middle cerebral artery occlusion animal model

et al. 2021

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“…Neurons are particularly sensitive to changes in mitochondrial dynamics due to their high energy demands [ 12 ]. The balance between mitochondrial fission and fusion is highly relevant to the pathological processes of many CNS diseases, including acute stroke [ 13 – 15 ] and some neurodegenerative diseases [ 16 ]. In mammals, dynamin-related protein 1 (Drp1) is the main protein regulating mitochondrial fission and acting as an intrinsic factor in mitochondria-dependent apoptosis pathway [ 17 , 18 ].…”

Section: Introductionmentioning

confidence: 99%

YiQiFuMai Powder Injection Protects against Ischemic Stroke via Inhibiting Neuronal Apoptosis and PKCδ/Drp1‐Mediated Excessive Mitochondrial Fission

Wang

et al. 2017

Oxidative Medicine and Cellular Longevity

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YiQiFuMai (YQFM) powder injection has been reported to be used in cardiovascular and nervous system diseases with marked efficacy. However, as a treatment against diseases characterized by hypoxia, lassitude, and asthenia, the effects and underlying mechanisms of YQFM in neuronal mitochondrial function and dynamics have not been fully elucidated. Here, we demonstrated that YQFM inhibited mitochondrial apoptosis and activation of dynamin-related protein 1 (Drp1) in cerebral ischemia-injured rats, producing a significant improvement in cerebral infarction and neurological score. YQFM also attenuated oxidative stress-induced mitochondrial dysfunction and apoptosis through increasing ATP level and mitochondria membrane potential (Δψm), inhibiting ROS production, and regulating Bcl-2 family protein levels in primary cultured neurons. Moreover, YQFM inhibited excessive mitochondrial fission, Drp1 phosphorylation, and translocation from cytoplasm to mitochondria induced by oxidative stress. We provided the first evidence that YQFM inhibited the activation, association, and translocation of PKCδ and Drp1 upon oxidative stress. Taken together, we demonstrate that YQFM ameliorates ischemic stroke-induced neuronal apoptosis through inhibiting mitochondrial dysfunction and PKCδ/Drp1-mediated excessive mitochondrial fission. These findings not only put new insights into the unique neuroprotective properties of YQFM associated with the regulation of mitochondrial function but also expand our understanding of the underlying mechanisms of ischemic stroke.

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“…Our proteomics study was performed according to a previously described method [ 18 ]. The right cerebral cortices were excised according to experimental groups and homogenized in buffer solution (8 M urea, 4% CHAPS, ampholytes, and 40 mM Tris-HCl).…”

Section: Methodsmentioning

confidence: 99%

“…Western blot analysis was performed as previously described [ 18 ]. Briefly, the right cerebral cortices were dissolved and homogenized in lysis buffer (1 M Tris-HCI, 5M sodium chloride, 0.5% sodium deoxycholate, 10% sodium dodecyl sulfate, 1% sodium azide, and 10% NP-40) containing 200 µM phenylmethylsulfonyl fluoride as a protein inhibitor.…”

Section: Methodsmentioning

confidence: 99%

“…These data support that DLP-1 is an essential protein for synaptic formation and mitochondrial functioning in neurons. We previously demonstrated that cerebral ischemic injury decreases DLP-1 expression [ 18 ]. Although several studies have demonstrated that hyperglycemic conditions exacerbate brain damage during cerebral ischemia, little is known about DLP-1 expression in ischemic brains in the context of diabetes.…”

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Hyperglycemia exacerbates downregulation of dynamin-like protein 1 in ischemic cerebral injury

2017

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Ischemic stroke is one of the leading causes of adult disability and death. Hyperglycemia is associated with an increased risk of stroke and poor outcomes after brain injury. Dynamin-like protein I (DLP-1) regulates mitochondrial fission and promotes mitochondrial dynamics. Neurodegenerative diseases are associated with mitochondrial dysfunction, and the downregulation of DLP-1 has been previously identified in a stroke animal model. Here, we investigated the changes in DLP-1 protein expression in an animal model of focal cerebral ischemia with induced hyperglycemia. Streptozotocin (40 mg/kg) was intraperitoneally injected into male rats to induce hyperglycemia, and middle cerebral artery occlusion (MCAO) was surgically induced 4 weeks after streptozotocin treatment. Brain tissue was isolated 24 hours after MCAO, and cerebral cortex samples were used for this study. Proteomics revealed a decrease in DLP-1 expression in MCAO animals when compared with controls, and this downregulation was more prominent in MCAO animals with hyperglycemia. Reverse-transcription polymerase chain reaction and Western blot analyses confirmed that DLP-1 was significantly downregulated in MCAO-injured animals with hyperglycemia compared to those without hyperglycemia. The decrease in DLP-1 indicates mitochondrial morphological changes and dysfunction. Together, these results suggest that the severe decrease of DLP-1 seen after brain injury under hyperglycemic conditions may exacerbate the damage to the brain.

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Ischemic brain injury decreases dynamin-like protein 1 expression in a middle cerebral artery occlusion animal model and glutamate-exposed HT22 cells

Cited by 7 publications

References 24 publications

Quercetin attenuates the reduction of parvalbumin in middle cerebral artery occlusion animal model

Quercetin attenuates the reduction of parvalbumin in middle cerebral artery occlusion animal model

YiQiFuMai Powder Injection Protects against Ischemic Stroke via Inhibiting Neuronal Apoptosis and PKCδ/Drp1‐Mediated Excessive Mitochondrial Fission

Hyperglycemia exacerbates downregulation of dynamin-like protein 1 in ischemic cerebral injury

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