Nicotinamide attenuates the injury-induced decrease of hippocalcin in ischemic brain injury

Koh, Phil-Ok

doi:10.1016/j.neulet.2013.04.010

Cited by 7 publications

(8 citation statements)

References 25 publications

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“…HPAC, a protein whose downregulation is induced by HS in the hypothalamus, belongs to a neuronal calcium sensor protein family (Takamatsu & Noguchi, ) and is a neuroprotective protein in ischemic brain injury and traumatic brain injury (Koh, ; Sun et al, ). Because of its important role in the brain and probable functions in HS‐induced hypothalamic injury, HPAC was chosen as the target candidate for further investigations.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, UTI has therapeutic effects that are based on its anti‐ischemia and anti‐inflammatory functions (Chen et al, ; Huang, Xie, Zhang, Dang, & Qiong, ; Zhang et al, ). Multiple other drugs reportedly contribute to neuroprotective functions by upregulating HPAC, such as nicotinamide and ferulic acid (Koh, , ). However, the exact mechanisms of UTI‐mediated upregulation of HPAC expression are undetermined.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, UTI has therapeutic effects that are based on its anti-ischemia and anti-inflammatory functions Huang, Xie, Zhang, Dang, & Qiong, 2008;Zhang et al, 2016). Multiple other drugs reportedly contribute to neuroprotective functions by upregulating HPAC, such as nicotinamide and ferulic acid (Koh, 2013b(Koh, , 2013a undetermined. In addition to reducing neuronal pathological injury, UTI increased heat tolerance in the heatstroke animals in our study, which was evidenced by a prolonged platform stage time at 39°C and 41°C and a prolonged total time before the Tc reached 42°C.…”

Section: Effects Of Uti On Hypothalamic Pathological Injury and Tc Changes In Heatstroke Micementioning

confidence: 99%

“…HPAC, a protein whose downregulation is induced by HS in the hypothalamus, belongs to a neuronal calcium sensor protein family and is a neuroprotective protein in ischemic brain injury and traumatic brain injury (Koh, 2013a;Sun et al, 2013). Because of its important role in the brain and may be related to its functions in attenuating calcium overload, counteracting caspase-12 activity and reducing endoplasmic reticulum stress.…”

Section: Effects Of Uti On Hypothalamic Pathological Injury and Tc Ch...mentioning

confidence: 99%

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Proteomic identification of hippocalcin and its protective role in heatstroke‐induced hypothalamic injury in mice

Hong

et al. 2018

Journal Cellular Physiology

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Heatstroke is a devastating condition that is characterized by severe hyperthermia and central nervous system dysfunction. However, the mechanism of thermoregulatory center dysfunction of the hypothalamus in heatstroke is unclear. In this study, we established a heatstroke mouse model and a heat-stressed neuronal cellular model on the pheochromocytoma-12 (PC12) cell line. These models revealed that HS promoted obvious neuronal injury in the hypothalamus, with high pathological scores. In addition, PC12 cell apoptosis was evident by decreased cell viability, increased caspase-3 activity, and high apoptosis rates. Furthermore, 14 differentially expressed proteins in the hypothalamus were analyzed by fluorescence two-dimensional difference gel electrophoresis and identified by matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Expression changes in hippocalcin (HPAC), a downregulated neuron-specific calcium-binding protein, were confirmed in the hypothalamus of the heatstroke mice and heat-stressed PC12 cells by immunochemistry and western blot. Moreover, HPAC overexpression and HPAC-targeted small interfering RNA experiments revealed that HPAC functioned as an antiapoptotic protein in heat-stressed PC12 cells and hypothalamic injury. Lastly, ulinastatin (UTI), a cell-protective drug that is clinically used to treat patients with heatstroke, was used in vitro and in vivo to confirm the role of HPAC; UTI inhibited heat stress (HS)-induced downregulation of HPAC expression, protected hypothalamic neurons and PC12 cells from HS-induced apoptosis and increased heat tolerance in the heatstroke animals. In summary, our study has uncovered and demonstrated the protective role of HPAC in heatstroke-induced hypothalamic injury in mice.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Effects Of Uti On Hypothalamic Pathological Injury and Tc Changes In Heatstroke Micementioning

confidence: 99%

Section: Effects Of Uti On Hypothalamic Pathological Injury and Tc Ch...mentioning

confidence: 99%

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Proteomic identification of hippocalcin and its protective role in heatstroke‐induced hypothalamic injury in mice

Hong

et al. 2018

Journal Cellular Physiology

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“…In relation to apoptotic DNA degradation, nicotinamide prevents apoptotic DNA injury in vascular cells (104,121), neurons (116,124,136,178), keratinocytes (179), corneal endothelial cells (180, and photoreceptor cells {Kiuchi, 2002 #3733, 181). Nicotinamide also can inhibit DNA replication in some cell systems (182).…”

Section: Apoptotic Cell Deathmentioning

confidence: 99%

New Insights for nicotinamide Metabolic disease autophagy and mTOR

Maiese

2020

Front Biosci

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Metabolic disorders, such as diabetes mellitus (DM), are increasingly becoming significant risk factors for the health of the global population and consume substantial portions of the gross domestic product of all nations. Although conventional therapies that include early diagnosis, nutritional modification of diet, and pharmacological treatments may limit disease progression, tight serum glucose control cannot prevent the onset of future disease complications. With these concerns, novel strategies for the treatment of metabolic disorders that involve the vitamin nicotinamide, the mechanistic target of rapamycin (mTOR), mTOR Complex 1 (mTORC1), mTOR Complex 2 (mTORC2), AMP activated protein kinase (AMPK), and the cellular pathways of autophagy and apoptosis offer exceptional promise to provide new avenues of treatment. Oversight of these pathways can promote cellular energy homeostasis, maintain mitochondrial function, improve glucose utilization, and preserve pancreatic β-cell function. Yet, the interplay among mTOR, AMPK, and autophagy pathways can be complex and affect desired clinical outcomes, necessitating further investigations to provide efficacious treatment strategies for metabolic dysfunction and DM.

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7,8-Dihydroxy-4-methylcoumarin Provides Neuroprotection by Increasing Hippocalcin Expression

Jin¹,

Wang²,

Li³

et al. 2015

Neurotox Res

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7,8-Dihydroxy-4-methylcoumarin (Dhmc) is a precursor in the synthesis of derivatives of 4-methyl coumarin, which has excellent radical scavenging properties. In this study, we investigated whether Dhmc protects against oxidative stress and ischemic brain injury. We found that Dhmc protected against glutamate toxicity in hippocampal HT-22 cells in a concentration-dependent manner in vitro. Dhmc inhibited glutamate-induced glutathione depletion and generation of reactive oxygen species, suggesting that Dhmc has an antioxidant effect. In addition, Dhmc inhibited glutamate-induced depletion of hippocalcin, a protein that buffers intracellular calcium and prevents calcium-induced cell death. In our in vivo studies, Dhmc reduced infarct volume in neonatal rats when administered 4 h after cerebral hypoxia/ischemia injury and attenuated the hypoxia/ischemia injury-induced decrease of hippocalcin expression in neonatal rats. Taken together, these results suggest that Dhmc prevents glutamate-induced toxicity by scavenging free radicals and regulating hippocalcin expression. Dhmc may represent a promising agent in the treatment of acute and chronic neurological disorders induced by oxidative stress.

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Nicotinamide attenuates the injury-induced decrease of hippocalcin in ischemic brain injury

Cited by 7 publications

References 25 publications

Proteomic identification of hippocalcin and its protective role in heatstroke‐induced hypothalamic injury in mice

Proteomic identification of hippocalcin and its protective role in heatstroke‐induced hypothalamic injury in mice

New Insights for nicotinamide Metabolic disease autophagy and mTOR

7,8-Dihydroxy-4-methylcoumarin Provides Neuroprotection by Increasing Hippocalcin Expression

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