Hyo Jung Kang
Ajou University
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Featured researches published by Hyo Jung Kang.
Neurobiology of Aging | 2004
Seung-Pil Yang; Dong-Goo Bae; Hyo Jung Kang; Byoung Joo Gwag; Yong Song Gho; Chi-Bom Chae
Alzheimers disease (AD) is accompanied by the progressive deposition of beta-amyloid (Abeta) in both senile plaques and cerebral blood vessels, loss of central neurons, and vessel damage. Cerebral hypoperfusion is one of the major clinical features in AD and likely plays a critical role in its pathogenesis. In addition to its major roles in angiogenesis, vascular endothelial growth factor (VEGF) has neurotrophic and neuroprotective effects. VEGF is an ischemia-inducible factor and increased expression of VEGF often occurs in AD. Although the presence of VEGF immunoreactivity in the AD brain has been described previously, the direct interaction of VEGF with Abeta has not been established. Here, we show that VEGF is co-localized with Abeta plaques in the brains of patients with AD. In vitro experiments show that VEGF binds to Abeta with high affinity (K(D) approximate to 50 pM). VEGF is co-aggregated with Abeta without any apparent effect on the rate of aggregation, strongly binds to pre-aggregated Abeta, and is very slowly released from the co-aggregated complex. Continuous deposition of VEGF in the amyloid plaques most likely results in deficiency of available VEGF under hypoperfusion and, thus, may contribute to neurodegeneration and vascular dysfunction in the progression of AD.
The Journal of Neuroscience | 2004
Hyo Jung Kang; Yoon S. Choi; Seung Beom Hong; Kee Won Kim; Ran Sook Woo; Seok Joon Won; Eun Ju Kim; Hee Kyung Jeon; So Young Jo; Tae Kook Kim; Robert M. Bachoo; Ian J. Reynolds; Byoung Joo Gwag; Han Woong Lee
The catalytic subunit of telomerase reverse transcriptase (TERT) protects dividing cells from replicative senescence in vitro. Here, we show that expression of TERT mRNA is induced in the ipsilateral cortical neurons after occlusion of the middle cerebral artery in adult mice. Transgenic mice that overexpress TERT showed significant resistance to ischemic brain injury. Among excitotoxicity, oxidative stress, and apoptosis comprising of routes of ischemic neuronal death, NMDA receptor-mediated excitotoxicity was reduced in forebrain cell cultures overexpressing TERT. NMDA-induced accumulation of cytosolic free Ca2+ ([Ca2+]c) was reduced in forebrain neurons from TERT transgenic mice, which was attributable to the rapid flow of [Ca2+]c into the mitochondria from the cytosol without change in Ca2+ influx and efflux through the plasma membrane. The present study provides evidence that TERT is inducible in postmitotic neurons after ischemic brain injury and prevents NMDA neurotoxicity through shift of the cytosolic free Ca2+ into the mitochondria, and thus plays a protective role in ameliorating ischemic neuronal cell death.
Journal of Neurochemistry | 2001
Kong Sook Han; Hyo Jung Kang; Eun Young Kim; Won Joo Yoon; Seonghyang Sohn; Hyuk Jae Kwon; Byoung Joo Gwag
Sustained alteration in [Ca2+]i triggers neuronal death. We examined morphological and signaling events of Ca2+‐deficiency‐induced neuronal death. Cortical cell cultures exposed to 20 µm 1,2‐bis(2‐aminophenoxy)ethane‐N,N,N′,N′‐tetraacetic acid (BAPTA‐AM), an intracellular calcium chelator, underwent neuronal apoptosis within 12 h that was evident by shriveled cell bodies, aggregated and condensed nuclear chromatin, and disrupted nuclear membrane. Thereafter, surviving neurons revealed typical necrosis, accompanied by swelling of cell body and mitochondria, over 24 h. Both apoptosis and necrosis were prevented by inclusion of 1 µg/mL cycloheximide, a protein synthesis inhibitor. Treatment with BAPTA‐AM induced translocation of Bax into mitochondria within 4 h and release of cytochrome c from mitochondria over 4–12 h. An active fragment of caspase‐3, a downstream mediator of cytochrome c, was observed within 8 h and cleaved PHF‐1‐positive tau. Administration of zVAD‐fmk, a broad inhibitor of caspases, or DEVD‐amc, a selective inhibitor of caspase‐3, selectively prevented the apoptosis component of BAPTA‐AM neurotoxicity. In contrast, BAPTA‐AM‐induced necrosis was propagated through sequential production of superoxide, mitochondrial and cytoplasmic reactive oxygen species. Combined treatment with caspase inhibitors and antioxidants blocked BAPTA‐AM neurotoxicity. The present study suggests that neurons deficient in [Ca2+]i undergo caspase‐3‐mediated apoptosis and reactive oxygen species (ROS)‐mediated necrosis.
Neuroreport | 2001
Jee Youn Kang; Hyo Jung Kang; Young Ki Chung; Byoung Joo Gwag; Jai Sung Noh
The effects of 5-hydroxytryptamine (5-HT) on several types of neuronal injury in mouse cortical cell cultures were tested. Co-treatment with 5-HT prevented free radical-mediated neuronal necrosis induced by FeCl2 or buthionine sulfoximine (BSO) in a dose-dependent manner. Subtype antagonists did not reverse the protective effect and 5-HT showed direct free radical scavenging activity evidenced by its ability to reduce the stable free radical 1,1-diphenyl-2-picrylhydrazyl (DPPH) in a cell-free system. Excitotoxic necrosis induced by NMDA or apoptosis induced by staurosporine was not sensitive to 5-HT treatment. These features raise the possibility that the endogenous neurotransmitter 5-HT may work as an innate antioxidant defense mechanism in the CNS.
Molecular Pharmacology | 2001
Soo Jung Eom; Eun Young Kim; Ji Eun Lee; Hyo Jung Kang; Jaekyung Shim; Seong Up Kim; Byoung Joo Gwag; Eui Ju Choi
Molecular Pharmacology | 2003
Hyo Jung Kang; Jai Sung Noh; Yun Soo Bae; Byoung Joo Gwag
Neurobiology of Disease | 2005
Hyo Jung Kang; Won Joo Yoon; Gyeong Joon Moon; Doo Yeon Kim; Seonghyang Sohn; Hyuk Jae Kwon; Byoung Joo Gwag
Neurobiology of Aging | 2004
Seon Eui Hong; Hyo Jung Kang; Byoung Joo Gwag
Neurobiology of Aging | 2004
Hyo Jung Kang; Han-Woong Lee; Byoung Joo Gwag
Archive | 2001
Kong Sook Han; Hyo Jung Kang; Eun Young Kim; Won Joo Yoon; Seonghyang Sohn; Hyuk Jae Kwon; Byoung Joo Gwag