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Astrogliosis Is a Possible Player in Preventing Delayed Neuronal Death
Jeong, Hey-Kyeong,Ji, Kyung-Min,Min, Kyoung-Jin,Choi, Insup,Choi, Dong-Joo,Jou, Ilo,Joe, Eun-Hye Korean Society for Molecular and Cellular Biology 2014 Molecules and cells Vol.37 No.4
Mitigating secondary delayed neuronal injury has been a therapeutic strategy for minimizing neurological symptoms after several types of brain injury. Interestingly, secondary neuronal loss appeared to be closely related to functional loss and/or death of astrocytes. In the brain damage induced by agonists of two glutamate receptors, N-ethyl-D-aspartic acid (NMDA) and kainic acid (KA), NMDA induced neuronal death within 3 h, but did not increase further thereafter. However, in the KA-injected brain, neuronal death was not obviously detectable even at injection sites at 3 h, but extensively increased to encompass the entire hemisphere at 7 days. Brain inflammation, a possible cause of secondary neuronal damage, showed little differences between the two models. Importantly, however, astrocyte behavior was completely different. In the NMDA-injected cortex, the loss of glial fibrillary acidic protein-expressing ($GFAP^+$) astrocytes was confined to the injection site until 7 days after the injection, and astrocytes around the damage sites showed extensive gliosis and appeared to isolate the damage sites. In contrast, in the KA-injected brain, $GFAP^+$ astrocytes, like neurons, slowly, but progressively, disappeared across the entire hemisphere. Other markers of astrocytes, including $S100{\beta}$, glutamate transporter EAAT2, the potassium channel Kir4.1 and glutamine synthase, showed patterns similar to that of GFAP in both NMDA- and KA-injected cortexes. More importantly, astrocyte disappearance and/or functional loss preceded neuronal death in the KA-injected brain. Taken together, these results suggest that loss of astrocyte support to neurons may be a critical cause of delayed neuronal death in the injured brain.
Jeong, Hey-Kyeong,Jou, Il-O,Joe, Eun-Hye Korean Society for Biochemistry and Molecular Bion 2010 Experimental and molecular medicine Vol.42 No.12
It has been suggested that brain inflammation is important in aggravation of brain damage and/or that inflammation causes neurodegenerative diseases including Parkinson's disease (PD). Recently, systemic inflammation has also emerged as a risk factor for PD. In the present study, we evaluated how systemic inflammation induced by intravenous (iv) lipopolysaccharides (LPS) injection affected brain inflammation and neuronal damage in the rat. Interestingly, almost all brain inflammatory responses, including morphological activation of microglia, neutrophil infiltration, and mRNA/protein expression of inflammatory mediators, appeared within 4-8 h, and subsided within 1-3 days, in the substantia nigra (SN), where dopaminergic neurons are located. More importantly, however, dopaminergic neuronal loss was not detectable for up to 8 d after iv LPS injection. Together, these results indicate that acute induction of systemic inflammation causes brain inflammation, but this is not sufficiently toxic to induce neuronal injury.
최혜영,최창용,공병기,임동한,장미경,정창남,나재운 한국공업화학회 2002 응용화학 Vol.6 No.1
α,β,γ-chitin were isolated from natural resources by treatment with NaOH solution and for deprotenization, and then by treatment with dilute HCI solution for demineralization. The chitin gel matrices were prepared using α,β,γ-chitin for application of drug delivery systems. In this study, α,β,γ-chitin were isolated from crab shell, squid pen and beetles of cuticle, respectively, and physicochemical properties were investigated using fourier transform infrared spectrometer, X-ray diffractometer, and differential scanning calorimeter. And then the chitin gel matrices were prepared using α,β,γ-chitin and dissolution characteristics of drug from chitin gel matrices were investigated. The dissolution profiles of α,β,γ-chitin gel matrices were determined by means of available compendium. Dissolution efficiency of these gel matrices were observed at 37 ± 0.5℃.
Choi, Insup,Kim, Jun,Jeong, Hey-Kyeong,Kim, Beomsue,Jou, Ilo,Park, Sang Myun,Chen, Linan,Kang, Un-Jung,Zhuang, Xiaoxi,Joe, Eun-hye Blackwell Publishing Ltd 2013 GLIA Vol.61 No.5
<P>PINK1 (PTEN induced putative kinase 1), a familial Parkinson's disease (PD)-related gene, is expressed in astrocytes, but little is known about its role in this cell type. Here, we found that astrocytes cultured from PINK1-knockout (KO) mice exhibit defective proliferative responses to epidermal growth factor (EGF) and fetal bovine serum. In PINK1-KO astrocytes, basal and EGF-induced p38 activation (phosphorylation) were increased whereas EGF receptor (EGFR) expression and AKT activation were decreased. p38 inhibition (SB203580) or knockdown with small interfering RNA (siRNA) rescued EGFR expression and AKT activation in PINK1-KO astrocytes. Proliferation defects in PINK1-KO astrocytes appeared to be linked to mitochondrial defects, manifesting as decreased mitochondrial mass and membrane potential, increased intracellular reactive oxygen species level, decreased glucose-uptake capacity, and decreased ATP production. Mitochondrial toxin (oligomycin) and a glucose-uptake inhibitor (phloretin) mimicked the PINK1-deficiency phenotype, decreasing astrocyte proliferation, EGFR expression and AKT activation, and increasing p38 activation. In addition, the proliferation defect in PINK1-KO astrocytes resulted in a delay in the wound healing process. Taken together, these results suggest that PINK1 deficiency causes astrocytes dysfunction, which may contribute to the development of PD due to delayed astrocytes-mediated repair of microenvironment in the brain.</P>
Ryoo, Soo-Ryoon,Cho, Hyun-Jeong,Lee, Hye-Won,Jeong, Hey Kyeong,Radnaabazar, Chinzorig,Kim, Yeun-Soo,Kim, Min-Jeong,Son, Mi-Young,Seo, Hyemyung,Chung, Sul-Hee,Song, Woo-Joo Blackwell Publishing Ltd 2008 Journal of Neurochemistry Vol.104 No.5
<P>Abstract</P><P>Most individuals with Down Syndrome (DS) show an early-onset of Alzheimer’s disease (AD), which potentially results from the presence of an extra copy of a segment of chromosome 21. Located on chromosome 21 are the genes that encode &bgr;-amyloid (A&bgr;) precursor protein (<I>APP</I> ), a key protein involved in the pathogenesis of AD, and dual-specificity tyrosine(Y)-phosphorylation regulated kinase 1A (<I>DYRK1A</I> ), a proline-directed protein kinase that plays a critical role in neurodevelopment. Here, we describe a potential mechanism for the regulation of AD pathology in DS brains by DYRK1A-mediated phosphorylation of APP. We show that APP is phosphorylated at Thr668 by DYRK1A <I>in vitro</I> and in mammalian cells. The amounts of phospho-APP and A&bgr; are increased in the brains of transgenic mice that over-express the human DYRK1A protein. Furthermore, we show that the amounts of phospho-APP as well as those of APP and DYRK1A are elevated in human DS brains. Taken together, these results reveal a potential regulatory link between APP and DYRK1A in DS brains, and suggest that the over-expression of DYRK1A in DS may play a role in accelerating AD pathogenesis through phosphorylation of APP.</P>
Ji, Kyung-Ae,Yang, Myung-Soon,Jeong, Hey-Kyeong,Min, Kyoung-Jin,Kang, Seung-Hee,Jou, Ilo,Joe, Eun-Hye John Wiley & Sons, Inc. 2007 Glia Vol.55 No.15
<P>Generally, it has been accepted that microglia play important roles in brain inflammation. However, recently several studies suggested possible infiltration of blood neutrophils and monocytes into the brain. To understand contribution of microglia and blood inflammatory cells to brain inflammation, the behavior of microglia, neutrophils, and monocytes was investigated in LPS (lipopolysaccharide)-injected substantia nigra pars compacta, cortex, and hippocampus of normal and/or leukopenic rats using specific markers of neutrophils (myeloperoxidase, MPO), and microglia and monocytes (ionized calcium binding adaptor molecule-1, Iba-1), as well as a general marker for these inflammatory cells (CD11b). CD11b-immunopositive (CD11b<SUP>+</SUP>) cells and Iba-1<SUP>+</SUP> cells displayed similar behavior in intact and LPS-injected brain at 6 h after the injection. Interestingly, however, CD11b<SUP>+</SUP> cells and Iba-1<SUP>+</SUP> cells displayed significantly different behavior at 12 h: Iba-1<SUP>+</SUP> cells disappeared while CD11b<SUP>+</SUP> cells became round in shape. We found that CD11b/Iba-1-double positive (CD11b<SUP>+</SUP>/Iba-1<SUP>+</SUP>) ramified microglia died within 6 h after LPS injection. The round CD11b<SUP>+</SUP> cells detected at 12 h were MPO<SUP>+</SUP>. These CD11b<SUP>+</SUP>/MPO<SUP>+</SUP> cells were not found in leukopenic rats, suggestive of neutrophil infiltration. MPO<SUP>+</SUP> neutrophils expressed inducible nitric oxide synthase, interleukin-1β, cyclooxygenase-2, and monocyte chemoattractant protein-1, but died within 18 h. CD11b<SUP>+</SUP> cells detected at 24 h appeared to be infiltrated monocytes, since these cells were once labeled with Iba-1 and were not found in leukopenic rats. Furthermore, transplanted monocytes were detectable in LPS-injected brain. These results suggest that at least a part of neutrophils and monocytes could have been misinterpreted as activated microglia in inflamed brain. © 2007 Wiley-Liss, Inc.</P>