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Bae, Jae-Sung,Furuya, Shigeki,Shinoda, Yoko,Endo, Shogo,Schuchman, Edward H.,Hirabayashi, Yoshio,Jin, Hee Kyung Mary Ann Liebert 2005 Human gene therapy Vol.16 No.8
<P>After transplantation, adult bone marrow-derived mesenchymal stem cells (BM-MSCs) may undergo transdifferentiation and/or cell fusion in response to new environments. However, the mechanism(s) that govern these cell fate switches remain unknown. Here we demonstrate that the pathology associated with murine Niemann-Pick disease type C (NP-C) cerebellum augments the ability of BM-MSCs to fuse with Purkinje neurons. The results suggest that the degenerative microenvironment of Purkinje neurons in the NP-C cerebellum modulates the cell fate switch of BM-MSCs via cell fusion.</P>
Bae, Jae-Sung,Han, Hyung Soo,Youn, Dong-Ho,Carter, Janet E.,Modo, Michel,Schuchman, Edward H.,Jin, Hee Kyung Wiley (John WileySons) 2007 Stem Cells Vol.25 No.5
<P>Recent studies have shown that bone marrow-derived MSCs (BM-MSCs) improve neurological deficits when transplanted into animal models of neurological disorders. However, the precise mechanism by which this occurs remains unknown. Herein we demonstrate that BM-MSCs are able to promote neuronal networks with functional synaptic transmission after transplantation into Niemann-Pick disease type C (NP-C) mouse cerebellum. To address the mechanism by which this occurs, we used gene microarray, whole-cell patch-clamp recordings, and immunohistochemistry to evaluate expression of neurotransmitter receptors on Purkinje neurons in the NP-C cerebellum. Gene microarray analysis revealed upregulation of genes involved in both excitatory and inhibitory neurotransmission encoding subunits of the ionotropic glutamate receptors (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, AMPA) GluR4 and GABA(A) receptor beta2. We also demonstrated that BM-MSCs, when originated by fusion-like events with existing Purkinje neurons, develop into electrically active Purkinje neurons with functional synaptic formation. This study provides the first in vivo evidence that upregulation of neurotransmitter receptors may contribute to synapse formation via cell fusion-like processes after BM-MSC transplantation into mice with neurodegenerative disease. Disclosure of potential conflicts of interest is found at the end of this article.</P>
피알라고 애드워드(Edward Joshua Pialago),정희여(Heeyeo Jung),유다영(Dayoung Yu),배성만(Seongman Bae),박찬우(Chan-Woo Park) 대한기계학회 2010 대한기계학회 춘추학술대회 Vol.2010 No.11
In the present study, the mechanical alloying of carbon nanotubes (CNTs) and copper powder by ball milling is being investigated. Results show that the physical characteristics such as the dispersion of CNTs and the presence or absence of the agglomeration of particles are depended on the milling time and CNT content of the powder mixture. Depending on the end application of the CNT-Cu powder composite, the desired composite can be fabricated by controlling the milling parameters such as mixture composition, milling time as well as temperature.
Gene Promoter Hypermethylation in Tumors and Plasma of Breast Cancer Patients
Young Kyung Bae,Young Ran Shim,Joon Hyuk Choi,Mi Jin Kim,Edward Gabrielson,Soo Jung Lee,Tae Yoon Hwang,Sei One Shin 대한암학회 2005 Cancer Research and Treatment Vol.37 No.4
Purpose: To measure the hypermethylation of four genes in primary tumors and paired plasma samples to determine the feasibility of gene promoter hypermethylation markers for detecting breast cancer in the plasma.Materials and Methods: DNA was extracted from the tumor tissues and peripheral blood plasma of 34 patients with invasive breast cancer, and the samples examined for aberrant hypermethylation in cyclin D2, retinoic acid receptor β (RAR β), twist and high in normal-1 (HIN-1) genes using methylation-specific PCR (MSP), and the results correlated with the clinicopathological parameters.Results: Promoter hypermethylation was detected at high frequency in the primary tumors for cyclin D2 (53%), RAR β (56%), twist (41%) and HIN-1 (77%). Thirty-threeof the 34 (97%) primary tumors displayed promoter hypermethylation in at least one of the genes examined. The corresponding plasma samples showed hyperme thylation of the same genes, although at lower frequencies (6% for cyclin D2, 16% for RAR β, 36% for twist, and 54% for HIN-1). Overall, 22 of the 33 (67%) primary tumors with hypermethylation of at least one of the four genes also had abnormally hypermethylated DNA in their matched plasma samples. No significant relationship was recognized between any of the clinical or pathological parameters (tumor size, axillary lymph node metastasis, stage, or Ki-67 labeling index) with the frequency of hypermethylated DNA in the primary tumor or plasma.Conclusion: The detection of aberrant promoter hypermethylation of cancer-related genes in the plasma may be a useful tool for the detection of breast cancer.
이용원,성연선,Edward Jeong Bae,오성훈,배인수,강효진 생화학분자생물학회 2015 Experimental and molecular medicine Vol.47 No.-
An F-box protein, β-TrCP recognizes substrate proteins and destabilizes them through ubiquitin-dependent proteolysis. It regulates the stability of diverse proteins and functions as either a tumor suppressor or an oncogene. Although the regulationby β-TrCP has been widely studied, the regulation of β-TrCP itself is not well understood yet. In this study, we found that the level of β-TrCP1 is downregulated by various protein kinase inhibitors in triple-negative breast cancer (TNBC) cells. A PI3K/mTOR inhibitor PI-103 reduced the level of β-TrCP1 in a wide range of TNBC cells in a proteasome-dependent manner. Concomitantly, the levels of c-Myc and cyclin E were also downregulated by PI-103. PI-103 reduced the phosphorylation of β-TrCP1 prior to its degradation. In addition, knockdown of β-TrCP1 inhibited the proliferation of TNBC cells. We furtheridentified that pharmacological inhibition of mTORC2 was sufficient to reduce the β-TrCP1 and c-Myc levels. These results suggest that mTORC2 regulates the stability of β-TrCP1 in TNBC cells and targeting β-TrCP1 is a potential approach to treathuman TNBC.
Lee, Jong Kil,Schuchman, Edward H,Jin, Hee Kyung,Bae, Jae-sung AlphaMed Press 2012 Stem cells Vol.30 No.7
<P>Microglia have the ability to eliminate amyloid β (Aβ) by a cell-specific phagocytic mechanism, and bone marrow (BM) stem cells have shown a beneficial effect through endogenous microglia activation in the brains of Alzheimer's disease (AD) mice. However, the mechanisms underlying BM-induced activation of microglia have not been resolved. Here we show that BM-derived mesenchymal stem cells (MSCs) induced the migration of microglia when exposed to Aβ in vitro. Cytokine array analysis of the BM-MSC media obtained after stimulation by Aβ further revealed elevated release of the chemoattractive factor, CCL5. We also observed that CCL5 was increased when BM-MSCs were transplanted into the brains of Aβ-deposited AD mice, but not normal mice. Interestingly, alternative activation of microglia in AD mice was associated with elevated CCL5 expression following intracerebral BM-MSC transplantation. Furthermore, by generating an AD-green fluorescent protein chimeric mouse, we ascertained that endogenous BM cells, recruited into the brain by CCL5, induced microglial activation. Additionally, we observed that neprilysin and interleukin-4 derived from the alternative microglia were associated with a reduction in Aβ deposition and memory impairment in AD mice. These results suggest that the beneficial effects observed in AD mice after intracerebral SC transplantation may be explained by alternative microglia activation. The recruitment of the alternative microglia into the brain is driven by CCL5 secretion from the transplanted BM-MSCs, which itself is induced by Aβ deposition in the AD brain.</P>
The Gut Microbiome: Human Health and Inflammatory Skin Diseases
( Emily A. Mann ),( Edward Bae ),( Darya Kostyuchek ),( Hye Jin Chung ),( Jean S. Mcgee ) 대한피부과학회 2020 Annals of Dermatology Vol.32 No.4
The human microbiome is a rich environment consisting of bacteria, fungi and other commensal microorganisms of the gut, mucosa and skin. The functional role of the gut microbiome includes facilitation in metabolism of macronutrients, maturation of the immune system, and production of pro- or anti-inflammatory signaling molecules and peptides. The identification of these resident organisms has brought about a new understanding of disease processes. Nevertheless, more questions remain regarding the interactions within the microbiome, its interactions with the host, and its contributions to the pathophysiology of disease. The purpose of this review is to examine the existing medical literature to highlight the role of the gut microbiome in human health, also paying attention to its role in several inflammatory skin diseases, namely atopic dermatitis, psoriasis, and rosacea. (Ann Dermatol 32(4) 265∼272, 2020)
( Byoung Kuk Jang ),( Edward Gane ),( Wai Kay Seto ),( Harry La Janssen ),( Florin A Caruntu ),( Hyung Joon Kim ),( Dzhamal Abdurakhmanov ),( Shuhei Nishiguchi ),( Andrzej Horban ),( Ho Bae ),( John F 대한간학회 2018 춘·추계 학술대회 (KASL) Vol.2018 No.1
Aims: Tenofovir alafenamide (TAF), a new prodrug of tenofovir (TFV), is now a preferred treatment in the 2017 EASL HBV Guidelines, and may be particularly useful in patients with risk factors for TDF associated renal and bone effects. We assessed the 1 year safety and efficacy in CHB patients with TDF risk factors who were switched from TDF to TAF. Methods: In two identically-designed Phase 3 studies, HBeAg(+) and HBeAg(-)patients were randomized 2:1 to TAF 25 mg or TDF 300 mg and treated in a double- blind fashion for 96 weeks; all patients received open-label (OL) TAF for an additional 48 weeks (through Week 144). Renal and bone safety parameters, and antiviral efficacy (HBV DNA < 29 IU/mL) and ALT normalization were assessed in the subset of switch patients with baseline risk factors for TDF use: Age >60 years, osteoporosis of hip or spine, ³Stage 2 CKD (GFRCG < 90 mL/ min), albuminurina (UACR >30 mg/g), hypophosphatemia (PO4 <2.5 mg/dL), or presence of comorbidities (e.g. HTN, DM). Results: Of 1298 patients randomized and treated in the 2 studies, 540(42%) switched to open- label TAF at Week 96 (TAF<sup>®</sup>TAF 360; TDF<sup>®</sup>TAF 180), of which 284(53%) patients had at least 1 TDF risk factor at baseline; 123(23%) patients had ³2 risk factors. Baseline demographics and disease characteristics were similar between treatment groups. At Week 144, significant improvements in renal (sCr, eGFRCG) parameters, hip and spine BMD were observed and summarized in the table. Antiviral efficacy was maintained at Week 144 in both groups and in TDF patients who switched to TAF, increased rates of ALT normalization were seen. Conclusions: In CHB patients with risk factors for potential TDF toxicity, switching from TDF to TAF resulted in improved bone and renal safety parameters while efficacy was maintained in this subgroup at one year.