중간엽줄기세포 매개 간세포증식인자 생체 외 송달을 통한 새로운 척수재생치료기술
DC Field | Value | Language |
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dc.contributor.advisor | 김병곤 | - |
dc.contributor.author | 정수령 | - |
dc.date.accessioned | 2019-10-21T07:11:52Z | - |
dc.date.available | 2019-10-21T07:11:52Z | - |
dc.date.issued | 2009-08 | - |
dc.identifier.other | 10119 | - |
dc.identifier.uri | https://dspace.ajou.ac.kr/handle/2018.oak/17141 | - |
dc.description | 학위논문(석사)--아주대학교 일반대학원 :의생명학과,2009. 8 | - |
dc.description.tableofcontents | ABSTRACT ⅰ TABLE OF CONTENTS ⅲ LIST OF FIGURES ⅴ LIST OF TABLE ⅵ LIST OF ABBREVIATION ⅶ Ⅰ. INTRODUCTION 1 Ⅱ. MATERIAL AND METHODS 5 A. PRIMARY ASTROCYTE CULTURES 5 B. ANIMALS AND SURGICAL PROCEDURES 6 C. IMMUNOCYTOCHEMISTRY 7 D. TISSUE PROCESSING AND IMMUNOHISTOCHEMISTRY 7 E. ENZYME-LINKED IMMUNOSORBENT ASSAY (ELISA) 8 F. WESTERN BLOT ANALYSIS 9 G. REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION (RT-PCR) 11 H. STASTITATIC ANALYSIS 12 Ⅲ. RESULTS 13 A. HGF prevents cytokine-induced astrocytic activation in vitro. 13 B. HGF decreases expression of chondroitin sulfate proteoglycans (CSPGs) 19 C. Effects of HGF on TGFβ secretion 22 D. Ex vivo delivery of HGF using mesenchymal stem cells in hemisection spinal cord injury. 27 E. HGF inhibits astrocytic activation and CSPGs production after spinal cord injury. 33 Ⅳ. DISCUSSION 38 Ⅴ. CONCLUSION 43 REFERENCE 44 국문요약 55 | - |
dc.language.iso | kor | - |
dc.publisher | The Graduate School, Ajou University | - |
dc.rights | 아주대학교 논문은 저작권에 의해 보호받습니다. | - |
dc.title | 중간엽줄기세포 매개 간세포증식인자 생체 외 송달을 통한 새로운 척수재생치료기술 | - |
dc.title.alternative | Jeong Soo Ryung | - |
dc.type | Thesis | - |
dc.contributor.affiliation | 아주대학교 일반대학원 | - |
dc.contributor.alternativeName | Jeong Soo Ryung | - |
dc.contributor.department | 일반대학원 의생명과학과 | - |
dc.date.awarded | 2009. 8 | - |
dc.description.degree | Master | - |
dc.identifier.localId | 567971 | - |
dc.identifier.url | http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000010119 | - |
dc.subject.keyword | spinal cord injury | - |
dc.subject.keyword | hepatocyte growth factor | - |
dc.subject.keyword | glial scars | - |
dc.subject.keyword | chondroitin sulfate proteoglycans | - |
dc.subject.keyword | transforming growth factor | - |
dc.subject.keyword | 중간엽줄기세포 | - |
dc.subject.keyword | 간세포증식인자 | - |
dc.description.alternativeAbstract | Formation of glial scars physically impedes growth of regenerating axons following CNS injuries such as spinal cord trauma. Glial scars also produce various species of chondroitin sulfate proteoglycans (CSPGs) that act as a potent inhibitor of axon growth. Thus, inhibition of glial scar formation and/or suppression of CSPGs production may support axonal regeneration following spinal cord injury. Hepatocyte growth factor (HGF), which was originally identified as a mitogen for hepatocytes, has been shown to strongly suppress fibrosis of internal organs such as liver and kidney. However, its role in the regulation of CNS glial scars has not been studied. The purpose of this study was to examine whether HGF can affect formation of glial scars and production of various CSPGs. Glial scar formation was mimicked in vitro by cytokine treatment in primary astrocyte culture. Treatment of TGFβ1 led to astrocytic hypertrophy that was associated with dramatic upregulation of intermediate filament, GFAP (glial fibrillary acidic protein), which was evidently suppressed by HGF cotreatment in a dose-dependent manner. HGF also inhibited TGFβ1-induced upregulation of neurocan, one of CSPG species. To explore whether glial scar formation is inhibited by HGF in vivo spinal cord injury model, HGF overexpressing mesenchymal stem cells (HGF-MSCs) were transplanted into hemisected spinal cord lesions at T8. The ex-vivo gene delivery approach effectively increased the HGF level and phosphorylation of its cognate receptor c-Met. Transplantation of HGF-MSCs reduced the formation glial scar and CSPGs deposition around the hemisection lesions. Western blot showed that the amount of neurocan significantly decreased in animals with HGF-MSCs transplantation. These findings were accompanied by decreases in TGFβ1 and β2, strong inducers of astrocyte activation. Our results suggest that HGF may potently regulate both glial scar formation and CSPGs production following spinal cord injury | - |
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