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허혈손상망막에 이식된 성체줄기세포의 소재 및 운명

권복실 ( Fu Shi Quan ),신지만 ( Ji Man Shin ),김인범 ( In Beom Kim ),염정은 ( Chung Eun Yeum ),채규태 ( Gue Tae Chae ),천명훈 ( Myung Hoon Chun ),오수자 ( Su Ja Oh ) 한국조직공학·재생의학회 2009 조직공학과 재생의학 Vol.6 No.4
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To investigate the differentiation potency of be engraft mesenchymal stem cells to the retinal cell population through the retina ischemia-reperfusion injury model of rat. Ischemic injury model was made by an elevation of intra-ocular pressure in young adult Sprague-Dawely rats. Adult stem cells of third passages labeled with DiI were applied by an intravitreous injection at 3, 5, and 7 days after the ischemia-reperfusion injury(PI), respectively, cared for 2 weeks, and in case of 7 days PI group were also cared for 4 and 6 weeks. For specification of engraft stem cells, immunofluorescent staining by antibodies against retinal neuronal marker molecules was done. Retinal ischemia led to reduce in both thickness and cell number, principally in the inner retina and to a lesser extent in the outer retina. DiI labeled stem cells were migrated and well associated with host retina tissue by 7 days PI. The retinas of stem cell engraft group were thicker than those of the ischemia group, however, and edematous caused maybe by cell suspension solution volume compared to those of normal control group. Stem cells were located mainly in the ganglion cell layer of 7 days PI engraft group, even though there was no co-localization of DiI and neuronal markers. These results suggest that stem cells influence endogenous neuroprotective mechanisms rather than differentiation into any retinal cell population against neuronal degeneration followed by ischemia injury. It has also been suggested that tissue-specific carriers are necessary for successful transplantation of stem cells into degenerated neral retinas.
2
인슐린의존성 당뇨병이 유도된 흰쥐의 신경망막에서 AII 무축삭세포의 연접이전 신경세포의 변화

박효숙(Hyo-Suk Park),박성진(Sung-Jin Park),신지만(Ji-Man Shin),천명훈(Myung-Hoon Chun),오수자(Su-Ja Oh) 대한해부학회 2007 Anatomy & Cell Biology Vol.40 No.3
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칼슘결합단백질인 parvalbumin은 신경망막에서 속핵층의 AII 및 넓은-수용영역 무축삭세포와 신경절세포층의 전위무축삭세포에서 발현되며, 당뇨병 상태에서 parvalbumin 발현은 AII 무축삭세포에서 저하되나, AII 무축삭세포와 전기연접을 형성하고 있는 원뿔이극세포에서 증가됨이 이미 보고되었다. 본 연구는 당뇨병 망막에서 AII 무축삭세포에서 parvalbumin 발현이 저하되는 원인을 규명하고자 AII 무축삭세포의 연접이전 신경세포들의 변화를 면역화학적 방법으로 추적하고자 하였다. 생후 8주 된 Sprague-Dawely계 흰쥐를 실험동물로 하여 streptozotocin의 정맥 내 주사로 당뇨병을 유발시켰으며, 300 mg/dL 이상의 혈당치를 나타낸 동물들을 각각 1, 4, 12 및 24주 경과시켜 사용하였다. 각 시기의 동물로부터 분리된 망막에 parvalbumin, protein kinase C (PKC)-α 및 tyrosine hydroxylase (TH) 항체를 사용한 면역조직화학법과 Western blot법을 시행하였다. 막대이극세포는 PKC-α에 면역 표지된 축삭종말을 주로 속얼기층의 5층으로 뻗고 있었다. 당뇨병 12주 및 24주 때 막대이극세포의 축삭은 짧아져 있었고 축삭종말은 다소 확장된 양상을 나타내었다. 당뇨병 때 PKC-α의 농도 변화는 크게 나타나지 않았다. TH 면역반응 신경세포는 속핵층의 무축삭세포로서 형태학적으로 두 종류로 구분되었다. 즉, 큰세포체와 길게 뻗은 일차 가지돌기를 지닌 세포 유형 (1형)과 작은 세포체와 가지돌기나무 (dendritic arborization)를 지닌 세포 유형(2형)이다. 속얼기층과 속핵층의 경계부위에 TH 면역반응 돌기들의 고리구조가 조밀하게 분포되어 있었다. 당뇨병 망막에서 1형 TH 무축삭세포의 면역반응성이 저하되어 나타났으나, 2형 무축삭세포의 반응성은 크게 변하지 않았다. 면역반응성의 저하와 더불어 TH 단백질의 농도 또한 당뇨병 시기 동안 저하되는 경향을 나타냈다. 이상의 결과로 망막의 TH 면역반응성 무축삭세포가 막대이극세포보다 당뇨병 상해에 대하여 더 민감한 반응을 보이며, 따라서 당뇨병 때 AII 무축삭세포에서의 parvalbumin 발현 저하가 주로 연접이전 도파민성 신경세포의 기능이상에 의한 것임을 유추할 수 있었다. It has been previously reported that parvalbumin expression was downregulated in AII amacrine cells, while upregulated in a subset of cone bipolar cells electrically synapse with AII amacrine cell in the streptozotocin-induced diabetic rat retina. In the present study, we aimed to trace biochemical changes of pre-synaptic neurons to AII amacrine cells in rat retina following diabetic injury. Diabetic condition was induced by streptozotocin injection into Sprague-Dawley rats aged of 8 weeks. The experimental term of induced diabetes was set at 1, 4, 12 and 24 weeks. Changes of pre-synaptic neurons were evaluated by immunohistochemistry and Western blot analysis with anti-protein kinase C (PKC)-α and anti-tyrosine hydroxylase (TH) antibodies. Rod bipolar cells immunolocalized with PKC-α antibody extended their enlarged axon terminals into stratum 5 of the inner plexiform layer. In later diabetes, the axon was shorten and its terminals of rod bipolar cell are slightly enlarged. The protein levels of PKC-α were slightly increased along with the duration of diabetes. TH immunoreactive neurons are morphologically classified into two subtypes of amacrine cells in the inner nuclear layer: one (type 1) has large soma with long and primary dendrites, classified with dopaminergic, and the other (type 2) has small soma with dendritic arborization. In the outermost inner plexiform layer, ring-like structures being composed of type 1 cell processes were densely distributed. In diabetic retina, the intensity of TH immunoreactivity in type 1 neurons was reduced. In accordance with morphological changes, the protein levels of TH were reduced during diabetes. These results demonstrate that TH immunoreactive dopaminergic amacrine cells are more susceptible to diabetic injury than the rod bipolar cells in the rat retina and may suggest that downregulation of parvalbumin expression in AII amacrine cells of diabetic retina is mainly due to dysfunction of pre-synaptic dopaminergic amacrine cells.