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Genetic and pharmacological correction of aberrant dopamine synthesis using patient iPSCs with BH4 metabolism disorders / BH4代謝病患者iPS細胞を用いた異常なドパミン合成の遺伝学的および薬理学的修復Ishikawa, Taizo 23 May 2017 (has links)
京都大学 / 0048 / 新制・論文博士 / 博士(医学) / 乙第13111号 / 論医博第2129号 / 新制||医||1022(附属図書館) / (主査)教授 齊藤 博英, 教授 松原 和夫, 教授 林 康紀 / 学位規則第4条第2項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Efficient and robust differentiation of endothelial cells from human induced pluripotent stem cells via lineage control with VEGF and cyclic AMP / VEGF及びcyclic AMP 投与による分化制御を利用したヒトiPS細胞からの高効率かつ高収量な血管内皮細胞分化誘導法の開発Ikuno, Takeshi 25 September 2017 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第20663号 / 医博第4273号 / 新制||医||1024(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 藤渕 航, 教授 木村 剛, 教授 岩田 想 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Significance of dopamine D1 receptor signalling for steroidogenic differentiation of human induced pluripotent stem cells / ヒトiPS細胞からステロイド産生細胞への分化におけるドーパミンD1受容体シグナルの重要性Matsuo, Koji 26 March 2018 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第21006号 / 医博第4352号 / 新制||医||1028(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 高橋 淳, 教授 濵﨑 洋子, 教授 渡邊 直樹 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Human AK2 links intracellular bioenergetic redistribution to the fate of hematopoietic progenitors / ヒトアデニル酸キナーゼ2は細胞内エネルギー分子の分配を介して血液前駆細胞の分化運命を制御するSaiki, Norikazu 23 May 2018 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(医科学) / 甲第21265号 / 医科博第92号 / 新制||医科||7(附属図書館) / 京都大学大学院医学研究科医科学専攻 / (主査)教授 斎藤 通紀, 教授 松田 道行, 教授 江藤 浩之 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Critical Functionality Effects from Storage Temperature on Human Induced Pluripotent Stem Cell-Derived Retinal Pigment Epithelium Cell Suspensions / ヒトiPS細胞由来網膜色素上皮細胞懸濁液の非凍結条件下における保存温度の影響Kitahata, Shohei 25 March 2019 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第21685号 / 医博第4491号 / 京都大学大学院医学研究科医学専攻 / (主査)教授 辻川 明孝, 教授 高橋 淳, 教授 井上 治久 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Modeling of sickle cell anemia utilizing disease-specific induced pluripotent stem cellsRozelle, Sarah Sundstrom 22 January 2016 (has links)
Sickle cell anemia, caused by a point mutation that affects the HBB gene, is one of the most common human genetic disorders world-wide and has a high morbidity and mortality. A single FDA approved drug, hydroxyurea, is available for its ability to induce fetal hemoglobin expression, a major modulator of disease severity. Not every patient responds to treatment and additional HbF-inducing drugs are needed. In this thesis, I outline an induced pluripotent stem cell-based approach to the study of sickle cell disease (SCD). In the lab, we are currently building a library of SCD-induced pluripotent stem cell (iPSC) lines from a cohort of SCD patients with different genetic backgrounds and fetal hemoglobin levels. Utilizing a directed-differentiation approach, iPSC can give rise to hematopoietic progenitors that are similar to megakaryocyte-erythroid progenitors and can be further specified to become cells of either lineage. I examined the hypothesis that an iPSC-based system would be capable of producing fully functional erythroid cells and also recapitulate the variation in fetal hemoglobin levels seen in SCD patients. Directed-differentiation of iPSCs produced erythroid-lineage cells that were responsive to oxygen levels and erythropoietin, and were capable of further maturation and increased hemoglobin production. A humanized mouse model demonstrated the ability of these cells to localize to the bone marrow, contribute to the peripheral blood, and survive in vivo for over two weeks. The maturation capability of SCD-specific iPSC-derived erythroid lineage cells was correlated with hemoglobin expression and compared to control cells. Characterization of in vitro and in vivo differences between control and SCD-specific iPSC-derived erythroid-lineage cells demonstrated variation amongst individuals, similar to the variation seen in patients. Both of these patient-specific iPSC-based in vitro and in vivo models allow for the examination of the effect of genetic variability on fetal hemoglobin expression and also for the modeling of patient-specific responses to drug treatment. This information will facilitate better clinical treatment of the disease.
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Modeling Defective Epigenetic Inheritance in Vascular Aging Using Hutchinson-Gilford Progeria Syndrome Vascular Smooth Muscle CellsChen, Zhaoyi 24 September 2020 (has links)
Cardiovascular disease (CVD) is the leading cause of death due to its prevalence in tandem with the propensity of atherosclerosis to worsen and cause myocardial infarction and stroke. The greatest risk factor for CVD development is age. The multifactorial etiology of atherosclerosis has made CVD difficult to model and consequently little is known about CVD onset and progression. Hutchinson-Gilford Progeria Syndrome (HGPS) is a severe human premature aging disorder caused by a mutation in Lamin A that leads to the accumulation of an aberrant Lamin A protein termed progerin. Patients who harbour this mutation develop atherosclerosis and die from myocardial infarction or stroke at an average age of 13 years old. Autopsies reveal deterioration of vascular smooth muscle cells (VSMCs) in HGPS patients, underlining a strong connection between VSMC loss and predisposition to CVD development. The major aim of this thesis was to model normative vascular aging and disease using HGPS induced pluripotent stem cell (iPSC)-derived VSMCs and monitor the onset of defective epigenetic inheritance in vitro. My results indicate reprogramming of patient fibroblasts to restores a normal nuclear phenotype. Patient derived iPSC lines generated from fibroblasts are nearly indistinguishable from healthy controls in terms of pluripotency, nuclear membrane integrity, as well as transcriptional and epigenetic profiles. However, differentiation of HGPS iPSCs to generate HGPS VSMCs recapitulates many aspects of normative vascular aging exemplified by increased ROS, DNA damage and transcriptomic aberrations. Furthermore, using a multi-omic approach including RNA-sequencing, and accelerated native isolation of protein on nascent DNA, HGPS VSMCs demonstrate loss of histone acetylation due to defective MOF abundance that contributed to impaired engagement with DNA damage repair pathway. This dissertation provides insights on the mechanisms that drive the epigenetic and transcriptomic changes in HGPS vasculature, illuminating druggable pathways that may also drive CVD in the general population.
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Cellular reprogramming of human acute myeloid leukemia patient somatic cellsSalci, Kyle 15 December 2015 (has links)
Acute myeloid leukemia (AML) is a fatal cancer of the human hematopoietic system characterized by the rapid accumulation of non-functional, immature hematopoietic cells in the bone marrow (BM) and peripheral blood (PB) of affected patients. Limited sources of safe hematopoietic stem/progenitor cells (HSPCs) for transplantation and incomplete mechanistic understandings of disease initiation, progression and maintenance have impeded advances in therapy required for improvement of long-term AML patient survival rates. Toward addressing these unmet clinical needs, the ability to generate induced pluripotent stem cells (iPSCs) from human somatic cells may provide platforms from which to develop patient-specific (autologous) cell-based therapies and disease models. However, the ability to generate iPSCs from human AML patient somatic cells had not been investigated prior to this dissertation. Accordingly, I hypothesized that cellular reprogramming of human AML patient somatic cells to iPSCs is possible and will enable derivation of autologous sources of normal and dysfunctional hematopoietic progenitor cells (HPCs).
I first postulated that reprogramming AML patient fibroblasts (AML Fibs) to pluripotency would provide a novel source of normal autologous HPCs. Our findings revealed that AML patient-specific iPSCs devoid of leukemia-associated aberrations found in the matched bone marrow (BM) could be generated from AML Fibs, and demonstrated that this cellular platform allowed for the derivation of healthy HPCs capable of normal differentiation to mature myeloid lineages in vitro. During the tenure of these experiments we also redefined conventional reprogramming methods by discovering that OCT4 transcription factor delivery combined with culture in pluripotent-supportive media was minimally sufficient to induce pluripotency in AML and normal Fibs.
Toward capturing and modeling the molecular heterogeneity observed across human AML samples in vitro, we next asked whether reprogramming of AML patient leukemic cells would enable generation of iPSCs and derivative HPCs that recapitulated dysfunctional differentiation features of primary disease. Our results demonstrated that conventional reprogramming conditions were insufficient to induce pluripotency in leukemic cells, but that generation of AML iPSCs could be reproducibly achieved in one AML sample when reprogramming conditions were modified. These AML iPSCs and their derivative HPCs harboured and expressed the leukemia-associated aberration found in the BM leukemic cells and similarly possessed dysfunctional differentiation capacities.
Together, this body of works provides the proof of principle that cellular reprogramming can be applied on a personalized basis to generate normal and dysfunctional HPCs from AML patient somatic cells. These foundational findings should motivate additional studies aimed at developing iPSC-based cell therapies and disease models toward improving AML patient quality of life and long-term survival rates. / Thesis / Doctor of Philosophy (PhD)
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iPS cells from Chediak-Higashi syndrome patients recapitulate the giant granules in myeloid cells / 患者由来iPS細胞を用いたチェディアック・東症候群のミエロイド細胞における病態再現Oh, Shigeharu 25 September 2023 (has links)
京都大学 / 新制・論文博士 / 博士(医学) / 乙第13569号 / 論医博第2295号 / 新制||医||1068(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 濵﨑 洋子, 教授 生田 宏一, 教授 滝田 順子 / 学位規則第4条第2項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Novel calmodulin variant p.E46K associated with severe CPVT produces robust arrhythmogenicity in human iPSC-derived cardiomyocytes / 重症CPVTを引き起こす新規カルモジュリン変異p.E46Kは、ヒトiPS細胞由来心筋細胞において重度な催不整脈性を示すGao, Jingshan 25 September 2023 (has links)
京都大学 / 新制・課程博士 / 博士(医学) / 甲第24878号 / 医博第5012号 / 新制||医||1068(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 萩原 正敏, 教授 湊谷 謙司, 教授 江藤 浩之 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
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