Induced pluripotent stem cells as a model for diabetes investigation

Mouse and human induced pluripotent stem cells (iPSCs) may represent a novel approach for modeling diabetes. Taking this into consideration, the aim of this study was to generate and evaluate differentiation potential of iPSCs from lep db/db (db/db) mice, the model of diabetes type 2 as well as from...

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Published in:	Scientific reports Vol. 5; no. 1; p. 8597
Main Authors:	Stepniewski, J., Kachamakova-Trojanowska, N., Ogrocki, D., Szopa, M., Matlok, M., Beilharz, M., Dyduch, G., Malecki, M. T., Jozkowicz, A., Dulak, J.
Format:	Journal Article
Language:	English
Published:	London Nature Publishing Group UK 26-02-2015 Nature Publishing Group
Subjects:	13/1 13/100 13/31 13/44 13/51 14/34 38 38/77 38/88 42 631/532/1360 631/532/2064/2158 Adult Alkaline phosphatase Angiogenesis Animals Biomarkers CD34 antigen Cell Differentiation Cells, Cultured Diabetes Diabetes mellitus Diabetes Mellitus, Type 2 - pathology Embryoid Bodies - metabolism Endothelial Progenitor Cells - metabolism Female Homeodomain Proteins - metabolism Humanities and Social Sciences Humans Induced Pluripotent Stem Cells - metabolism Insulin Lewis X Antigen - metabolism Male Mice, Inbred C57BL Mice, Obese Middle Aged multidisciplinary Nanog Homeobox Protein Nuclear Proteins - metabolism Oct-4 protein Octamer Transcription Factor-3 - metabolism Pluripotency Rodents Science Stem cell transplantation Stem cells
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Abstract	Mouse and human induced pluripotent stem cells (iPSCs) may represent a novel approach for modeling diabetes. Taking this into consideration, the aim of this study was to generate and evaluate differentiation potential of iPSCs from lep db/db (db/db) mice, the model of diabetes type 2 as well as from patients with Maturity Onset Diabetes of the Young 3 (HNF1A MODY). Murine iPSC colonies from both wild type and db/db mice were positive for markers of pluripotency: Oct3/4A, Nanog, SSEA1, CDy1 and alkaline phosphatase and differentiated in vitro and in vivo into cells originating from three germ layers. However, our results suggest impaired differentiation of db/db cells into endothelial progenitor-like cells expressing CD34 and Tie2 markers and their reduced angiogenic potential. Human control and HNF1A MODY reprogrammed cells also expressed pluripotency markers: OCT3/4A, SSEA4, TRA-1–60, TRA-1-81, formed embryoid bodies (EBs) and differentiated into cells of three germ layers. Additionally, insulin expressing cells were obtained from those partially reprogrammed cells with direct as well as EB-mediated differentiation method. Our findings indicate that disease-specific iPSCs may help to better understand the mechanisms responsible for defective insulin production or vascular dysfunction upon differentiation toward cell types affected by diabetes.
AbstractList	Mouse and human induced pluripotent stem cells (iPSCs) may represent a novel approach for modeling diabetes. Taking this into consideration, the aim of this study was to generate and evaluate differentiation potential of iPSCs from lep db/db (db/db) mice, the model of diabetes type 2 as well as from patients with Maturity Onset Diabetes of the Young 3 (HNF1A MODY). Murine iPSC colonies from both wild type and db/db mice were positive for markers of pluripotency: Oct3/4A, Nanog, SSEA1, CDy1 and alkaline phosphatase and differentiated in vitro and in vivo into cells originating from three germ layers. However, our results suggest impaired differentiation of db/db cells into endothelial progenitor-like cells expressing CD34 and Tie2 markers and their reduced angiogenic potential. Human control and HNF1A MODY reprogrammed cells also expressed pluripotency markers: OCT3/4A, SSEA4, TRA-1–60, TRA-1-81, formed embryoid bodies (EBs) and differentiated into cells of three germ layers. Additionally, insulin expressing cells were obtained from those partially reprogrammed cells with direct as well as EB-mediated differentiation method. Our findings indicate that disease-specific iPSCs may help to better understand the mechanisms responsible for defective insulin production or vascular dysfunction upon differentiation toward cell types affected by diabetes. Mouse and human induced pluripotent stem cells (iPSCs) may represent a novel approach for modeling diabetes. Taking this into consideration, the aim of this study was to generate and evaluate differentiation potential of iPSCs from lepdb/db (db/db) mice, the model of diabetes type 2 as well as from patients with Maturity Onset Diabetes of the Young 3 (HNF1A MODY). Murine iPSC colonies from both wild type and db/db mice were positive for markers of pluripotency: Oct3/4A, Nanog, SSEA1, CDy1 and alkaline phosphatase and differentiated in vitro and in vivo into cells originating from three germ layers. However, our results suggest impaired differentiation of db/db cells into endothelial progenitor-like cells expressing CD34 and Tie2 markers and their reduced angiogenic potential. Human control and HNF1A MODY reprogrammed cells also expressed pluripotency markers: OCT3/4A, SSEA4, TRA-1-60, TRA-1-81, formed embryoid bodies (EBs) and differentiated into cells of three germ layers. Additionally, insulin expressing cells were obtained from those partially reprogrammed cells with direct as well as EB-mediated differentiation method. Our findings indicate that disease-specific iPSCs may help to better understand the mechanisms responsible for defective insulin production or vascular dysfunction upon differentiation toward cell types affected by diabetes. Abstract Mouse and human induced pluripotent stem cells (iPSCs) may represent a novel approach for modeling diabetes. Taking this into consideration, the aim of this study was to generate and evaluate differentiation potential of iPSCs from lep db/db (db/db) mice, the model of diabetes type 2 as well as from patients with Maturity Onset Diabetes of the Young 3 (HNF1A MODY). Murine iPSC colonies from both wild type and db/db mice were positive for markers of pluripotency: Oct3/4A, Nanog, SSEA1, CDy1 and alkaline phosphatase and differentiated in vitro and in vivo into cells originating from three germ layers. However, our results suggest impaired differentiation of db/db cells into endothelial progenitor-like cells expressing CD34 and Tie2 markers and their reduced angiogenic potential. Human control and HNF1A MODY reprogrammed cells also expressed pluripotency markers: OCT3/4A, SSEA4, TRA-1–60, TRA-1-81, formed embryoid bodies (EBs) and differentiated into cells of three germ layers. Additionally, insulin expressing cells were obtained from those partially reprogrammed cells with direct as well as EB-mediated differentiation method. Our findings indicate that disease-specific iPSCs may help to better understand the mechanisms responsible for defective insulin production or vascular dysfunction upon differentiation toward cell types affected by diabetes. Mouse and human induced pluripotent stem cells (iPSCs) may represent a novel approach for modeling diabetes. Taking this into consideration, the aim of this study was to generate and evaluate differentiation potential of iPSCs from lep(db/db) (db/db) mice, the model of diabetes type 2 as well as from patients with Maturity Onset Diabetes of the Young 3 (HNF1A MODY). Murine iPSC colonies from both wild type and db/db mice were positive for markers of pluripotency: Oct3/4A, Nanog, SSEA1, CDy1 and alkaline phosphatase and differentiated in vitro and in vivo into cells originating from three germ layers. However, our results suggest impaired differentiation of db/db cells into endothelial progenitor-like cells expressing CD34 and Tie2 markers and their reduced angiogenic potential. Human control and HNF1A MODY reprogrammed cells also expressed pluripotency markers: OCT3/4A, SSEA4, TRA-1-60, TRA-1-81, formed embryoid bodies (EBs) and differentiated into cells of three germ layers. Additionally, insulin expressing cells were obtained from those partially reprogrammed cells with direct as well as EB-mediated differentiation method. Our findings indicate that disease-specific iPSCs may help to better understand the mechanisms responsible for defective insulin production or vascular dysfunction upon differentiation toward cell types affected by diabetes.
ArticleNumber	8597
Author	Dyduch, G. Kachamakova-Trojanowska, N. Malecki, M. T. Szopa, M. Jozkowicz, A. Stepniewski, J. Dulak, J. Beilharz, M. Ogrocki, D. Matlok, M.
Author_xml	– sequence: 1 givenname: J. surname: Stepniewski fullname: Stepniewski, J. organization: Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University – sequence: 2 givenname: N. surname: Kachamakova-Trojanowska fullname: Kachamakova-Trojanowska, N. organization: Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University – sequence: 3 givenname: D. surname: Ogrocki fullname: Ogrocki, D. organization: Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University – sequence: 4 givenname: M. surname: Szopa fullname: Szopa, M. organization: Clinic of Metabolic Diseases, Jagiellonian University Medical College, University Hospital Krakow Poland – sequence: 5 givenname: M. surname: Matlok fullname: Matlok, M. organization: II Clinic of General Surgery, Collegium Medicum, Jagiellonian University – sequence: 6 givenname: M. surname: Beilharz fullname: Beilharz, M. organization: Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University – sequence: 7 givenname: G. surname: Dyduch fullname: Dyduch, G. organization: Department of Clinical and Experimental Pathomorphology, Jagiellonian University Medical College – sequence: 8 givenname: M. T. surname: Malecki fullname: Malecki, M. T. organization: Clinic of Metabolic Diseases, Jagiellonian University Medical College, University Hospital Krakow Poland – sequence: 9 givenname: A. surname: Jozkowicz fullname: Jozkowicz, A. organization: Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University – sequence: 10 givenname: J. surname: Dulak fullname: Dulak, J. organization: Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Malopolska Centre of Biotechnology, Jagiellonian University
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Snippet	Mouse and human induced pluripotent stem cells (iPSCs) may represent a novel approach for modeling diabetes. Taking this into consideration, the aim of this... Abstract Mouse and human induced pluripotent stem cells (iPSCs) may represent a novel approach for modeling diabetes. Taking this into consideration, the aim...
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Title	Induced pluripotent stem cells as a model for diabetes investigation
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