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Studies on Mature Endothelial Cells and CD34+ Stem Cells

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Studies on Mature Endothelial Cells and CD34+ Stem Cells Exploring Mechanisms for Improvement of Cardiovascular Disease; Studies on Mature + Endothelial Cells and CD34 Stem Cells Sherin M. Bakhashab Institute of Cellular Medicine Faculty of Medical Sciences University of Newcastle A thesis submitted in fulfilment of the requirements for the degree of Doctor of Philosophy May 2015 Abstract ABSTRACT Cardiovascular disease (CVD) is the major cause of morbidity and mortality worldwide and in particular in diabetes mellitus (DM). Although metformin has been shown to reduce CVD in Type-2 DM clinical trials, the underlying cardioprotective mechanism remains unexplored. Objective: to determine the effect of metformin on mature endothelial and stem cells exposed to hypoxia, hyperglycaemia or both conditions combined. Human umbilical vein endothelial cells (HUVEC) were studied by scratch test for migration and flow cytometry for apoptosis after culture in euglycaemia or hyperglycaemia, and/or hypoxia with or without metformin. mRNA was assayed by whole transcript microarrays. Genes of interest were confirmed by quantitative real-time PCR (qRT-PCR), proteins by western blot assay or flow cytometry. Metformin increased cell survival and migration via activation of vascular endothelial growth factor (VEGF) signalling, through upregulation of matrix metalloproteinase 16, and ERK/mitogen-activated protein kinase signalling under hyperglycaemia-hypoxia. Paracrine secretion of CD34+ cells treated with euglycaemia or hyperglycaemia, and/or hypoxia with or without metformin was assessed by measuring pro-inflammatory cytokines, VEGFA, chemokine (C-X-C Motif) ligand 10 (CXCL10), tissue inhibitor of metalloproteinase 1 (TIMP1) and efficacy to promote in vitro tube formation by HUVECs. Additionally, miR-126 was evaluated in exosomes and exosome-depleted medium, which was found to be increased by metformin. mRNA from treated CD34+ cells was assayed by microarray and genes of interest were validated by qRT-PCR. An anti-inflammatory effect of metformin was detected under euglycaemia and euglycaemia-hypoxia through upregulation of STEAP family member 4. Metformin enhanced angiogenesis via increased VEGFA and miR-126 under hyperglycaemia-hypoxia. Metformin downregulated the expression of angiogenic inhibitors CXCL10 and TIMP1, which were upregulated under hyperglycaemia-hypoxia. ii Abstract In conclusion, our data from HUVEC and CD34+ cells are commensurate with a vascular protective effect of metformin in a model of a diabetic state combined with hypoxia, and add to understanding of the underlying mechanism. iii Dedication Dedication I dedicated this thesis to my parents, For my mother and the pride that I know she would have felt if she was with us today For my father enduring love and generous support Declaration DECLARATION The work described in this thesis was undertaken in the laboratory of Visiting Professor Jolanta Weaver at the Institute of Cellular Medicine (Newcastle University) in fulfilment of the degree of Doctor of Philosophy. This thesis is the result of my work, and I have acknowledged the contributions of others. No portion of the work referred to in the thesis has been submitted in support of an application for another degree or qualification of this or any other university or other institution of learning. Sherin Bakhashab 2015 Acknowledgments ACKNOWLEDGEMENTS I would like to extend my sincere gratitude to my supervisor Prof. Jolanta Weaver for giving me the opportunity to perform this research in her laboratory and for passing on her knowledge and guidance to me. Additionally, I am thankful for Prof. Weaver continuous help and support in this project. I would like to express a special thanks to Dr. Michael Glanville for his great help and advice in molecular techniques. I am particularly grateful to Mrs. Elizabeth Anne Douglas for her help in ordering reagents required for my work. I would like to acknowledge the excellent teamwork by Dr. Fahad Ahmed, Ayat Bashir and other members of our group in Haematological Sciences Laboratory. As a Joint Supervision Program Ph.D. student at Newcastle University and King Abdulaziz University (KAU), Saudi Arabia, I would like to thank all the people in KAU who supported me with their time and help. I would like especially to thank Prof. Ammar Amin, Supervisor General of the Joint Supervision Program, my KAU supervisors Prof. Abdulrahman Al-Malki, and Dr. Sahira Lary. I was lucky to be associated with the Centre of Excellence in Genomic Medicine Research (CEGMR), Jeddah, Saudi Arabia, where I was able to perform part of my research. I would therefore like to express my gratitude to Prof. Mohammed Al-Qahtani, the director of CEGMR and Prof. Mamdooh Qari for allowing access to the CEGMR labs and facilities. I am thankful to Dr. Farid Ahmed, for his help in tissue culture and flow cytometry techniques and his guidance in preparing this thesis. I would also like to thank Dr. Hans- Juergen Schulten for his excellent support in microarray technology. I thank Prof. David Jones and Dr. Gabriele Saretzki for their input and guidance during the internal assessment stages of my Ph.D. I would like to express my appreciation to Prof. Dianne Ford and Prof. Stefan Przyborski for volunteering to be my examiners. Financial support for this work has been generously provided by Joint Supervision Program, KAU, Jeddah, Saudi Arabia and King Abdulaziz City for Science and Technology (KACST), Saudi Arabia. vi Acknowledgments Finally, I am forever grateful for the open-handed support of my husband, Ali Binladen, and close family members who have shared the excitements and struggles of my Ph.D. years. vii Table of Contents Table of Contents Chapter 1. Introduction .................................................................................................. 1 1.1 Diabetes mellitus and cardiovascular disease ....................................................... 2 1.1.1 Definition and classification of diabetes mellitus .......................................... 2 1.1.2 Complications of diabetes ............................................................................. 3 1.2 Vasculogenesis and angiogenesis ......................................................................... 3 1.2.1 Origin of vascular endothelium ..................................................................... 3 1.2.2 Endothelial cell differentiation and vascular development ............................. 5 1.2.3 Molecular mechanisms involved in angiogenesis .......................................... 7 1.3 Endothelial dysfunction in diabetes .................................................................... 12 1.4 Molecular mechanisms of ischaemic cardiovascular disease .............................. 14 1.4.1 Hypoxia ...................................................................................................... 14 1.4.2 Structure and function of HIF-1 .................................................................. 14 1.5 Role of microRNAs in vascular biology ............................................................. 19 1.5.1 MicroRNA biogenesis and mechanism of action ......................................... 19 1.5.2 Identification and quantification of miRNAs ............................................... 22 1.5.3 Role of miRNAs in angiogenesis ................................................................ 22 1.6 Human stem cells ............................................................................................... 24 1.6.1 Stem cell classification based on origin ....................................................... 25 1.6.2 The stem cell niche ..................................................................................... 25 1.7 CD34+ stem cells ............................................................................................... 28 1.7.1 CD34+ cells as a therapeutic agent .............................................................. 28 1.7.2 Paracrine function of human CD34+ stem cells ........................................... 29 1.8 Metformin ......................................................................................................... 31 viii Table of Contents 1.8.1 History of metformin .................................................................................. 31 1.8.2 Mechanism of action of metformin as anti-diabetic drug ............................. 32 1.8.3 Action of metformin on cardiovascular disease ........................................... 35 1.9 Aims of the thesis .............................................................................................. 36 Chapter 2. Material and Methods ................................................................................. 38 2.1 Cell culture techniques ....................................................................................... 38 2.1.1 Tissue supply .............................................................................................. 38 2.1.2 Isolation of HUVEC from umbilical cord.................................................... 38 2.1.3 Incubation of HUVEC with various concentrations of glucose and hypoxia 40 2.1.4 Metformin treatment ................................................................................... 41 2.1.5 Isolation of mononuclear cells from umbilical cord blood ........................... 42 2.1.6 Isolation of CD34+ stem cells ...................................................................... 42 2.1.7 CD34+ cell culture .....................................................................................
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