M
M. Reza Saadatzadeh
Researcher at Indiana University
Publications - 40
Citations - 1462
M. Reza Saadatzadeh is an academic researcher from Indiana University. The author has contributed to research in topics: Medicine & Cancer research. The author has an hindex of 14, co-authored 27 publications receiving 1326 citations. Previous affiliations of M. Reza Saadatzadeh include University of Tokyo & Indiana University – Purdue University Indianapolis.
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Journal ArticleDOI
Human CD34+AC133+VEGFR-2+ cells are not endothelial progenitor cells but distinct, primitive hematopoietic progenitors
Jamie Case,Laura E. Mead,Waylan K. Bessler,Daniel N. Prater,Hilary White,M. Reza Saadatzadeh,Janak R. Bhavsar,Mervin C. Yoder,Laura S. Haneline,David A. Ingram +9 more
TL;DR: It is found that CD34+AC133+VEGFR-2+ cells are HPCs that do not yield EC progeny, and the biological mechanism for their correlation with cardiovascular disease needs to be reexamined.
Journal ArticleDOI
Robust Functional Vascular Network Formation In Vivo by Cooperation of Adipose Progenitor and Endothelial Cells
Dmitry O. Traktuev,Daniel N. Prater,Stephanie Merfeld-Clauss,Aravind Sanjeevaiah,M. Reza Saadatzadeh,Michael P. Murphy,Brian Johnstone,David A. Ingram,Keith L. March +8 more
TL;DR: This study is the first to demonstrate prompt and consistent assembly of a vascular network by human ASCs and endothelial cells and vascularization by these cells of parenchymal cells in implants.
Journal ArticleDOI
Clonogenic endothelial progenitor cells are sensitive to oxidative stress.
David A. Ingram,Theresa R. Krier,Laura E. Mead,Colleen McGuire,Daniel N. Prater,Janak R. Bhavsar,M. Reza Saadatzadeh,Khadijeh Bijangi-Vishehsaraei,Fang Li,Mervin C. Yoder,Laura S. Haneline +10 more
TL;DR: A framework for understanding how oxidative injury leads to vascular disease and potentially limits the efficacy of transplantation of EPCs into ischemic tissues enriched for reactive oxygen species and oxidized metabolites is outlined.
Journal ArticleDOI
Oxidant hypersensitivity of Fanconi anemia type C-deficient cells is dependent on a redox-regulated apoptotic pathway.
M. Reza Saadatzadeh,Khadijeh Bijangi-Vishehsaraei,Ping Hong,Heidi Bergmann,Laura S. Haneline +4 more
TL;DR: The data argue that the predisposition of Fancc -/- hematopoietic stem/progenitor cells to apoptosis is mediated in part through altered redox regulation and ASK1 hyperactivation.
Journal ArticleDOI
Enhanced TNF-α–induced apoptosis in Fanconi anemia type C–deficient cells is dependent on apoptosis signal-regulating kinase 1
Khadijeh Bijangi-Vishehsaraei,Khadijeh Bijangi-Vishehsaraei,M. Reza Saadatzadeh,M. Reza Saadatzadeh,Adam Werne,Adam Werne,Kristina A. Wilson McKenzie,Kristina A. Wilson McKenzie,Reuben Kapur,Reuben Kapur,Hidenori Ichijo,Hidenori Ichijo,Laura S. Haneline,Laura S. Haneline +13 more
TL;DR: Data indicate that the predisposition of Fancc-/- hematopoietic progenitors to apoptosis is mediated in part through altered redox regulation and Ask1 hyperactivation, and targeting the Ask1 pathway by using either antioxidants or a p38 inhibitor protected Fancc's MEFs and c-kit+ cells from TNF-alpha-induced apoptosis.