Michael R. Blackburn
University of Texas Health Science Center at Houston
211 Papers
2.8K Citations
Michael R. Blackburn is an academic researcher from University of Texas Health Science Center at Houston. The author has contributed to research in topics: Adenosine & Adenosine deaminase. The author has an hindex of 63, co-authored 205 publications. Previous affiliations of Michael R. Blackburn include University of Texas at Austin & Thomas Jefferson University.
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Papers
A1 adenosine receptors mediate hypoglycemia-induced neuronal injury.
TL;DR: Data show that hypoglycemia induces A1ARs activation leading to alterations in [Ca2+]i, which plays a prominent role in leading to hypoglyCEmia-induced neuronal death.
Role of A2B Adenosine Receptors in Regulation of Paracrine Functions of Stem Cell Antigen 1-Positive Cardiac Stromal Cells
Sergey Ryzhov,Anna E. Goldstein,Sergey V. Novitskiy,Michael R. Blackburn,Italo Biaggioni,Igor Feoktistov +5 more
TL;DR: This study tested the hypothesis that stimulation of adenosine receptors on cardiac Sca-1+ cells up-regulates their secretion of proangiogenic factors and found that ScA-1 is expressed in subsets of mouse cardiac stromal CD31− and endothelial CD31+ cells.
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Endogenous osteopontin promotes ozone-induced neutrophil recruitment to the lungs and airway hyperresponsiveness to methacholine
Ramon X. Barreno,Jeremy B. Richards,Daniel J. Schneider,Kevin R. Cromar,Arthur Nádas,Christopher B. Hernandez,Lance M. Hallberg,Roger E. Price,S. Shahrukh Hashmi,Michael R. Blackburn,Ikram U. Haque,Richard A. Johnston,Richard A. Johnston +12 more
TL;DR: It is demonstrated that OPN is increased in the air spaces following acute exposure to O₃ and functionally contributes to the development of O ₃-induced pulmonary inflammation and airway and lung parenchymal hyperresponsiveness to methacholine.
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Sustained adenosine exposure causes lung endothelial apoptosis: a possible contributor to cigarette smoke-induced endothelial apoptosis and lung injury.
Qing Lu,Pavlo Sakhatskyy,Julie Newton,Paul Shamirian,Vivian Hsiao,Sean Curren,Gustavo Andres Gabino Miranda,Mesias Pedroza,Michael R. Blackburn,Sharon Rounds +9 more
TL;DR: It is shown that CS exposure increased lung tissue adenosine levels in mice, an effect associated with increased lung EC apoptosis and the development of emphysema, and inhibition ofadenosine uptake may become a new therapeutic target in treatment of CS-induced lung diseases.
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Genetically engineered mice demonstrate that adenosine deaminase is essential for early postimplantation development
TL;DR: Genetically modified mice are utilized to delineate the relative contribution and importance of decidual and trophoblast ADA at the maternal-fetal interface and provide genetic evidence that Ada expression at the mothers' Fetal interface is essential for early postimplantation development in mice.
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