Michael Blackburn, PhD
Dean Emeritus / Professor (Ret.)
The University of Texas Health Science Center at Houston
McGovern Medical School
Department of Biochemistry and Molecular Biology
Chronic lung diseases are the third leading cause of death in the United States and there are currently no effective therapies for these disorders. Examples of chronic lung disease include chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, asthma and pulmonary hypertension. My laboratory focuses on uncovering novel signaling pathways that control the excessive remodeling that is seen in these diseases with the goal of developing novel treatment options. Graduate students in my laboratory will use tissues and cells from patients with chronic lung disease as well as sophisticated genetically modified mice to conduct basic and translational research on in this area.
Publications
- Enhancing Extracellular Adenosine Levels Restores Barrier Function in Acute Lung Injury Through Expression of Focal Adhesion Proteins
- MicroRNA-98 reduces nerve growth factor expression in nicotine-induced airway remodeling
- Downregulation of CFIm25 amplifies dermal fibrosis through alternative polyadenylation
- Transforming growth factor β1 alters the 3'-UTR of mRNA to promote lung fibrosis
- Comprehensive characterization of circular RNAs in ~ 1000 human cancer cell lines
- Interferon regulatory factor 7 (IRF7) represents a link between inflammation and fibrosis in the pathogenesis of systemic sclerosis
- Adenosine and hyaluronan promote lung fibrosis and pulmonary hypertension in combined pulmonary fibrosis and emphysema
- Correction: MicroRNA-101 attenuates pulmonary fibrosis by inhibiting fibroblast proliferation and activation
- Cleavage factor 25 deregulation contributes to pulmonary fibrosis through alternative polyadenylation
- Coordination of ENT2-dependent adenosine transport and signaling dampens mucosal inflammation
- Elevated ecto-5'-nucleotidase: a missing pathogenic factor and new therapeutic target for sickle cell disease
- Short-Term Hypoxia Dampens Inflammation in vivo via Enhanced Adenosine Release and Adenosine 2B Receptor Stimulation
- Suppression of cleavage factor Im 25 promotes the proliferation of lung cancer cells through alternative polyadenylation
- Switching-Off Adora2b in Vascular Smooth Muscle Cells Halts the Development of Pulmonary Hypertension
- The Antifibrotic Effect of A2B Adenosine Receptor Antagonism in a Mouse Model of Dermal Fibrosis
Education & Training
PhD, Thomas Jefferson University, 1993
Research Info
Adenosine signaling and the regulation of COPD and Pulmonary Fibrosis