Harry Karmouty-Quintana, PhD
Lab: MSB 6.034/6.310
Research: Mechanisms of Pulmonary Hypertension associated with Chronic Lung Diseases. Chronic lung diseases such as Chronic Obstructive Pulmonary Disease (COPD) and Idiopathic Pulmonary Fibrosis (IPF) are currently the 3rd largest killers in the US. An important and deadly complication of COPD and IPF is the development of Pulmonary Hypertension (PH). PH is a deadly disorder that is characterized by remodeling of the vasculature, increased blood pressure in the pulmonary circulation (>25mmHg) that results in right-sided heart attack and death. Currently, there are no treatments available for this disorder, in part due to our lack of understanding of the pathogenesis of PH in patients with chronic lung disease. Our research has identified the adenosine A2B receptor, a receptor that is elevated following conditions of cell injury and stress, and hyaluronan, a component of the lung extracellular matrix, as potential targets for the treatment of PH in chronic lung disease. Our research efforts are focused on uncovering the mechanisms of adenosine signaling and hyaluronan that lead to PH in chronic lung disease.
Fun Facts: Fun Facts: I previously trained in Montreal, Quebec at McGill University from 2006 to 2010 where I completed my first postdoc on airway smooth muscle remodeling in asthma. Prior to that I lived in Basel, Switzerland, where I pursued my PhD on “Experimental Pulmonary Diseases assessed by Magnetic Resonance Imaging”, a joint venture with Novartis and King’s College London (UK) where I graduated in 2006. Having spent a lot of time in cold countries, I was happy to move to Houston in May 2010 where I started as a postdoc and was promoted to Research Assistant Professor in September 2012. Other than lung diseases, I am interested in ocean life; I have a saltwater aquarium at home and I am a certified scuba diver! Originally from Barcelona, I may be hard to find if FC Barcelona is playing a champions league game or against Real Madrid!
Fayong Luo, MD, PhD
Lab: MSB 6.034
Research: Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease responsible for up to 30,000 deaths per year in the U.S. Despite decades of research, the pathogenesis of IPF is still not fully understood and there is no FDA approved treatment available. My research focuses on investigating the potential role of adenosine signaling pathways in IPF and other lung diseases with chronic injuries. By intratracheal or intraperitoneal injection of bleomycin, mouse lung fibrosis models are established. Mouse and rat lung epithelial cells are also used for in vitro study of adenosine signaling pathways. Extracellular adenosine levels are critical in acute or chronic lung injuries and are controlled by equilibrative nucleoside transporter (ENT) proteins. ENT protein expression can be further regulated in direct or indirect ways by hypoxia inducible factor-1α (hif-1 α) and transforming growth factor β (TGF-β), which are important molecules that play crucial rules in lung fibrosis. By investigating the potential networks among TGF-β, ENTs and adenosine, we will be able to better understand the pathogenesis of lung fibrosis, and therefore, generate novel drugs or therapeutic strategies for IPF.
Fun facts: I received my MD degree in China in 2008 with a focus on oncology. That same year I came to Tulane University School of Medicine to pursue my PhD degree in pulmonary diseases. Five years of living in New Orleans transformed me into a huge fan of Cajun food, jazz, and the Saints football team. Meanwhile, I am glad the Saints will only play against the Texans every four years in regular season so I do not have to make a difficult choice very often. In my leisure time I love taking road trips. When I obtain my first NIH RO1, I would like to drive from the east coast across the west coast for celebration.
Tingting Weng, PhD
Lab: MSB 6.034
Research: Investigating the role of deoxyadenosine signaling in chronic lung disease and the role of adenosine signaling in acute lung injury. The goal of my research is to understand the mechanisms of hypoxia-induced deoxycytidine kinase (DCK) expression in chronic lung diseases; the role of DCK in these diseases is examined by using the DCK inhibitor 2′-deoxycytidine. Hypoxia and the DCK pathway are characterized utilizing lung samples from IPF and COPD patients. I have recently started a project to study the role of adenosine signaling in acute lung injury; my goal is to understand the molecular mechanisms of how adenosine can protect vascular leakage through the A2B receptor.
Fun Facts: I joined the Blackburn lab in the spring of 2010 and was awarded an AHA Postdoctoral Fellowship in 2012. In my free time I enjoy sketching and drawing – skills that I believe will “significantly” impact the success of my research projects!
Jonathan Davies, MD
Visiting Scientist, Neonatal-Perinatal Medicine Fellow
Lab: MSB 6.036
Research: Adenosine Signaling in Hyperoxic Lung Injury and Bronchopulmonary Dysplasia. Bronchopulmonary dysplasia (BPD) remains a significant morbidity among premature neonates. Treatments for these patients, including supplemental oxygen, cause lung injury and inflammation that lead to BPD. Few interventions are available to prevent or treat chronic lung disease in at-risk neonates. The nucleoside adenosine has been shown to play a key role in pulmonary inflammation in adult chronic lung diseases, including idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease and asthma. Altering the adenosine signaling pathway in animal models of adult chronic lung disease has been shown to curtail the fibrosis and disrupted alveolar remodeling that are involved in these disease processes. Knowledge of this pathway has led to the identification of targets for the development of novel pharmacologic therapies. The role of the adenosine signaling pathway in BPD has not been evaluated, but there is evidence that suggests adenosine plays a key role in BPD, including the protective effect of caffeine, an adenosine receptor antagonist. My project involves testing the hypothesis that the adenosine pathway plays a critical role in the development of BPD and altering the adenosine pathway can protect against the development of BPD.
Fun Facts: I am currently a 3rd year neonatology fellow at Baylor College of Medicine. I joined the Blackburn lab in Fall 2012. I was born and raised in Houston, completed my medical degree at the University of Texas Southwestern Medical School, and pediatric residency at Children’s National Medical Center in Washington, DC before returning to Houston for a fellowship in neonatal-perinatal medicine. I have received the Whitlock Award and AAP Marshall Klaus Award for neonatal-perinatal research. I am married and have two children named Charlie and Matthew. They both love playing soccer, making a mess of the house, and visiting me at lab where they get to act like real scientists.
Kemly Philip, MBioE
Graduate Research Assistant
Lab: MSB 6.036
Research: Investigating the role of alternatively activated macrophages in the hypoxic adenosine response. Idiopathic pulmonary fibrosis (IPF) is one of the most common interstitial lung diseases affecting up to 200,000 people in the United States alone. As the cause of almost 40,000 deaths yearly, IPF presents an immense disease burden due to the lack of effective treatment options. Our lab has shown that extracellular adenosine accumulation leads to chronic lung disease as evidenced by immunocyte infiltration, airspace destruction, pro-fibrotic interleukin-6 increase, and pulmonary fibrosis. These effects are mediated via the Adora2b receptor, which also promotes differentiation of macrophages and may ultimately mediate the transition from the beneficial effects of adenosine to chronic pro-inflammatory effects in the setting of hypoxia. Thus, I plan to utilize in vitro and in vivo mouse models to focus on understanding this interaction between adenosine signaling, hypoxia, macrophage polarization, and pulmonary fibrosis.
Fun Facts: I was born and raised in Houston, TX within minutes of the Medical Center. I studied at Bellaire High School (05′) and went on to graduate from Rice University with my Bachelors (09′) and Masters (10′) in Bioengineering. I joined the MD/PhD program at UT Houston in June 2010, completed the first three years of medical school, and have recently joined Dr. Blackburn’s lab for my graduate work. In my spare time, I love to read mystery novels, watch movies, and spend time with my family, friends, and my two dogs – Bella and Juliet. I also enjoy community service and the arts. I currently serve as a student leader for the Frontera de Salud chapter at UT Houston Medical School, an executive committee member for the Houston Global Health Collaborative, and a mentor for the Big Owls/Little Owls Program with Rice University. I have continued my passion for the arts through involvement in UTH Acapella and various Indian Classical/Bollywood dance companies across Houston including Rangeela and the Anjali Center for Performing Arts.