Research

Tingting Weng, PhD

Assistant Professor
Lab: MSB 6.034
Telephone: 713-500-6024

One of my research projects is the investigation of the role of deoxyadenosine signaling in chronic lung disease and the role of adenosine signaling in acute lung injury. The goal of this 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 also recently started a project to study the role of adenosine signaling in acute lung injury, with the goal to understand the molecular mechanisms of how adenosine can protect vascular leakage through the A2B receptor.

Another project is focusing on the role of Nudt21 in tissue fibrosis. My interest in this project was strengthened by the finding that Nudt21 is a key regulator of alternative polyadenylation in proliferating tissues such as cancer cells. I have expanded these studies to investigate aging and pulmonary fibrosis, as well as skin fibrosis. Through this research, I have uncovered novel roles of Nudt21 with regards to fibrotic gene expression and pathogenesis of lung and skin fibrosis.


Junsuk (Josh) Ko

Graduate Student
Lab: MSB 6.036
Telephone: 713-500-6047

The goal of my research is to understand the role of mRNA modification (alternative polyadenylation) in pulmonary fibrosis. Alternative polyadenylation (APA) is a post-transcriptional regulation that controls the length of 3′ untranslated regions (3’UTRs) of mRNA. Since this process generates mRNAs with different lengths of 3’UTR in mammalian cells, it is known that 3’UTR shortening by APA leads to mRNA stabilization and, thus, enhanced protein translation due to the lack of necessary elements for mRNA degradation, such as miRNA binding sites and AU-rich elements (ARE). Our lab discovered that cleavage factor 25 (CFIm25), which is a key regulator of APA, is associated with pulmonary fibrosis. My research efforts are focused on elucidating the mechanisms of CFIm25 dysregulation, which leads to the exacerbation of pulmonary fibrosis.


Jonathan Davies, MD

Visiting Scientist, Neonatal-Perinatal Medicine Fellow
Lab: MSB 6.036
Telephone: 713-500-6047

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.