Pulm_Div_Ding

Associate Professor of Medicine and Cell Biology

Division of Pulmonary, Allergy & Critical Care Medicine
1530 3rd Avenue So, THT-422
University of Alabama at Birmingham
Birmingham, AL 35294

Contact Information

Campus Address:

 THT 422

Academic Office location:

 THT 437

Office Phone:

 (205) 996-2512

Office Fax (Academic):

 (205) 934-1721

Email Address:

 qding@uab.edu

Brief Bio

Dr. Qiang Ding is an Associate Professor of Medicine in the Division of Pulmonary, Allergy, and Critical Care Medicine. Dr. Ding recieved his PhD degree in molecular and cellular pathology at the University of Alabama at Birmingham. After completeing his postdoctoral fellowship training in the UAB Department of Pathology, Dr. Ding joined the UAB Division of Pulmonary, Allergy, and Critical Care medicine at the rank of Assistant Professor. Dr. Ding is actively involved in education and service for the medical community. He holds a secondary appointment in the Department of Cell, Developmental, and Integrative Biology (CDIB), is a member of the Intellectual and Developmental Disabilities Research Center (IDDRC), and is a faculty member of the Graduate Biomedical Science PhD program at UAB.

Academic & Research Interests

Dr. Ding's research focuses on cellular and extracellular environment interaction in various diseases and how such interaction affects the molecular mechanisms contributing to tissue injury and disregulated tissue repairing.

Dr. Ding's laboratory is currently investigating the role of fibroblast migration and myofibroblast differentiation in the development of lung fibrosis, and the molecular mechanisms which contribute to fibroblast migration and myfibroblast differentiation.

Focal adhesion kinase (FAK) plays an important role in regulatoin of fibroblast migratoin, differentiation, and proliferation. The Ding Lab has found that focal adhesion kinase (FAK) regulates cell proliferation through regulation of the expression of extracellular matrix proteins and Cyclin D1. The cytoplasmic protein FAK-related non-kinase (FRNK) acts to limit FAK-dependent cell migration and proliferation. Data from this laboratory indicates that FRNK acts to limit myofibroblast differentiation induced by transforming growth factor beta-1 (TGF-beta-1), a core signaling process in the development of lung fibrosis.

The Ding Lab is also interested in exploring the expression of FRNK, its signaling pathways, and how that signaling regulates the pro-fibrotic phenotype and plasticity of the cell types involved. Recently, the lab investigated post-transcriptional regulation and its role in pathogenesis, along with examining the theraputic potentials of small molecular inhibitors of involved signaling pathways in treating pulmonary fibrosis, cancer, and excessive tissue injury.

Key Publications
Ding Q, Grammer JR, Nelson MA, Guan JL, Stewart JE, and Gladson CL. p27(Kip1) and Cyclin D1 Are Necessary for Focal Adhesion Kinase (FAK) Regulation of Cell Cycle Progression in Glioblastoma Cells Propagated In Vitro and In Vivo in the Scid Mouse Brain. J Biol Chem. 2005; Feb 25; 280(8):6802-15


Liu G, Friggeri A, Yang Y, Milosevic J, Ding Q, Thannickal VJ, Kaminski N, Abraham E.  miR-21 mediates fibrogenic activation of pulmonary fibroblasts and lung fibrosis. J Exp Med. 2010 Aug 2;207(8):1589- 97. [Epub 2010 Jul 19]. PMID: 20643828

Ding Q, Luckhardt TR, Hecker L, Zhou Y, Liu G, DeAndrade JA, and Thannickal VJ. New Insights into the Pathogenesis and Treatment of IPF: An Update. Drugs. 2011 May 28;71(8):981-001. PMID: 21668038

Zhan S, Cai GQ, Zheng A, Wang Y, Jia J, Fang H, Yang Y, Hu M, Ding Q. Tumor necrosis factor- alpha regulates the Hypocretin system via mRNA degradation and ubiquitination. Biochim Biophys Acta, Molecular Basis of Disease. 2011 Apr;1812(4):565-71. PMID: 2109425


Huang X, Yang N, Fiore VF, Barker TH, Sun Y, Morris SW, Ding Q, Thannickal VJ, Zhou Y. Matrix stiffness-induced myofibroblast differentiation is mediated by intrinsic mechanotransduction. Am J Respir Cell Mol Biol 2012; S47(3):340-348. PMID:22461426  

Cai GQ, Chou CF, Hu M, Zheng A, Reichardt LF, Guan JL, Fang H, Luckhardt TR, Zhou Y, Thannickal VJ, Ding Q. Neuronal Wiskott-Aldrich Syndrome protein is critical for formation of α-smooth muscle actin filaments during myofibroblast differentiation. Am J. Physiol Lung Cell Mol Physiol 2012; 303(8):L692-702. PMID: 22886502

Gladson CL, Ding Q, Craik CS, Chapman HA, Olman MA. Urokinase-type Plasminogen Activator Receptor (uPAR) Ligation Induces a Raft-localized Integrin Signaling Switch That Mediates the Hypermotile Phenotype of Fibrotic Fibroblasts. J Biol Chem. 2014 May 2;289(18):12791-804. Epub 2014 Mar 18.

Hu M, Che P, Han X, Cai GQ, Liu G, Antony V, Luckhardt T, Siegal GP, Zhou Y, Liu RM, Desai LP, O'Reilly PJ, Thannickal VJ, Ding Q. Therapeutic targeting of Src kinase in myofibroblast differentiation and pulmonary fibrosis. J Pharmacol Exp Ther. 2014;
Oct;351(1):87-95. PMID: 25047515

Ding Q, Antony V, Thannickal VJ, Liu RM. >Ding Q. S100A4 promotes cancer progression through a dual signaling pathway mediated by Src and focal adhesion kinase. Sci Rep. 2015 Feb 3;5:8453. PMID: 25677816

Please click here for Dr. Ding's complete publications listing.

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