Research Areas
Figure 1. The roles of hyaluronan (HA) during lung injury and fibrosis, shown in four alveoli. 1) Epithelial HA-TLR interaction provides basal NF-κB activation to prevent type II cell apoptosis. 2) During tissue injury, HA accumulates, and low-molecular-mass HA fragments stimulate macrophages to release chemokines, cytokines, and growth factors. 3) CD44 on macrophages can promote the inflammatory resolution and HA clearance. 4) Cytokines and growth factors in turn stimulate fibroblasts to produce collagen, fibronectin and HA, which further worsen fibrosis.
Innate Immunity and Matrix Interactions Regulate Lung Injury and Repair
We are interested in the role of innate immune components (Toll-like receptors) in lung injury, repair and fibrosis. We are using genetically modified mice targeting TLR receptors, TLR signaling molecules, and hyaluronan synthase to investigate the mechanism of TLR components in pulmonary fibrosis.
Molecular Mechanisms of Lung Fibrogenesis
We are interested in the sources of fibrotic fibroblasts, the role of beta-arrestins in fibrogenesis, and the transcriptional control of fibroblast activation.
Role of Chemokines and Chemokine Receptors in Lung Injury and Repair
We are studying the immunoregulatory and molecular roles of CXCL10, CXCR3, CXCL12, and CCL2 in lung injury and repair, using transgenic and knockout mice to define the mechanisms of these chemokines and their receptors in pulmonary fibrosis, especially stem cell recruitment and maintenance, inflammatory cell recruitment and activation, and epithelial cell integrity.
Role of MicroRNA Lung Injury
We are also studying the role of microRNA in lung injury and repair, by examining microRNA expression pattern during tissue injury and generating genetically modified mice targeting specific miRNAs
Figure 3. Genetic cell lineage tracing was used to identify the sources of fibrotic fibroblasts.
Contact the Jiang Lab
127 S. San Vicente Blvd.
Pavilion, A-9404
Los Angeles, CA 90048