As an immunologist, Dr. Qing Lin’s research focuses on the role of damage-associated molecular pattern (DAMP) signaling in vascular inflammation. His studies demonstrated for the first time that toll-like receptor (TLR)-3 activation enhances skin wound repair and the TLR3 activator poly(I:C) has potential therapeutic value for wound healing in humans. In corneal wound healing, his work found that the DAMP molecule high-mobility group box-1 (HMGB1) initiates TLR4-dependent inflammatory responses that induces pathological angiogenesis. Dr. Lin also investigated vascular remodeling in injured lung and found that HMGB1 signaling is critical for the development of pulmonary arterial hypertension. The long-term goal of Dr. Lin’s research is to fully elucidate the role of inflammation in abnormal vascular growth and remodeling.
Lab Summary (Principal Investigator: Qing Lin, M.D., Ph.D.)
Our lab focuses on elucidating the immuno-regulatory mechanisms in: 1) pulmonary arterial hypertension and 2) skin wound healing.
Pulmonary arterial hypertension: We seek to understand how inflammation drives the uncontrolled proliferation of vascular smooth muscle cells and subsequently relentless vascular remodeling in the lung. By investigating the role of damage-associated molecular pattern (DAMP) signaling in regulating the inflammation-to-proliferation function switch of neutrophils and macrophages, we expect to gain key insights into the contributions of these immune cells to pulmonary vascular inflammation and remodeling.
Skin wound healing: Wound therapy remains a clinical challenge. Large burns or impaired-healing diabetic ulcers require enhanced wound repair. Human scarring following trauma or surgery is another major medical problem. Addressing the complex post-injury immune response is critical to defining an effective therapy for both repair and regeneration. We are particularly interested in understanding whether and how vascular inflammation influences the balance between fibrotic and regenerative skin wound healing.
Our overarching goal is to elucidate the wound healing mechanisms in lung and skin, and develop better strategies and novel targets for treatment of vascular inflammation-related diseases including pulmonary arterial hypertension, skin wounds, and systemic sclerosis.
Technology Expertise Keywords
Immunology; Molecular Biology; Cell Signaling
View all on PubMed
Lin Q, Wang L, Lin Y, Liu X, Ren X, Wen S, Du X, Lu T, Su SY, Yang X, Huang W, Zhou S, Wen F, Su SB. Toll-like receptor 3 ligand polyinosinic:polycytidylic acid promotes wound healing in human and murine skin. J Invest Dermatol. 2012;132:2085-2092
Lin Q, Yang XP, Fang D, Ren X, Zhou H, Fang J, Liu X, Zhou S, Wen F, Yao X, Wang JM, Su SB. High-mobility group box-1 mediates toll-like receptor 4-dependent angiogenesis. Arterioscler Thromb Vasc Biol. 2011;31:1024-1032
Lin Q, Wesson RN, Maeda H, Wang Y, Cui Z, Liu JO, Cameron AM, Gao B, Montgomery RA, Williams GM, Sun Z. Pharmacological mobilization of endogenous stem cells significantly promotes skin regeneration after full-thickness excision: the synergistic activity of AMD3100 and tacrolimus. J Invest Dermatol. 2014;134:2458-2468
Lin Q, Fan C, Skinner JT, Hunter EN, Macdonald AA, Illei PB, Yamaji-Kegan K, Johns RA. RELMα licenses macrophages for damage-associated molecular pattern activation to instigate pulmonary vascular remodeling. J Immunol. 2019;203:2862-2871. Featured in the 2020 January issue of "Vascular Biology Publication Alerts".
Lin Q, Fan C, Gomez-Arroyo J, Van Raemdonck K, Meuchel LW, Skinner JT, Allen D. Everett AD, Fang X, Macdonald AA, Yamaji-Kegan K, Johns RA. HIMF (hypoxia-induced mitogenic factor) signaling mediates the HMGB1 (high mobility group box 1)-dependent endothelial and smooth muscle cell cross talk in pulmonary hypertension. Arterioscler Thromb Vasc Biol. 2019;39:2505-2519. Chosen as the "Editor's Pick"
Wound Healing via Autologous Stem Cell Mobilization
Patent # US 20160106710 A1 | 03/16/2021
Application of Toll-like receptor-3 agonist to preparation of medicines for promoting wound healing
Patent # CN101780279 | 07/12/2012
Methods of recruiting SDF-producing macrophages
Patent # US20210251954A1 |