Qing Lin
Ohio State University, OH·Microbiology & Immunology
Skin scars that form after an injury or surgery can disfigure people, cause pain and limit movement, and there are still no effective treatments to prevent them. Healing usually lays down fibrous scar tissue instead of rebuilding the original skin.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Physiology
- Topics
mast cells
Mrgprb2
G-protein-coupled receptor
- Grants
- 1 known grant, through Jan 2030
What they work on
- Test whether turning Mrgprb2 signaling, a mast-cell surface receptor pathway, up or down changes skin scarring and regeneration, using gene-modified mouse lines in wound healing models.
- Dissect how Mrgprb2 signaling promotes inflammation and fibrosis (scar-tissue buildup) during healing in mouse skin wounds.
- Test whether mast cells activated through Mrgprb2 or its human version MRGPRX2 change how immune cells behave and drive fibroblast growth and migration, using mouse and human wound-related cells in culture.
- Determine whether MRGPRX2-activated mast cells trigger endothelial-to-mesenchymal transition, in which blood-vessel lining cells become scar-forming cells, in human cell co-culture studies.
- Measure MRGPRX2 signaling in human scar tissue from dermatology and plastic surgery clinics, and in human skin wound models kept alive outside the body during early healing.
More about the research
A central question is whether the immune response right after injury can be steered toward true regeneration. This project focuses on mast cells, immune cells in the skin that are among the first to respond to damage, and on a receptor they carry that may help decide whether a wound scars.
Why it matters
People left with scars after trauma or surgery often face disfigurement, pain, loss of function or restricted movement. By identifying a mast-cell receptor that may drive scarring, this work could point to MRGPRX2 as a drug target for therapies that reduce scarring and improve healing. It could also inform treatments for other fibrotic skin diseases.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Risheng Xu
Johns Hopkins University, MD·Neuroscience·Early-career
Identify which mast-cell inflammatory signals, such as TNFα and CCL2, are controlled by the receptor Mrgprb2 after ischemic stroke induced by transient middle cerebral artery occlusion in mice.
Soban Umar
University of California-Los Angeles, CA·Medicine & Clinical Research
Determine how the Snai1–LOXL2–CTGF axis drives endothelial-to-mesenchymal transition, where vessel-lining cells become scar-forming cells, in right ventricles of PH rats and in human coronary artery endothelial cells.
Ryan Driskell
Washington State University, WA·Biology
Test whether Lef1, a Wnt-pathway transcription factor, is the master regulator of newborn papillary fibroblast function by switching it on in adult mouse skin fibroblasts and using wounding and chamber grafting assays to see if scarring gives way to regeneration.
The school
Ohio State University: 71 labs on PI Pages, $1.6B a year on research, 882 research doctorates a year.
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