Local Growth Factor Presentation by Macrophages

Fibrosis comprises different connective tissue disorders that ultimately result in deposition of detrimental scar tissue in injured or inflamed organs. The culprit cells for organ scarring are called myofibroblasts because they secrete fibrous collagen matrix (“fibro”) that is contracted (“myo”) into scar tissue. Excessive myofibroblast activities are responsible for loss of function of vital organs after injury, such as the heart after an infarct – this life-threatening condition is called fibrosis.

Fibrosis ensues from normal repair partly because unresolved inflammation promotes continued activation of myofibroblasts to make and pull fibrous collagen matrix into stiff scar tissue. Our lab found that inflammatory macrophages carry an inactive fibrosis-inducing factor on their surface. We propose that myofibroblast can grab onto and activate this factor by pulling it our of a ‘straight-jacket’. The receptors involved in the grabbing process will need to be identified.

It is our aim to identify the molecular players mediating macrophage-induced fibroblast activation. We propose that preventing these cells to touch or blocking the interaction signaling molecules will ultimately reduce tissue scarring. We will study macrophages and fibroblasts derived from mouse tissue in unique co-culture environments. We will delete and inhibit already identified receptors on the macrophage and/or myofibroblast sur

Faculty Supervisor:

Boris Hinz

Student:

Partner:

Reutlingen University

Discipline:

Life Sciences

Sector:

Education

University:

University of Toronto

Program: