We have found that ?-catenin protein is highly up-regulated in disc tissues derived from patients with disc degeneration and have created a ?-catenin conditional activation mouse model which displays severe defects in disc tissue morphology and pain. ?-catenin plays a key role in the development of disc degeneration and one of the key signaling mechanisms is to activate Runx2 expression which subsequently regulates Mmp13 expression in Col2-expressing cells in disc tissue. In this study, we will determine the role of Runx2 and CCL2 in ?-catenin-induced disc degeneration

Public Health Relevance

The intervertebral disc (IVD) degeneration is a natural progression of the aging process associated with chronic back pain. ?-catenin protein is highly up-regulated in disc tissues derived from patients with disc degeneration and ?-catenin conditional activation mouse model displays severe defects in disc tissue morphology and pain. We propose to determine the role of Runx2 and CCL2 in ?-catenin-induced disc degeneration. The goal of this research is to discover potential targets for the development of effective therapies of human Degenerative Disc Disease (DDD) and associated pain mechanisms..

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Small Research Grants (R03)
Project #
1R03AG061460-01
Application #
9652267
Study Section
Skeletal Biology Structure and Regeneration Study Section (SBSR)
Program Officer
Williams, John
Project Start
2019-01-01
Project End
2020-11-30
Budget Start
2019-01-01
Budget End
2019-11-30
Support Year
1
Fiscal Year
2019
Total Cost
Indirect Cost
Name
Rush University Medical Center
Department
Orthopedics
Type
Schools of Medicine
DUNS #
068610245
City
Chicago
State
IL
Country
United States
Zip Code
60612