UNIVERSITY OF NORTH CAROLINA AT CHAPEL HILL
Total received in grants · trailing 12 months
$2.3M
$0for every U.S. household÷ 131M U.S. households
In perspective
0.0%of all $162.9B in tracked grants
1separate grants, trailing 12 months
UNIVERSITY OF NORTH CAROLINA AT CHAPEL HILL has received $2.3M across 1 federal grant of $1M or more on record.
Data as of July 24, 2026. Source: USAspending.gov, prime contract awards $1M+. Federal spending data lags and has known gaps. This is not a real-time or complete record.
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| Agency | Description | Amount |
|---|---|---|
| Department of Health and Human Services | INTEGRIN SIGNALING IN OSTEOARTHRITIS - PROJECT SUMMARY THE LONG-TERM GOAL OF THIS PROJECT IS TO DETERMINE THE BASIC MECHANISMS BY WHICH SIGNALS GENERATED THROUGH THE Α5Β1 INTEGRIN RECEPTOR CONTRIBUTE TO THE PROGRESSION OF OSTEOARTHRITIS (OA). THE PREMISE OF THIS WORK IS THAT ACTIVATION OF THE Α5Β1 INTEGRIN BY FRAGMENTS OF THE MATRIX PROTEIN FIBRONECTIN (FN), ACTING AS A “MATRIKINE”, INITIATES A CASCADE OF EVENTS INTENDED TO REMODEL AND REPAIR THE DAMAGED ECM, AS SEEN IN THE WOUND HEALING RESPONSE. HOWEVER, DURING OA THE SIGNALS GENERATED BY Α5Β1 INTEGRIN ACTIVATION, LIKELY IN COMBINATION WITH OTHER OA FACTORS SUCH AS ABNORMAL JOINT STRESS, ACTIVATE A FEED FORWARD SIGNALING LOOP THAT RESULTS IN A PROINFLAMMATORY ENVIRONMENT AND PROGRESSIVE MATRIX DESTRUCTION RESULTING IN A CHRONIC “NON-HEALING” WOUND. TO MITIGATE THIS PROCESS AND HALT OA PROGRESSION, THERE IS A CRITICAL NEED TO DETERMINE THE BASIC CELLULAR MECHANISMS THAT PRODUCE OA MEDIATORS IN RESPONSE TO THE ACTIVATION OF Α5Β1 INTEGRIN BY MATRIX DEGRADATION PRODUCTS. WE FOCUS ON A NOVEL MECHANISM OF SPATIALLY REGULATED, COMPARTMENTALIZED, SIGNALING MEDIATED BY REDOXOSOMES, WHICH CAN ALSO APPLY TO SIGNALING BY OTHER OA MEDIATORS INCLUDING CYTOKINES SUCH AS IL-1 THAT UTILIZE A SIMILAR PATHWAY. THIS WORK WILL OPEN A NOVEL AREA OF MECHANISTIC BASIC OA RESEARCH NEEDED TO DISCOVER NEW WAYS OF SELECTIVELY TARGETING COMPARTMENTALIZED PATHOLOGIC SIGNALS GENERATED THROUGH REDOXOSOMES AND AVOID MODIFYING PHYSIOLOGIC SIGNALING. AS A MODEL SYSTEM TO DEFINE THE SIGNALING PATHWAYS AND TRANSCRIPTIONAL CHANGES RELEVANT TO OA, WE USE A PURIFIED, SPECIFIC, Α5Β1 INTEGRIN BINDING BIOACTIVE FN FRAGMENT (FN7-10) THAT ACTS AS A MATRIKINE. RNASEQ ANALYSIS REVEALED THAT CHANGES IN GENE EXPRESSION INDUCED BY FN7-10 SIGNIFICANTLY CORRELATED WITH GENES THAT ARE DIFFERENTIALLY EXPRESSED IN HUMAN OA CARTILAGE. WE DISCOVERED THAT THE PATHOLOGIC Α5Β1 SIGNALING ACTIVATED BY FN7-10 OCCURS IN A COMPARTMENTALIZED, TEMPOROSPATIAL MANNER, THROUGH ENDOSOMES CALLED “REDOXOSOMES”. THIS ALLOWS FOR AN EFFICIENT COUPLING OF SIGNALING TO THE TRANSCRIPTIONAL RESPONSE. WE HAVE DEVELOPED A NOVEL TRANSGENIC MOUSE FOR INDUCIBLE EXPRESSION OF FN7-10 THAT WILL ALLOW US TO STUDY MECHANISMS OF Α5Β1 SIGNALING IN VIVO. AIM 1 WILL DEFINE THE MECHANISM BY WHICH Α5Β1 INTEGRIN SIGNALS GENERATED BY FN7-10 PROMOTE EXPRESSION OF PROINFLAMMATORY AND MATRIX DEGRADING GENES. AIM 2 WILL DETERMINE THE MECHANISM BY WHICH ACTIVATION OF Α5Β1 SIGNALING DRIVES OA PHENOTYPES IN VIVO. IMPACT: A MECHANISTIC UNDERSTANDING OF Α5Β1 SIGNALING AND THE ROLE OF REDOXOSOMES IN OA WILL PROVIDE THE INFORMATION NEEDED TO DEVELOP NEW TARGETED THERAPIES DESIGNED TO SLOW OR HALT THE PROGRESSION OF OA. SPECIFICALLY TARGETING THE COMPARTMENTALIZED REDOX SIGNALING IN OR NEAR ENDOSOMES WILL BE A MAJOR ADVANCE OVER THE CURRENT APPROACH WHERE SMALL MOLECULES CAN INHIBIT BOTH PATHOLOGIC AND PHYSIOLOGIC SIGNALING. | $2,265,261 |