About the Lab

Major Focus of Kapoor Lab

Osteoarthritis Biomarkers (Early detection):

Goal: Identification of reliable and specific OA Biomarkers that can assist in detecting and determining the degree of joint destruction during OA. Our biomarker exploration studies are currently focusing on two joints: knee and spine (facet). For biomarker exploration, we are employing a multi-tier approach using Next Generation Sequencing, Metabolomics, cytokine-multiplexing etc in combination with patient demographics and risk factors. Our team of scientists within Kapoor Lab and key collaborators including basic scientists, clinicians, epidemiologists, computational biologists are involved in this study.

Injectable Therapies to stop Joint Destruction During Osteoarthritis:

Goal: Identifying and targeting potential therapeutic targets that can reduce or stop joint inflammation, fibrosis, cartilage destruction and help restore joint function.

Kapoor Lab is currently working on three major injectable therapies:

1 - Chondro-protective therapy: Chondrocyte cell death within the articular cartilage is the major event that initiates cartilage destruction during OA. Our recent studies suggest that autophagy proteins are crucial for survival of chondrocytes within articular cartilage. We have identified crucial autophagy mediators that can help increase the survival of chondrocytes within articular cartilage. We are currently testing some major autophagy-activating agents in OA models to identify their chondro-protective potential.

2 - microRNA Blockers: We have discovered some specific microRNAs that are elevated in the cartilage and bio fluids of subjects with knee and spine OA. These microRNAs increase inflammation and catabolic activity in the cartilage and contribute to its degeneration. We are currently testing the efficacy and safety of microRNA inhibitors in preclinical spine and knee OA models.

3 - Anti-fibrotic therapy: We recently identified that soluble ephrin-B2 (shedded form of ephrin-B2 protein belonging to protein-tyrosine kinase family) as a novel pro-fibrotic mediator and as a potential anti-fibrotic therapeutic target. We specifically identified how ephrin-B2 is shed by ADAM10 metalloproteinase and how this shedded form of ephrin-B2 promotes tissue fibrosis. We are currently testing the therapeutic potential of targeting the ephrin pathway to limit fibrosis in animal models OA, scleroderma and idiopathic pulmonary fibrosis.