Promoting intervertebral disc health and healing
Welcome to the Illien-Junger Lab at the Emory University School of Medicine. Our lab is part of the diverse and highly collaborative Department of Orthopaedics. Our research focus is on Intervertebral disc degeneration, specifically, our lab explores the molecular pathways that regulate intervertebral disc cellularity, and investigates how diets affect spinal health, using transgenic mice and mouse aging studies, and intervertebral disc organ and cell culture studies.
Protein phosphatases in intervertebral disc degeneration
Hallmarks of intervertebral disc degeneration include chronic inflammation, cell loss, and matrix degradation. Survival pathways, such as the Akt signaling pathway regulate cellularity and matrix production in intervertebral discs, and their inactivation is known to contribute to a pro-inflammatory environment, a catabolic shift and increased cell loss via apoptosis. Regulation of survival pathways are highly tissue specific. We are studying the intervertebral disc specific role of the protein phosphatase PHLPP, specifically, if its pharmacological inhibition can promote cell health and reduce spontaneous degeneration in mouse models, and human cell culture studies.
Targeting protein phosphatases to promote intervertebral disc healing
Discectomies are common surgical interventions that treat radiculopathy by removing herniated and loose intervertebral disc tissues. However, the remaining intervertebral disc tissue can continue to degenerate resulting in long-term clinical problems. Intervertebral discs have a very limited healing capacity. Our lab studies the role of the protein phosphatase PHLPP in decelerating intervertebral disc degeneration following large needle puncture injury, which simulates discectomy surgeries. Targeting this specific phosphatase could halt the degenerative cascade after discectomies by preventing cell death and matrix degradation after acute intervertebral disc injury.
Diet to maintain intervertebral disc health
Diabetes and low back pain are debilitating diseases and modern epidemics. Diabetes and obesity are also highly correlated with intervertebral disc degeneration and back pain. Advanced glycation endproducts (AGEs) increase reactive-oxygen-species and inflammation, and are one cause for development of diabetes. AGEs accumulate in tissues due to hyperglycemia or prolonged consumption of foods processed at high heat. We found that chronic ingestion of AGE rich diets lead to AGE accumulation in intervertebral discs and vertebrae, contributing to intervertebral disc tissue crosslinking and collagen damage, which are known contributors to intervertebral disc degeneration.