Back to 2012 Annual Meeting Program
Neural Wound Healing: Why Surgery May Not Be Enough for Carpal Tunnel Syndrome
Jason R. Kang, BS; Weiping Wang, PhD; Nima Nassiri, BS; Peter Hahn, BS; Derek Frum; Tahseen Mozaffar, MD; Ranjan Gupta
University of California Irvine, Irvine, CA, USA
Chronic nerve compression (CNC) injuries such as carpal tunnel syndrome cause significant morbidity in millions of individuals with the ensuing loss of sensation and motor function. Recent advancements in our understanding of the cellular and molecular basis of CNC injury have prompted a reinterpretation of compressive neuropathies as a form of neural wound healing. Wound healing is a well-recognized biological phenomenon classically described as inflammation, angiogenesis, cellular proliferation, and connective tissue remodeling. Previous studies have demonstrated the prevalence of tissue inflammation, increased neural vasculature, and Schwann cell proliferation during the progression of CNC injury. However, the role of connective tissue remodeling in compressive neuropathies is not clearly understood. In peripheral nerves, Schwann cells and fibroblasts are intimately associated with a rich connective tissue network of proteins, glycoproteins, and proteoglycans known as the extracellular matrix (ECM). Our current study utilizes in vivo rat and mouse models of CNC injury to investigate changes in ECM composition of peripheral nerves with and without injury. Quantitative polymerase chain reaction was performed to assess changes in gene expression of fibronectin, laminin, and collagen type IV at various time points. Additionally, protein immunoblot and immunohistochemistry assays for these structural ECM proteins were performed to detect and measure their levels. qPCR analysis revealed that CNC injury increased gene expression of fibronectin, laminin, collagen type IV by 10.7
Back to 2012 Annual Meeting Program