Tracy Criswell, PhD, Assistant Professor

Dr. Tracy Criswell received her Bachelor’s degree in Biology from the University of Cincinnati in 1998 (Magna Cum Laude) and her PhD in Cellular and Molecular Bases of Disease from Case Western Reserve University in 2004. Her thesis work focused on identifying the cellular effects of low dose ionizing radiation exposure on breast cancer. After the completion of her PhD, Dr. Criswell joined the laboratory of Dr. Carlos Arteaga at Vanderbilt University where her research focused on the role of TGFβ signaling in breast cancer metastases. In 2009, she joined the Wake Forest Institute for Regenerative Medicine as a senior research fellow and was subsequently promoted to a faculty position in 2012. Dr. Criswell is currently an Assistant Professor at the Wake Forest Institute for Regenerative Medicine with cross appointments in Integrative Physiology and Pharmacology, Molecular Medicine and Translational Science and the Virginia Tech-Wake Forest University School of Biomedical Engineering and Science.

SYNOPSIS OF AREA OF INTEREST:

  1. The development of novel cellular, biological and pharmacological therapies for the treatment of skeletal muscle injury.
  2. The effects of age and gender on skeletal muscle regeneration.

DETAILED AREA OF INTEREST:

Musculoskeletal injuries and disorders are the primary cause of disability in the United States. In young and healthy individuals, skeletal muscle tissue has a remarkable ability to undergo regeneration when prompted to do so in response to local damage or injury. However, aged muscle shows compromised ability to recover after injury, resulting in decreased muscle function and often, loss of independence in the elderly. The recovery of muscle function following injury requires the activation and differentiation of resident satellite cells, or alternatively termed muscle progenitor stem cells (MPCs), and a cellular microenvironment that is conducive to this process. It is likely that the age related decrease in muscle regeneration capacity results from imbalances in one or both of these requirements.

The mechanisms behind sarcopenia, or age-related loss of muscle volume and function, are not well understood, but are thought to involve many physiological and metabolic changes, including decreased innervation, increased adipose deposition and chronic inflammation. The combined contribution of these components to decreased skeletal muscle regenerative capacity in the elderly has not been extensively studied. The field of regenerative medicine offers the promise of novel approaches to the treatment of age related loss of tissue function. Cell therapy approaches have recently been introduced as a clinical intervention in order to repair damaged and/or lost tissue, but these approaches are hindered by the hostile environment of the injured tissue such as increased fibrosis, poor tissue perfusion affecting cell survival and host immune rejection of allogeneic grafts. Moreover, a majority of this research is being conducted in young animals, which are known to have efficient endogenous regeneration capacity. Thus, these studies have demonstrated only a modest effect of MPC therapy on functional recovery.  We have developed a model of compression-induced muscle injury in rats that results in multi-component damage to the muscular, neural and, vascular compartments (Criswell et al., 2011).  This model closely mimics the damage found in patients that have experienced crush-type injuries.  We believe that the extracellular changes represented in our injury model offer clear advantages over more conventional models that leave the vascular and neural networks largely intact, and provides an ideal model for identifying and validating novel therapeutic treatments for skeletal muscle dysfunction.

 

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