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Aron Parekh

Assistant Professor of Otolaryngology
Assistant Professor of Biomedical Engineering
Assistant Professor of Cancer Biology

Intellectual Neighborhoods

Research Focus

The Parekh Laboratory is focused on mechanobiology research in cancer and wound healing. Proper cell and extracellular matrix (ECM) interactions are responsible for maintaining functional homeostasis in tissues and organs. Alterations in this reciprocal relationship following disease or injury are guided by changes in the local ECM mechanical environment as well as signaling molecules and interactions with other cell types. These changes drive the ensuing disease state and tissue repair response by altering cellular phenotypes resulting in outcomes such as cancer cell invasion and pathological remodeling of healing wounds, respectively. In order to modulate these mechanobiological responses, a fundamental understanding of the biochemical and biophysical factors that influence these processes are required. These factors dictate cellular phenotypes and thus determine the manner in which cells further interact with their ECM microenvironment. Clinical modalities can be developed by identifying therapeutic targets that drive these pathological responses toward a more favorable outcome by interfering with these cell/ECM interactions. Therefore, our general research goal is to understand how mechanical forces drive pathologic cellular phenotypes in cancer and wound healing by utilizing biochemical and biomechanical approaches that include in vitro, ex vivo, in vivo, and in silico techniques and/or models.

Publications:

  • Jerrell RJ, Leih MJ, Parekh A. “The altered mechanical phenotype of fetal fibroblasts hinders myofibroblast differentiation.” Wound Repair and Regeneration. 2019;27:29-38. (Selected for the cover of Volume 27, Issue 1).
  • Kahue CN, Jerrell RJ, Parekh A. “Expression of human papillomavirus oncoproteins E6 and E7 inhibits invadopodia activity but promotes cell migration in HPV-positive head and neck squamous cell carcinoma cells.” Cancer Reports. 2018;1:e1125. (Selected for the cover of Volume 1, Issue 3. A top downloaded paper of 2017-2018.)
  • Jerrell RJ, Parekh A. “Matrix rigidity differentially regulates invadopodia activity through ROCK1 and ROCK2.” Biomaterials. 2016;84:119-129.
  • Jerrell RJ, Parekh A. “Cellular traction stresses mediate extracellular matrix degradation by invadopodia.” Acta Biomaterialia. 2014;10:1886-1896.