Aron Parekh

Prostaglandin E2 differentially modulates human fetal and adult dermal fibroblast migration and contraction: implication for wound healing.

Prostaglandin E2 inhibition of keloid fibroblast migration, contraction, and transforming growth factor (TGF)-beta1-induced collagen synthesis.

Collagen gel anisotropy measured by 2-D laser trap microrheometry.

Differential regulation of free-floating collagen gel contraction by human fetal and adult dermal fibroblasts in response to prostaglandin E2 mediated by an EP2/cAMP-dependent mechanism.

Differences in tissue-remodeling potential of aortic and pulmonary heart valve interstitial cells.

Fetal dermal fibroblasts retain a hyperactive migratory and contractile phenotype under 2-and 3-dimensional constraints compared to normal adult fibroblasts.

Extracellular matrix rigidity promotes invadopodia activity.

Prostaglandin E2 differentially regulates contraction and structural reorganization of anchored collagen gels by human adult and fetal dermal fibroblasts.

Repair of the tympanic membrane with urinary bladder matrix.

Regulation of cancer invasiveness by the physical extracellular matrix environment.

Generating elastin-rich small intestinal submucosa-based smooth muscle constructs utilizing exogenous growth factors and cyclic mechanical stimulation.

Assessing the effects of transforming growth factor-beta1 on bladder smooth muscle cell phenotype. I. Modulation of in vitro contractility.

Assessing the effects of transforming growth factor-beta1 on bladder smooth muscle cell phenotype. II. Modulation of collagen organization.

Ex vivo deformations of the urinary bladder wall during whole bladder filling: contributions of extracellular matrix and smooth muscle.

Sensing and modulation of invadopodia across a wide range of rigidities.

Strain history and TGF-β1 induce urinary bladder wall smooth muscle remodeling and elastogenesis.

Synthetic and tissue-derived models for studying rigidity effects on invadopodia activity.

Cellular traction stresses mediate extracellular matrix degradation by invadopodia.