R. Rivkah Isseroff

A fibrin-based bioengineered ocular surface with human corneal epithelial stem cells.

Calcium channel blockers inhibit galvanotaxis in human keratinocytes.

Beta-adrenergic receptor activation inhibits keratinocyte migration via a cyclic adenosine monophosphate-independent mechanism.

Melanocytes do not migrate directionally in physiological DC electric fields.

Power-line frequency electromagnetic fields do not induce changes in phosphorylation, localization, or expression of the 27-kilodalton heat shock protein in human keratinocytes.

PP2A activation by beta2-adrenergic receptor agonists: novel regulatory mechanism of keratinocyte migration.

Electrical stimulation of wound healing.

Human dermal fibroblasts do not exhibit directional migration on collagen I in direct-current electric fields of physiological strength.

Power line frequency electromagnetic fields do not increase the rate of protein synthesis in human skin fibroblasts as previously reported.

Stochastic models for cell motion and taxis.

Human melanocytes do not express EGF receptors.

Heat shock protein 27 is expressed in normal and malignant human melanocytes in vivo.

Cyclic AMP mediates keratinocyte directional migration in an electric field.

Beta 2-adrenergic receptor activation delays dermal fibroblast-mediated contraction of collagen gels via a cAMP-dependent mechanism.

Arsenite pre-conditioning reduces UVB-induced apoptosis in corneal epithelial cells through the anti-apoptotic activity of 27 kDa heat shock protein (HSP27).

Topical negative pressure devices: use for enhancement of healing chronic wounds.

Beta2-adrenergic receptor activation delays wound healing.

The beta 2-adrenergic receptor activates pro-migratory and pro-proliferative pathways in dermal fibroblasts via divergent mechanisms.

beta-Adrenergic receptor antagonists accelerate skin wound healing: evidence for a catecholamine synthesis network in the epidermis.

beta4 integrin and epidermal growth factor coordinately regulate electric field-mediated directional migration via Rac1.

UVB irradiation-induced changes in the 27-kd heat shock protein (HSP27) in human corneal epithelial cells.

Beta-adrenergic receptor agonists delay while antagonists accelerate epithelial wound healing: evidence of an endogenous adrenergic network within the corneal epithelium.

Wound re-epithelialization: modulating keratinocyte migration in wound healing.

Beta adrenergic receptors in keratinocytes.

Association between the use of beta-adrenergic receptor agents and the development of venous leg ulcers.

Responses of the 27-kDa heat shock protein to UVB irradiation in human epidermal melanocytes.

Dynamics of neutrophil infiltration during cutaneous wound healing and infection using fluorescence imaging.

Beta2-adrenergic receptor signaling mediates corneal epithelial wound repair.

Direct binding of integrin alphavbeta3 to FGF1 plays a role in FGF1 signaling.

An epinephrine-dependent mechanism for the control of UV-induced pigmentation.

beta-Adrenergic receptor modulation of wound repair.

Stress-mediated increases in systemic and local epinephrine impair skin wound healing: potential new indication for beta blockers.

Vincent Azubike Ziboh (1929-2009).

Single cell mechanics of keratinocyte cells.

Keratinocyte proximity and contact can play a significant role in determining mesenchymal stem cell fate in human tissue.

Does inflammation have a role in the pathogenesis of venous ulcers? A critical review of the evidence.

The linear excisional wound: an improved model for human ex vivo wound epithelialization studies.

β2AR antagonists and β2AR gene deletion both promote skin wound repair processes.

Toll-like receptors in wound healing: location, accessibility, and timing.

Plant-based modulation of Toll-like receptors: an emerging therapeutic model.

The epithelial sodium channel mediates the directionality of galvanotaxis in human keratinocytes.

Catecholamine stress alters neutrophil trafficking and impairs wound healing by β2-adrenergic receptor-mediated upregulation of IL-6.

Electrical Stimulation Therapy and Wound Healing: Where Are We Now?

Acute wounding alters the beta2-adrenergic signaling and catecholamine synthetic pathways in keratinocytes.

Recovery and cultivation of keratinocytes from shipped mouse skin.