Keloids demonstrate high-level epidermal expression of vascular endothelial growth factor - 24/08/11

Doi : 10.1016/j.jaad.2003.11.061

Amy Kim Gira, MD ^a, Lawrence F Brown, MD ^c, Carl V Washington, MD ^a, Cynthia Cohen, MD ^b, Jack L Arbiser, MD, PhD ^a,^⁎
^a Department of Dermatology, Emory University School of Medicine and Atlanta Veterans Administration Medical Center, Atlanta, Georgia, USA
^b Department of Pathology, Emory University School of Medicine and Atlanta Veterans Administration Medical Center, Atlanta, Georgia, USA
^c Department of Pathology, Beth Israel Deaconness Medical Center, Harvard Medical School, Boston, Massachusetts, USA

^*Reprint requests: Jack L. Arbiser, Department of Dermatology, Emory University School of Medicine, WMB 5309, 1639 Pierce Dr, Atlanta, GA 30322, USA.

Abstract

Background

Keloids are a major cause of morbidity, and arise after operation, injury, or cutaneous infection. Clinically, keloids differ from hypertrophic scars in that they grow beyond the original borders of the injury. Keloids occur most commonly for patients of African and Asian descent, and treatment options are multiple, indicating that there is no entirely satisfactory treatment for keloids. Angiogenesis inhibition has been shown to be effective in treatment of malignancy in both animal models and human beings.

Objective

We sought to determine whether keloids produce the potent angiogenic factor vascular endothelial growth factor (VEGF).

Methods

We performed in situ hybridization for VEGF on keloid tissue and normal skin.

Results

Our study demonstrated abundant production of VEGF in keloids and, surprisingly, the major source of VEGF was the overlying epidermis.

Conclusions

Our results suggest that the overlying epidermis is the major source of keloid angiogenesis. These findings demonstrate that keloids are angiogenic lesions. Topical antiangiogenic therapy, directed at either down-regulating epidermal VEGF or inhibiting keratinocyte-derived VEGF activity on its endothelial receptors, may be useful in the treatment of keloids.

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Plan

Materials and methods

Results

Discussion

Supported by grant RO1 AR47901 and P30 AR42687 Emory Skin Disease Research Core Center Grant from the National Institutes of Health and a Department of Veterans Affairs Merit Award (J. L. A.).
Conflicts of interest: None identified.