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Prepublished online as a Blood First Edition Paper on September 5, 2002; DOI 10.1182/blood-2002-05-1516.
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Blood, 15 January 2003, Vol. 101, No. 2, pp. 560-567
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
A critical role of placental growth factor in the induction of
inflammation and edema formation
Hajimu Oura,
Jennifer Bertoncini,
Paula Velasco,
Lawrence F. Brown,
Peter Carmeliet, and
Michael Detmar
From the Cutaneous Biology Research Center, Department
of Dermatology, Massachusetts General Hospital and Harvard Medical
School; and Department of Pathology, Beth Israel Deaconess Medical
Center and Harvard Medical School; both of Boston; and Center for
Transgene Technology and Gene Therapy, University of Leuven,
Belgium.
Angiogenesis is a prominent feature of a number of inflammatory
human diseases, including rheumatoid arthritis, psoriasis, and
cutaneous delayed-type hypersensitivity (DTH) reactions. Up-regulation of placental growth factor (PlGF), a member of the vascular endothelial growth factor (VEGF) family, has been found in several conditions associated with pathologic angiogenesis; however, its distinct role in
the control of angiogenesis has remained unclear. To directly investigate the biologic function of PlGF in cutaneous inflammation and
angiogenesis, DTH reactions were investigated in the ear skin of
wild-type mice, of PlGF-deficient mice, and of transgenic mice with
targeted overexpression of human PlGF-2 in epidermal keratinocytes, driven by a keratin 14 promoter expression construct. Chronic transgenic delivery of PlGF-2 to murine epidermis resulted in a
significantly increased inflammatory response, associated with more
pronounced vascular enlargement, edema, and inflammatory cell
infiltration than seen in wild-type mice. Conversely, PlGF deficiency
resulted in a diminished and abbreviated inflammatory response,
together with a reduction of inflammatory angiogenesis and edema
formation. VEGF expression was up-regulated at a comparable level in
the inflamed skin of all genotypes. These findings reveal that
placental growth factor plays a critical role in the control of
cutaneous inflammation, and they suggest inhibition of PlGF bioactivity
as a potential new approach for anti-inflammatory therapy.
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