MONOCYTE CHEMOATTRACTANT PROTEIN-1 MESSENGER-RNA EXPRESSION IN HEMANGIOMAS AND VASCULAR MALFORMATIONS

Citation
Ff. Isik et al., MONOCYTE CHEMOATTRACTANT PROTEIN-1 MESSENGER-RNA EXPRESSION IN HEMANGIOMAS AND VASCULAR MALFORMATIONS, The Journal of surgical research, 61(1), 1996, pp. 71-76
Citations number
29
Categorie Soggetti
Surgery
ISSN journal
00224804
Volume
61
Issue
1
Year of publication
1996
Pages
71 - 76
Database
ISI
SICI code
0022-4804(1996)61:1<71:MCPMEI>2.0.ZU;2-F
Abstract
Hemangiomas are vascular tumors that appear at or shortly after birth and undergo a rapid growth before involuting. During the proliferative phase, hemangiomas are infiltrated by macrophages, cells that are cap able of initiating angiogenesis. Vascular malformations grow slowly, c ommensurate with the child, and do not regress or become infiltrated b y macrophages. We demonstrate by in situ hybridization increased monoc yte chemoattractant protein-1 (MCP-1) mRNA expression during hemangiom a and vascular malformation growth. We found markedly upregulated expr ession of MCP-1 mRNA in all proliferative hemangioma specimens, expres sed by alpha-actin(+) perivascular smooth muscle cells and interstitia l HAM 56(+) macrophages. In contrast, 9 of 10 clinically involuting he mangiomas displayed no expression of MCP-1 mRNA. We found no expressio n of MCP-1 mRNA in vascular malformations, which correlates with the m inimal monocytic infiltration of these lesions. We also showed that de xamethasone and interferon-cu downregulate MCP-1 mRNA in cultured huma n vascular smooth muscle cells. Glucocorticoids can be efficacious in 30-50% of cases when given in the proliferative phase of hemangioma gr owth, but have no beneficial effect on vascular malformations. Interfe ron-a has been used to dramatically induce regression of steroid-refra ctory hemangiomas. Both of these agents' beneficial action on prolifer ative hemangiomas may, in part, result from reduced MCP-1 production a nd reduced influx of angiogenic macrophages. (C) 1996 Academic Press, Inc.