PMID- 8769945
OWN - NLM
STAT- MEDLINE
DCOM- 19961230
LR  - 20131121
IS  - 0022-4804 (Print)
IS  - 0022-4804 (Linking)
VI  - 61
IP  - 1
DP  - 1996 Feb 15
TI  - Monocyte chemoattractant protein-1 mRNA expression in hemangiomas and vascular 
      malformations.
PG  - 71-6
AB  - 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 capable of initiating angiogenesis. 
      Vascular malformations grow slowly, commensurate with the child, and do not 
      regress or become infiltrated by macrophages. We demonstrate by in situ 
      hybridization increased monocyte chemoattractant protein-1 (MCP-1) mRNA 
      expression during hemangioma and vascular malformation growth. We found markedly 
      upregulated expression of MCP-1 mRNA in all proliferative hemangioma specimens, 
      expressed by alpha-actin perivascular smooth muscle cells and interstitial HAM 
      56+ macrophages. In contrast, 9 of 10 clinically involuting hemangiomas displayed 
      no expression of MCP-1 mRNA. We found no expression of MCP-1 mRNA in vascular 
      malformations, which correlates with the minimal monocytic infiltration of these 
      lesions. We also showed that dexamethasone and interferon-alpha downregulate 
      MCP-1 mRNA in cultured human vascular smooth muscle cells. Glucocorticoids can be 
      efficacious in 30-50% of cases when given in the proliferative phase of 
      hemangioma growth, but have no beneficial effect on vascular malformations. 
      Interferon-alpha has been used to dramatically induce regression of 
      steroid-refractory hemangiomas. Both of these agents' beneficial action on 
      proliferative hemangiomas may, in part, result from reduced MCP-1 production and 
      reduced influx of angiogenic macrophages.
FAU - Isik, F F
AU  - Isik FF
AD  - Department of Surgery, University of Washington Medical Center, Seattle 98195, 
      USA.
FAU - Rand, R P
AU  - Rand RP
FAU - Gruss, J S
AU  - Gruss JS
FAU - Benjamin, D
AU  - Benjamin D
FAU - Alpers, C E
AU  - Alpers CE
LA  - eng
GR  - DK 47659/DK/NIDDK NIH HHS/United States
GR  - HL 42270/HL/NHLBI NIH HHS/United States
GR  - HL 47151/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Surg Res
JT  - The Journal of surgical research
JID - 0376340
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interferon-alpha)
RN  - 0 (RNA, Messenger)
RN  - 7S5I7G3JQL (Dexamethasone)
SB  - IM
MH  - Blood Vessels/*abnormalities
MH  - Blotting, Northern
MH  - Cells, Cultured
MH  - Chemokine CCL2/*genetics
MH  - Dexamethasone/pharmacology
MH  - Hemangioma/*metabolism/pathology
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - Interferon-alpha/pharmacology
MH  - Muscle, Smooth, Vascular/cytology/metabolism
MH  - RNA, Messenger/*metabolism
EDAT- 1996/02/15 00:00
MHDA- 1996/02/15 00:01
CRDT- 1996/02/15 00:00
PHST- 1996/02/15 00:00 [pubmed]
PHST- 1996/02/15 00:01 [medline]
PHST- 1996/02/15 00:00 [entrez]
AID - S0022-4804(96)90083-9 [pii]
AID - 10.1006/jsre.1996.0083 [doi]
PST - ppublish
SO  - J Surg Res. 1996 Feb 15;61(1):71-6. doi: 10.1006/jsre.1996.0083.