PMID- 1918946
OWN - NLM
STAT- MEDLINE
DCOM- 19911028
LR  - 20061115
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 147
IP  - 7
DP  - 1991 Oct 1
TI  - Murine endothelioma cell lines transformed by polyoma middle T oncogene as target 
      for and producers of cytokines.
PG  - 2122-9
AB  - We studied cytokine-related functional properties of four mouse endotheliomas 
      from different anatomical sites obtained by transformation with middle T 
      oncogene. We examined mRNA expression of IL-6, IL-1 alpha, macrophage-CSF, 
      granulocyte/macrophage-CSF, and two members of an emerging super-family of 
      chemotactic cytokines (JE/monocyte chemoattractant protein-1 (MCP-1) and KC). 
      Exposure to IL-1 augmented or induced cytokine gene transcripts in three 
      endothelioma lines (eEnd.1, sEnd.1, and tEnd) with maximal expression in tEnd.1 
      cells. Endothelioma cells also responded to TNF-alpha and LPS. Levels of IL-6 and 
      monocyte chemotactic activity (a JE/MCP activity) correlated with mRNA 
      expression. IL-1 also induced production of procoagulant activity and 
      platelet-activating factor in endothelioma cells, with heterogeneity in the 
      levels of response among individuals lines. Murine melanoma B16-F1, human colon 
      carcinoma HT29 cells, CB33MT lymphoblastoid cells, and monocytes adhered to 
      endothelioma monolayers and the adhesive properties of these cell lines were 
      modulated by IL-1 beta, with marked differences among themselves. Murine EC 
      derived from brain capillaries, used as control, shared several properties with 
      bEnd.4 line. Endothelioma lines cause tumors by recruiting host cells. The 
      capacity to produce cytokines that directly or indirectly attract host vascular 
      cells, may play an important role in hemangioma induction in vivo. Murine 
      endothelioma lines, generated by transformation with the polyoma middle T 
      oncogene, retain functional properties of normal endothelium, and may represent 
      an invaluable tool for analysis of the immunobiology and heterogeneity of EC in 
      different tissues.
FAU - Bussolino, F
AU  - Bussolino F
AD  - Dipartimento di Genetica, Biologia e Chimica Medica, Universita di Torino, Italy.
FAU - De Rossi, M
AU  - De Rossi M
FAU - Sica, A
AU  - Sica A
FAU - Colotta, F
AU  - Colotta F
FAU - Wang, J M
AU  - Wang JM
FAU - Bocchietto, E
AU  - Bocchietto E
FAU - Padura, I M
AU  - Padura IM
FAU - Bosia, A
AU  - Bosia A
FAU - DeJana, E
AU  - DeJana E
FAU - Mantovani, A
AU  - Mantovani A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Antigens, Polyomavirus Transforming)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (Platelet Activating Factor)
RN  - 0 (RNA, Messenger)
RN  - 81627-83-0 (Macrophage Colony-Stimulating Factor)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Animals
MH  - Antigens, Polyomavirus Transforming/genetics
MH  - Cell Adhesion
MH  - Chemokine CCL2
MH  - Chemotactic Factors/*biosynthesis
MH  - Cytokines/*biosynthesis/genetics/pharmacology
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/biosynthesis
MH  - Hemangioendothelioma/*metabolism/pathology
MH  - Interleukin-1/biosynthesis
MH  - Interleukin-6/biosynthesis
MH  - Macrophage Colony-Stimulating Factor/biosynthesis
MH  - Mice
MH  - Oncogenes
MH  - Platelet Activating Factor/biosynthesis
MH  - RNA, Messenger/analysis
MH  - Tumor Cells, Cultured
EDAT- 1991/10/01 00:00
MHDA- 1991/10/01 00:01
CRDT- 1991/10/01 00:00
PHST- 1991/10/01 00:00 [pubmed]
PHST- 1991/10/01 00:01 [medline]
PHST- 1991/10/01 00:00 [entrez]
PST - ppublish
SO  - J Immunol. 1991 Oct 1;147(7):2122-9.