Influence of IFN- alpha and IFN- gamma on Lymphangiogenesis.

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Influence of IFN- alpha and IFN- gamma on Lymphangiogenesis.

Postby patoco » Wed Sep 20, 2006 8:28 pm

Influence of IFN- alpha and IFN- gamma on Lymphangiogenesis.

August 6, 2006

Shao X, Liu C.
Department of Anatomy, Medical College of Qingdao University, Qingdao,
PR China 266021.

Malignant cancers commonly spread by local invasion followed by
metastasis through venous or lymphatic passages or both to distant
sites. Angiogenesis and its relation to tumor growth and metastasis
have been extensively researched. To date, however, the role played by
lymphangiogenesis and metastasis of cancer has been overlooked.
Inhibition of lymphangiogenesis, compared with inhibition of
angiogenesis, may provide new insight to the mechanisms of metastasis
of cancers.

The current study was designed to examine the effect of two commonly
used inhibitors of angiogenesis, interferon-alpha (IFN-alpha ) and
IFN-gamma, on the growth and proliferation of lymphatic endothelial
(LE) cells isolated from pig thoracic duct under in vitro condition.
The LE cells were isolated and marked using specific markers, such as VEGFR-3 and LYVE-1, before experimental studies.

The results showed that treatment of LE cells derived from the thoracic
duct with these two inhibitors caused a decrease in the rate of cell
proliferation in a dose-dependent manner, as assessed by MTT assays
(tetrazolium salt colorimetric assay). Cell migration rate was assessed
by the speed at which the cell migrated out from the scrape-wound
margin; the speed of migration of LE cells was significantly inhibited
in a dose-dependent fashion compared with controls. Treatment with both
IFN-alpha and IFN-gamma caused an increase in apoptosis of LE cells, as
assessed by Hoechst staining and caspase-3 staining.

Our results showed that both IFN-alpha and IFN-gamma were able to
inhibit LE cell growth in a dose-dependent manner and that the
inhibition may be through induction of apoptosis of endothelial cells.

PMID: 16881867 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum

Related Article:

IFN--mediated inhibition of tumor angiogenesis by natural killer T-cell ligand, -galactosylceramide

Yoshihiro Hayakawa, Kazuyoshi Takeda, Hideo Yagita, Mark J. Smyth, Luc
Van Kaer, Ko Okumura, and Ikuo Saiki

>From the Department of Pathogenic Biochemistry, Institute of Natural
Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan; the Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo, Japan; the Cancer Immunology Program, Sir Donald and Lady Trescowthick Laboratories, Peter MacCallum Cancer Institute, East Melbourne, Victoria, Australia; and the Howard Hughes Medical Institute, Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN.

Abstract

Alpha-galactosylceramide (-GalCer), which is a specific ligand for
CD1d-restricted variable-14 chain (V14) natural killer T (NKT) cells,
exerts a potent antitumor effect. We recently demonstrated that
interferon- (IFN-) secreted by both NKT cells and NK cells plays a
critical role in mediating the antimetastatic effect of -GalCer;
however, the IFN--dependent antitumor mechanisms remain poorly defined.

In the present study, we demonstrate IFN--dependent inhibition of tumor
angiogenesis by -GalCer. In -GalCer-treated mice, subcutaneous tumor
growth and tumor-induced angiogenesis were inhibited in an
IFN--dependent manner. The -GalCer-activated splenic or hepatic
mononuclear cells inhibited murine endothelial cell proliferation in
vitro, and this inhibitory effect was mediated mostly by IFN- produced
by NKT cells and NK cells. NK cell depletion resulted in significant
but partial inhibition of tumor growth and angiogenesis in vivo. These
results suggest that the IFN--mediated inhibition of tumor angiogenesis
is critically involved in the effector mechanisms of antitumor effects
evoked by -GalCer. (Blood. 2002;100:1728-1733)

© 2002 by The American Society of Hematology.

Complete Article Available:

http://www.bloodjournal.org/cgi/content/full/100/5/1728

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