Inducer-stimulated Fas targets activated endothelium for destruction by anti-angiogenic thrombospondin-1 and pigment epithelium-derived factor

Nature Medicine
Olga V VolpertNoel P Bouck

Abstract

Natural inhibitors of angiogenesis are able to block pathological neovascularization without harming the preexisting vasculature. Here we show that two such inhibitors, thrombospondin-1 and pigment epithelium-derived factor, derive specificity for remodeling vessels from their dependence on Fas/Fas ligand (FasL)-mediated apoptosis to block angiogenesis. Both inhibitors upregulated FasL on endothelial cells. Expression of the essential partner of FasL, Fas/CD95 receptor, was low on quiescent endothelial cells and vessels but greatly enhanced by inducers of angiogenesis, thereby specifically sensitizing the stimulated cells to apoptosis by inhibitor-generated FasL. The anti-angiogenic activity of thrombospondin-1 and pigment epithelium-derived factor both in vitro and in vivo was dependent on this dual induction of Fas and FasL and the resulting apoptosis. This example of cooperation between pro- and anti-angiogenic factors in the inhibition of angiogenesis provides one explanation for the ability of inhibitors to select remodeling capillaries for destruction.

References

Jan 1, 1996·Advances in Cancer Research·N BouckS C Hsu
Aug 11, 1997·The Journal of Cell Biology·D W DawsonN P Bouck
May 30, 1998·Proceedings of the National Academy of Sciences of the United States of America·O V VolpertN P Bouck
Mar 23, 1999·Nature Medicine·H J KaplanT A Ferguson
Apr 17, 1999·The Journal of Biological Chemistry·M DhanabalV P Sukhatme
Sep 30, 1999·Experimental Cell Research·E DejanaM G Lampugnani
Nov 2, 1999·Biochemical and Biophysical Research Communications·J TranR S Kerbel
Feb 10, 2000·The American Journal of Pathology·D S O'ConnorD C Altieri
Mar 31, 2000·Nature Medicine·P Carmeliet
Jun 22, 2000·American Journal of Physiology. Gastrointestinal and Liver Physiology·T SodemanG J Gores
Aug 5, 2000·Science·P Golstein
Sep 23, 2000·European Journal of Cell Biology·G BossiG M Griffiths
Oct 26, 2000·Nature·P H Krammer
Feb 24, 2001·Cancer Metastasis Reviews·L E Benjamin
Feb 28, 2001·Proceedings of the National Academy of Sciences of the United States of America·V StellmachN Bouck
Apr 9, 2001·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·M Shichiri, Y Hirata
Jun 26, 2001·Journal of Cellular Physiology·K MoriP A Campochiaro
Aug 4, 2001·Biochemical and Biophysical Research Communications·M A FreybergP Friedl

❮ Previous
Next ❯

Citations

May 21, 2005·Cellular and Molecular Life Sciences : CMLS·A A TimurQ Wang
Jan 15, 2008·Cellular and Molecular Life Sciences : CMLS·S KazerounianJ Lawler
Nov 16, 2006·Journal of Molecular Medicine : Official Organ of the Gesellschaft Deutscher Naturforscher Und Ärzte·N I Fernandez-GarciaB Jimenez
Apr 15, 2008·Breast Cancer Research and Treatment·Karen O YeeJack Lawler
Feb 14, 2009·Cancer Metastasis Reviews·Hang T TaDave E Dunstan
Jun 25, 2013·Clinical & Experimental Metastasis·John M LattierHans E Grossniklaus
Jan 1, 2010·Cancer Microenvironment : Official Journal of the International Cancer Microenvironment Society·Kent E WilliamsAllan R Albig
Feb 27, 2004·Biochimica Et Biophysica Acta·Jane Sottile
Apr 26, 2003·Matrix Biology : Journal of the International Society for Matrix Biology·Lucas C Armstrong, Paul Bornstein
Sep 17, 2002·Current Opinion in Cell Biology·Paul Bornstein, E Helene Sage
Jun 6, 2003·Cytokine & Growth Factor Reviews·Hae-ock Lee, Thomas A Ferguson
Jul 13, 2002·Trends in Molecular Medicine·Noël Bouck
Jun 28, 2003·Trends in Molecular Medicine·Joyce Tombran-Tink, Colin J Barnstable
May 9, 2012·Expert Reviews in Molecular Medicine·Debabrata Patra, Linda J Sandell
Aug 8, 2008·Expert Reviews in Molecular Medicine·Joshua C AndersonCandece L Gladson
Oct 2, 2008·Molecular Therapy : the Journal of the American Society of Gene Therapy·Ping ChenJoseph T Bruder
Mar 15, 2013·Nature Reviews. Cancer·S Patricia Becerra, Vicente Notario
Feb 25, 2006·Nature Reviews. Immunology·Ralph C BuddJürg Tschopp
Aug 19, 2007·Molecular Therapy : the Journal of the American Society of Gene Therapy·Katsutoshi YokoiPeter A Campochiaro
Apr 27, 2005·Proceedings of the National Academy of Sciences of the United States of America·Trudy F C MackayStephanie M Rollmann
Aug 23, 2008·Proceedings of the National Academy of Sciences of the United States of America·Esma LejmiJean Plouët
Aug 21, 2008·Proceedings of the National Academy of Sciences of the United States of America·Akihiko YamamotoRobert R H Anholt
Aug 12, 2009·Proceedings of the National Academy of Sciences of the United States of America·Yishan SunMichael J Welsh
Feb 20, 2009·The Journal of Biological Chemistry·Adrien BernardZhenlin Li
Jun 9, 2004·The Journal of Experimental Medicine·Tetiana A ZaichukOlga V Volpert
Jul 21, 2010·Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences·Dominic A EdwardTracey Chapman
Jun 22, 2011·Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences·Rinaldo C Bertossa
May 4, 2012·Cold Spring Harbor Perspectives in Medicine·Patrick R Lawler, Jack Lawler
Aug 31, 2011·Cold Spring Harbor Perspectives in Biology·Josephine C Adams, Jack Lawler
May 28, 2009·Science Signaling·Roy L Silverstein, Maria Febbraio
Apr 15, 2009·Molecular and Cellular Biology·Vladislava JuricLester F Lau
Mar 29, 2003·Journal of Clinical Pathology·M GuanY Lu
Oct 3, 2002·Annual Review of Medicine·Gregg L Semenza
Apr 16, 2009·Cancer Research·Bin RenRoya Khosravi-Far
Feb 19, 2009·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Yelena MirochnikOlga V Volpert
Dec 17, 2008·Molecular Cancer Therapeutics·Jie Ma, David J Waxman

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptotic Caspases

Apoptotic caspases belong to the protease enzyme family and are known to play an essential role in inflammation and programmed cell death. Here is the latest research.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis