Targeted Disruption of Endothelial Cell-selective Adhesion Molecule Inhibits Angiogenic Processes in Vitro and in Vivo

Ishida, Tatsuro; Kundu, Ramendra K.; Yang, Eugene; Hirata, Ken Ichi; Ho, Yen Dong; Quertermous, Thomas

doi:10.1074/jbc.m304890200

Cited by 102 publications

(95 citation statements)

References 43 publications

(35 reference statements)

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“…37 A recently identified TJ protein, ESAM, however, has been found to promote in vitro tube formation in endothelial-like yolk sac cells and the genetic ablation of ESAM leads to decreased tumor size and vascularization. 16 These findings indicate that TJs might offer a new frontier for the regulation of angiogenesis. Our finding of the role of JAM-A in FGF-2-induced neovascularization is the second record to demonstrate an involvement of a TJ protein in angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

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Fibroblast Growth Factor-2 Failed to Induce Angiogenesis in Junctional Adhesion Molecule-A-Deficient Mice

Cooke

Naik

2006

ATVB

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Objective-We have previously shown that JAM-A regulates fibroblast growth factor-2 (FGF-2)-induced endothelial cell morphology, proliferation, and migration. Whether JAM-A is involved in FGF-2-induced angiogenesis in vivo is not known. We used JAM-A null mice to conclusively determine the role of JAM-A in FGF-2-induced neovascularization. Methods and Results-We generated JAM-A null (JAM-A Ϫ/Ϫ ) mice using gene trap technology. These mice, although viable and fertile, exhibited distorted Mendelian and sex ratios, suggesting partial embryonic lethality. Retinal fluorescein angiogram did not reveal any significant morphological differences in the vasculature of JAM-A

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Section: Discussionmentioning

confidence: 99%

“…16 Briefly, 1 mL of phosphate-buffered saline containing 25 mg of 2ϫ10 6 molecular weight FITC-dextran was injected into the portal vein. Thirty minutes later, mice were euthanized by CO 2 asphyxiation; the eyes were removed and fixed in 4% paraformaldehyde in phosphate-buffered saline for 3 hours.…”

Section: Retinal Fluorescein Angiogrammentioning

confidence: 99%

Fibroblast Growth Factor-2 Failed to Induce Angiogenesis in Junctional Adhesion Molecule-A-Deficient Mice

Cooke

Naik

2006

ATVB

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“…The congenic C57BL/6 strain (C57BL/ 6SJL; CD45.1 alloantigen) was purchased from The Jackson Laboratory (Bar Harbor, ME) and used for transplantation experiments. ESAM KO mice were developed by Dr. T. Ishida (Kobe University, Kobe, Japan) as previously reported (18). Mating of heterozygous male and female mice was routinely performed to generate homozygous ESAM KO mice.…”

Section: Micementioning

confidence: 99%

The Endothelial Antigen ESAM Monitors Hematopoietic Stem Cell Status between Quiescence and Self-Renewal

Sudo

Yokota

Oritani

et al. 2012

The Journal of Immunology

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Whereas most hematopoietic stem cells (HSC) are quiescent in homeostasis, they actively proliferate in response to bone marrow (BM) injury. Signals from the BM microenvironment are thought to promote entry of HSC into the cell cycle. However, it has been cumbersome to assess cycle status of viable HSC and thus explore unique features associated with division. In this study, we show that expression of endothelial cell-selective adhesion molecule (ESAM) can be a powerful indicator of HSC activation. ESAM levels clearly mirrored the shift of HSC between quiescence and activation, and it was prominent in comparison with other HSC-related Ags. ESAMhi HSC were actively dividing, but had surprisingly high long-term reconstituting capacity. Immunohistochemical analyses showed that most ESAMhi HSC were located near vascular endothelium in the BM after 5-fluorouracil treatment. To determine the importance of ESAM in the process of BM recovery, ESAM knockout mice were treated with 5-fluorouracil and their hematopoietic reconstruction was examined. The ESAM deficiency caused severe and prolonged BM suppression, suggesting that ESAM is functionally indispensable for HSC to re-establish homeostatic hematopoiesis. With respect to intracellular regulators, NF-κB and topoisomerase II levels correlated with the ESAM upregulation. Thus, our data demonstrate that the intensity of ESAM expression is useful to trace activated HSC and to understand molecular events involved in stem cell states.

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“…Claudins (Furuse et al, 1998), (Furuse et al, 2002), (Nitta et al, 2003), (Turksen and Troy, 2002), (Tatum et al, 2010), (Nakano et al, 2009), (Gow et al, 1999), (Gow et al, 2004), (Ben-Yosef et al, 2003), (Tamura et al, 2008), (Simon et al, 1999), (Miyamoto et al, 2005), (Hou et al, 2009), (Angelow et al, 2008) Occludin (Furuse et al, 1993), (Traweger et al, 2002), (Sakakibara et al, 1997), (Saitou et al, 2000), (Furuse et al, 1998), (Du et al, 2010), (Runkle et al, 2011) MarvelD3 (Raleigh et al, 2010), (Steed et al, 2009) Tricellulin (Ikenouchi et al, 2005), (Ikenouchi et al, 2008) LSR (Masuda et al, 2011) JAMs (Hirabayashi and Hata, 2006), (Weber et al, 2007), (Kostrewa et al, 2001), (Laukoetter et al, 2007), (Pellegrini et al, 2011), (Ishida et al, 2003) …”

Section: Recommended Readingmentioning

confidence: 99%

Current Frontiers and Perspectives in Cell Biology

2012

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Targeted Disruption of Endothelial Cell-selective Adhesion Molecule Inhibits Angiogenic Processes in Vitro and in Vivo

Cited by 102 publications

References 43 publications

Fibroblast Growth Factor-2 Failed to Induce Angiogenesis in Junctional Adhesion Molecule-A-Deficient Mice

Fibroblast Growth Factor-2 Failed to Induce Angiogenesis in Junctional Adhesion Molecule-A-Deficient Mice

The Endothelial Antigen ESAM Monitors Hematopoietic Stem Cell Status between Quiescence and Self-Renewal

Current Frontiers and Perspectives in Cell Biology

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