Cooperative interaction of Angiopoietin-like proteins 1 and 2 in zebrafish vascular development

Kubota, Yoshiaki; Oike, Yuichi; Satoh, Shinya; Tabata, Yoko; Niikura, Yuichi; Morisada, Tohru; Akao, Masaki; Urano, Takashi; Ito, Yasuhiro; Miyamoto, Takeshi; Nagai, Norihiro; Koh, Gou Young; Watanabe, Sumiko; Suda, Toshio

doi:10.1073/pnas.0501902102

Cited by 92 publications

(99 citation statements)

References 34 publications

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“…This phenomenon represents the first step of the metastatic process and implies the presence of blood vessels and lymphatics within and around the tumor as well as interactions between tumor and endothelial cells. Unlike angiopoietins and other members of the angiopoietin-like family that have been shown to regulate angiogenesis, namely ANGPTL1 (22, 23), ANGPTL2 (23), and ANGPTL3 (24), ANGPTL4 did not affect lymph or blood vessel density of primary Lewis lung carcinoma (3LL) tumors but decreased their in vivo intravasating potential.…”

Section: Discussionmentioning

confidence: 99%

Angiopoietin-like 4 prevents metastasis through inhibition of vascular permeability and tumor cell motility and invasiveness

Galaup

Cazes

Jan

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

225

219

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Angiopoietin-like 4 (ANGPTL4), a secreted protein of the angiopoietin-like family, is induced by hypoxia in both tumor and endothelial cells as well as in hypoxic perinecrotic areas of numerous cancers. Here, we investigated whether ANGPTL4 might affect tumor growth as well as metastasis. Metastatic 3LL cells were therefore xenografted into control mice and mice in which ANGPTL4 was expressed by using in vivo DNA electrotransfer. Whereas primary tumors grew at a similar rate in both groups, 3LL cells metastasized less efficiently to the lungs of mice that expressed ANGPTL4. Fewer 3LL emboli were observed in primary tumors, suggesting that intravasation of 3LL cells was inhibited by ANGPTL4. Furthermore, melanoma B16F0 cells injected into the retro-orbital sinus also metastasized less efficiently in mice expressing ANGPTL4. Although B16F0 cells were observed in lung vessels, they rarely invaded the parenchyma, suggesting that ANGPTL4 affects extravasation. In addition, recombinant B16F0 cells that overexpress ANGPTL4 were generated, showing a lower capacity for in vitro migration, invasion, and adhesion than control cells. Expression of ANGPTL4 induced reorganization of the actin cytoskeleton through inhibition of actin stress fiber formation and vinculin localization at focal contacts. Together, these results show that ANGPTL4, through its action on both vascular and tumor compartments, prevents the metastatic process by inhibiting vascular activity as well as tumor cell motility and invasiveness.angiogenesis ͉ cancer ͉ hypoxia

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Section: Discussionmentioning

confidence: 99%

Angiopoietin-like 4 prevents metastasis through inhibition of vascular permeability and tumor cell motility and invasiveness

Galaup

Cazes

Jan

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

225

219

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“…This finding is striking in radialized hec mutant embryos, where zangptl2 expression encompasses the entirety of the yolk cell. zangptl2 is homologous to a family of secreted angiopoietin-related factors, which are important for promoting tissue remodeling and cell migration during vascularization, although previous studies do not support a role for zangptl2 function in yolk extension formation (Kubota et al, 2005a). However, zangptl2 expression suggests that the induction of gene expression in the YSL may be important for changes in this cellular layer, which in turn may lead to the anterior movement of tail bud-derived cells and/or the generation of the forces that shape the yolk extension.…”

Section: Coordinated Changes Associated With Yolk Extension Formationmentioning

confidence: 98%

Analysis of axis induction mutant embryos reveals morphogenetic events associated with zebrafish yolk extension formation

Gingerich

Lindeman

Putiri

et al. 2006

Developmental Dynamics

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We analyze patterning and morphogenetic events during somitogenesis in hecate mutant embryos, which exhibit early axis induction defects. The posterior region, in the absence of a dorsal axis, is capable of forming organized gene expression patterns. The aberrant morphogenesis of mutant embryos is associated with anteriorly directed cell movements, underlying the enveloping layer, from the posterior region. In both wild-type and mutant embryos, these changes result in an accumulation of cells, whose location correlates with a constriction in the posterior yolk cell, which in the wild-type corresponds to the yolk extension. The region encompassing the constriction corresponds to a region of expression of zangptl2 in the yolk syncytial layer, which expands anteriorly together with the anteriorly migrating tail bud-derived cell population.

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“…Angiopoietin-1 tightens vessels by promoting interactions between cells of the vascular wall, whereas angiopoietin-2 loosens these interactions and stimulates the growth of immature vessels. 5,6 Angiopoietin-like proteins also play a role in the modulation of angiogenesis, as shown for ANGPTL1, 7,8 ANGPTL2,8,9 ANGPTL3, 10 and ANGPTL4. 2,3,11,12 [15][16][17] In the pathological context of ischemic diseases, ANGPTL4 could modulate angiogenesis by modifying the microenvironment in response to hypoxia.…”

mentioning

confidence: 99%

“…Angiopoietin-1 tightens vessels by promoting interactions between cells of the vascular wall, whereas angiopoietin-2 loosens these interactions and stimulates the growth of immature vessels. 5,6 Angiopoietin-like proteins also play a role in the modulation of angiogenesis, as shown for ANGPTL1, 7,8 ANGPTL2, 8,9 ANGPTL3, 10 and ANGPTL4. 2,3,11,12 ANGPTL4, previously known as hepatic fibrinogen/angiopoietin-related protein (HFARP), 3 peroxi-some proliferator-activated receptor-␥ (PPAR-␥), angiopoietinrelated gene (PGAR), 13 or fasting-induced adipose factor (FIAF), 14 is also involved in lipid and glucose metabolism.…”

mentioning

confidence: 99%

Extracellular Matrix–Bound Angiopoietin-Like 4 Inhibits Endothelial Cell Adhesion, Migration, and Sprouting and Alters Actin Cytoskeleton

Cazes

Galaup

Chomel

et al. 2006

Circulation Research

165

138

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Abstract-Angiopoietin-like 4 (ANGPTL4) is a secreted protein that belongs to the angiopoietin family and is involved in angiogenesis and metabolism regulation. We previously reported the induction of angptl4 by hypoxia in endothelial cells and in human ischemic tissues from peripheral artery disease. We here observed in a mouse model of hindlimb ischemia that the mRNA upregulation in the vessels correlates with the accumulation of the full-length protein in ischemic tissues. We then investigated its functions in endothelial cells. In response to hypoxia, endogenous ANGPTL4 accumulates in the subendothelial extracellular matrix (ECM). Although the secreted protein undergoes proteolysis leading to truncated fragments present in the medium, only full-length ANGPTL4 interacts with the ECM. Competition and direct binding assays indicate that the strong interaction of ANGPTL4 with the ECM is heparin/heparan sulfate proteoglycan dependent. The balance between matrix-associated and soluble forms of ANGPTL4 points to the role of the ECM in the regulation of its bioavailability. The angiogenic function of the ECM-bound full-length protein was investigated using either the form associated with the conditioned ECM from ANGPTL4-transfected HEK293 cells or the purified immobilized protein. We show that matrix-associated and immobilized ANGPTL4 limit the formation of actin stress fibers and focal contacts in the adhering endothelial cells and inhibit their adhesion. Immobilized ANGPTL4 also decreases motility of endothelial cells and inhibits the sprouting and tube formation. Altogether, these findings show that hypoxic endothelial cells accumulate ANGPTL4 in the ECM, which in turn negatively regulates their angiogenic capacities through an autocrine pathway. Key Words: extracellular matrix Ⅲ endothelial cells Ⅲ angiogenesis Ⅲ hypoxia C ardiovascular disorders such as coronary and peripheral artery diseases lead to a deficient blood supply to tissues and a decrease in oxygen partial pressure, ie, hypoxia. Because of their location at the interface of circulating blood and peripheral tissues, endothelial cells are exposed to hypoxia. A critical adaptation to hypoxia is angiogenesis, which consists in the formation of new blood vessels extending from the preexisting vasculature. 1 This phenomenon occurs through the activation of the endothelial cells by a multistep process including changes of cell/extracellular matrix (ECM) interactions. In ischemic cardiovascular pathologies, reactive angiogenesis is a beneficial event. Therefore, unraveling the interplay of multiple molecular signals and events that occur in hypoxia and lead to functional new blood vessels is a challenging issue.We previously identified angiopoietin-like 4 gene (angptl4) as a hypoxia-induced target in vitro in the human microvascular endothelial cell line (HMEC-1) and in vivo in the vessels of ischemic tissues from peripheral artery disease. 2 Human ANGPTL4 is a secreted glycoprotein that belongs to the angiopoietin family. 3 It is composed of 406 amino acids...

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Cooperative interaction of Angiopoietin-like proteins 1 and 2 in zebrafish vascular development

Cited by 92 publications

References 34 publications

Angiopoietin-like 4 prevents metastasis through inhibition of vascular permeability and tumor cell motility and invasiveness

Angiopoietin-like 4 prevents metastasis through inhibition of vascular permeability and tumor cell motility and invasiveness

Analysis of axis induction mutant embryos reveals morphogenetic events associated with zebrafish yolk extension formation

Extracellular Matrix–Bound Angiopoietin-Like 4 Inhibits Endothelial Cell Adhesion, Migration, and Sprouting and Alters Actin Cytoskeleton

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