| Deficiency of autotaxin/lysophospholipase D results in head cavity formation in mouse embryos through the LPA receptor-Rho-ROCK pathway. | |
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MedLine Citation:
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PMID: 20692235 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Autotaxin, encoded by the Enpp2 gene, generates lysophosphatidic acid (LPA) extracellularly, eliciting various cellular responses through specific LPA receptors. Previous studies have revealed that Enpp2(-/-) mice die at E9.5 owing to angiogenic defects in the yolk sac. Moreover, Enpp2(-/-) embryos show growth retardation, allantois malformation, no axial turning, and head cavity formation. We have also demonstrated that lysosome biogenesis is impaired in yolk sac visceral endoderm cells of Enpp2(-/-) embryos as a result of the downregulation of the Rho-ROCK (Rho-associated coiled-coil containing protein kinase)-LIM kinase pathway. In this study, we examine what signaling defect(s) is responsible for head cavity formation and yolk sac angiogenic defects. By using a whole embryo culture system, we show that 10 μM Ki16425, an antagonist for the LPA receptors, induces head cavity formation and yolk sac angiogenic defects in wild-type embryos. Moreover, 1 μM Ki16425 induces both phenotypes in Enpp2 heterozygous embryos at significantly higher incidence than in wild-type embryos, suggesting an interaction between autotaxin and LPA receptor signaling. Furthermore, we show that inhibition of the Rho-ROCK pathway induces head cavity formation, whereas multiple pathways are involved in yolk sac angiogenic defects. These results reveal the signal transduction defects that underlie the abnormalities in Enpp2(-/-) embryos. |
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Authors:
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Seiichi Koike; Kazuko Keino-Masu; Masayuki Masu |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-08-06 |
Journal Detail:
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Title: Biochemical and biophysical research communications Volume: 400 ISSN: 1090-2104 ISO Abbreviation: Biochem. Biophys. Res. Commun. Publication Date: 2010 Sep |
Date Detail:
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Created Date: 2010-09-13 Completed Date: 2010-10-11 Revised Date: 2011-11-07 |
Medline Journal Info:
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Nlm Unique ID: 0372516 Medline TA: Biochem Biophys Res Commun Country: United States |
Other Details:
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Languages: eng Pagination: 66-71 Citation Subset: IM |
Copyright Information:
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Copyright © 2010 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Molecular Neurobiology, Graduate School of Comprehensive Human Sciences, Institute of Basic Medical Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8577, Japan. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Actins
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metabolism Animals Blood Vessels / abnormalities Embryo, Mammalian / abnormalities*, metabolism Head / abnormalities* Mice Mice, Mutant Strains Multienzyme Complexes / genetics* Neovascularization, Physiologic / genetics Phosphodiesterase I / genetics* Phosphoric Diester Hydrolases / genetics* Pyrophosphatases / genetics* Receptors, Lysophosphatidic Acid / antagonists & inhibitors, metabolism* Rho Factor / antagonists & inhibitors, metabolism* Signal Transduction / genetics Yolk Sac / abnormalities, blood supply rho-Associated Kinases / antagonists & inhibitors, metabolism* |
| Chemical | |
Reg. No./Substance:
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0/Actins; 0/Multienzyme Complexes; 0/Receptors, Lysophosphatidic Acid; 0/Rho Factor; EC 2.7.11.1/rho-Associated Kinases; EC 3.1.4.-/Phosphoric Diester Hydrolases; EC 3.1.4.1/Phosphodiesterase I; EC 3.1.4.39/alkylglycerophosphoethanolamine phosphodiesterase; EC 3.6.1.-/Pyrophosphatases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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