Defective blood vessel development and pericyte/pvSMC distribution in alpha 4 integrin-deficient mouse embryos
Blood vessel development is in part regulated by pericytes/presumptive vascular smooth muscle cells (PC/pvSMCs). Here, we demonstrate that interactions between PC/pvSMCs and extracellular matrix play a critical role in this event. We show that the cranial vessels in alpha4 integrin-deficient mouse e...
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| Veröffentlicht in: | Developmental biology 2006-05, Vol.293 (1), p.165-177 |
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| creator | Grazioli, Alison Alves, Christina S Konstantopoulos, Konstantinos Yang, Joy T |
| description | Blood vessel development is in part regulated by pericytes/presumptive vascular smooth muscle cells (PC/pvSMCs). Here, we demonstrate that interactions between PC/pvSMCs and extracellular matrix play a critical role in this event. We show that the cranial vessels in alpha4 integrin-deficient mouse embryos at the stage of vessel remodeling are increased in diameter. This defect is accompanied by a failure of PC/pvSMCs, which normally express alpha4beta1 integrin, to spread uniformly along the vessels. We also find that fibronectin but not VCAM-1 is localized in the cranial vessels at this stage. Furthermore, cultured alpha4 integrin-null PC/pvSMCs plated on fibronectin display a delay in initiating migration, a reduction in migration speed, and a decrease in directional persistence in response to a polarized force of shear flow. These results suggest that specific motile activities of PC/pvSMCs regulated by mechanical signals imposed by the interstitial extracellular matrix may also be required in vivo for the distribution and function of the PC/pvSMCs during blood vessel development. |
| doi_str_mv | 10.1016/j.ydbio.2006.01.026 |
| format | Article |
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Here, we demonstrate that interactions between PC/pvSMCs and extracellular matrix play a critical role in this event. We show that the cranial vessels in alpha4 integrin-deficient mouse embryos at the stage of vessel remodeling are increased in diameter. This defect is accompanied by a failure of PC/pvSMCs, which normally express alpha4beta1 integrin, to spread uniformly along the vessels. We also find that fibronectin but not VCAM-1 is localized in the cranial vessels at this stage. Furthermore, cultured alpha4 integrin-null PC/pvSMCs plated on fibronectin display a delay in initiating migration, a reduction in migration speed, and a decrease in directional persistence in response to a polarized force of shear flow. These results suggest that specific motile activities of PC/pvSMCs regulated by mechanical signals imposed by the interstitial extracellular matrix may also be required in vivo for the distribution and function of the PC/pvSMCs during blood vessel development.</description><subject>Animals</subject><subject>Cell Movement - physiology</subject><subject>Cells, Cultured</subject><subject>Embryo, Mammalian</subject><subject>Fibronectins - biosynthesis</subject><subject>Fibronectins - genetics</subject><subject>Integrin alpha4 - genetics</subject><subject>Integrin alpha4 - physiology</subject><subject>Integrin alpha4beta1 - biosynthesis</subject><subject>Integrin alpha4beta1 - genetics</subject><subject>Integrin alpha4beta1 - physiology</subject><subject>Integrin beta1 - physiology</subject><subject>Mice</subject><subject>Myocytes, Smooth Muscle - physiology</subject><subject>Neovascularization, Pathologic - embryology</subject><subject>Neovascularization, Pathologic - genetics</subject><subject>Pericytes - metabolism</subject><subject>Pericytes - physiology</subject><subject>Vascular Cell Adhesion Molecule-1 - biosynthesis</subject><subject>Vascular Cell Adhesion Molecule-1 - genetics</subject><issn>0012-1606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkD1PwzAYhD2AaCn8AiTkiS3pazu1nRGVT6mIAZijOH4NrpI4xEmk_HuKgJnpbnjudDpCLhikDJhc79PZGh9SDiBTYClweUSWAIwnTIJckNMY9wAgtBYnZMHkhudKbJakvUGH1eAnpKYOwdIJY8SaWpywDl2D7UDL1tIOe1_NA6676eVpS62PQ-_NOPjQUt_Ssu4-Spod7IDvvW8Ti85X_jvdhDEixcb0c4hn5NiVdcTzX12Rt7vb1-1Dsnu-f9xe75KOKRgS4RgKjkpmkmlukDuhTGalc5I5zDXk6DjLAEoDWlrGN1oZY5zAvOJglViRq5_erg-fI8ahaHyssK7LFg97Cqm0Vpzzf0GmmMqUhAN4-QuOpkFbdL1vyn4u_q4UX-t_dw8</recordid><startdate>20060501</startdate><enddate>20060501</enddate><creator>Grazioli, Alison</creator><creator>Alves, Christina S</creator><creator>Konstantopoulos, Konstantinos</creator><creator>Yang, Joy T</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20060501</creationdate><title>Defective blood vessel development and pericyte/pvSMC distribution in alpha 4 integrin-deficient mouse embryos</title><author>Grazioli, Alison ; Alves, Christina S ; Konstantopoulos, Konstantinos ; Yang, Joy T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p170t-3f1e32e7646182be2f37b4d6ff61fe9809ef21400ab086d12587bbbf3e9c20d73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Cell Movement - physiology</topic><topic>Cells, Cultured</topic><topic>Embryo, Mammalian</topic><topic>Fibronectins - biosynthesis</topic><topic>Fibronectins - genetics</topic><topic>Integrin alpha4 - genetics</topic><topic>Integrin alpha4 - physiology</topic><topic>Integrin alpha4beta1 - biosynthesis</topic><topic>Integrin alpha4beta1 - genetics</topic><topic>Integrin alpha4beta1 - physiology</topic><topic>Integrin beta1 - physiology</topic><topic>Mice</topic><topic>Myocytes, Smooth Muscle - physiology</topic><topic>Neovascularization, Pathologic - embryology</topic><topic>Neovascularization, Pathologic - genetics</topic><topic>Pericytes - metabolism</topic><topic>Pericytes - physiology</topic><topic>Vascular Cell Adhesion Molecule-1 - biosynthesis</topic><topic>Vascular Cell Adhesion Molecule-1 - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Grazioli, Alison</creatorcontrib><creatorcontrib>Alves, Christina S</creatorcontrib><creatorcontrib>Konstantopoulos, Konstantinos</creatorcontrib><creatorcontrib>Yang, Joy T</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Developmental biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Grazioli, Alison</au><au>Alves, Christina S</au><au>Konstantopoulos, Konstantinos</au><au>Yang, Joy T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Defective blood vessel development and pericyte/pvSMC distribution in alpha 4 integrin-deficient mouse embryos</atitle><jtitle>Developmental biology</jtitle><addtitle>Dev Biol</addtitle><date>2006-05-01</date><risdate>2006</risdate><volume>293</volume><issue>1</issue><spage>165</spage><epage>177</epage><pages>165-177</pages><issn>0012-1606</issn><abstract>Blood vessel development is in part regulated by pericytes/presumptive vascular smooth muscle cells (PC/pvSMCs). Here, we demonstrate that interactions between PC/pvSMCs and extracellular matrix play a critical role in this event. We show that the cranial vessels in alpha4 integrin-deficient mouse embryos at the stage of vessel remodeling are increased in diameter. This defect is accompanied by a failure of PC/pvSMCs, which normally express alpha4beta1 integrin, to spread uniformly along the vessels. We also find that fibronectin but not VCAM-1 is localized in the cranial vessels at this stage. Furthermore, cultured alpha4 integrin-null PC/pvSMCs plated on fibronectin display a delay in initiating migration, a reduction in migration speed, and a decrease in directional persistence in response to a polarized force of shear flow. These results suggest that specific motile activities of PC/pvSMCs regulated by mechanical signals imposed by the interstitial extracellular matrix may also be required in vivo for the distribution and function of the PC/pvSMCs during blood vessel development.</abstract><cop>United States</cop><pmid>16529735</pmid><doi>10.1016/j.ydbio.2006.01.026</doi><tpages>13</tpages></addata></record> |
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| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; ScienceDirect Journals (5 years ago - present) |
| subjects | Animals Cell Movement - physiology Cells, Cultured Embryo, Mammalian Fibronectins - biosynthesis Fibronectins - genetics Integrin alpha4 - genetics Integrin alpha4 - physiology Integrin alpha4beta1 - biosynthesis Integrin alpha4beta1 - genetics Integrin alpha4beta1 - physiology Integrin beta1 - physiology Mice Myocytes, Smooth Muscle - physiology Neovascularization, Pathologic - embryology Neovascularization, Pathologic - genetics Pericytes - metabolism Pericytes - physiology Vascular Cell Adhesion Molecule-1 - biosynthesis Vascular Cell Adhesion Molecule-1 - genetics |
| title | Defective blood vessel development and pericyte/pvSMC distribution in alpha 4 integrin-deficient mouse embryos |
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