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Bcl-2 expression modulates cell adhesion and migration promoting branching of ureteric bud cells.

Bcl-2 expression modulates cell adhesion and migration promoting branching of ureteric bud cells. Research Abstract Details 

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  • Bcl-2 expression modulates cell adhesion and migration promoting branching of ureteric bud cells. Abstract Text:

    nader sheibaniNader Sheibani,elizabeth a scheefElizabeth A Scheef,terri a dimaioTerri A Dimaio,yongji wangYongji Wang,shuji kondoShuji Kondo,christine m sorensonChristine M Sorenson,

    Bcl-2 is the founding member of a family of proteins that influence apoptosis. During kidney development bcl-2 not only acts as a survival factor, but may also impact cell adhesive mechanisms and by extension branching morphogenesis. The interrelationship between cell adhesion, migration and apoptosis, important during development, is poorly understood. Here we examined the impact lack of bcl-2, an inhibitor of apoptosis, has on ureteric bud (UB) cell adhesion, migration, and branching morphogenesis. Bcl-2 -/- UB cells demonstrated increased cell migration, increased cell invasion and decreased adhesion to vitronectin and fibronectin compared with wild-type cells. Bcl-2 +/+ UB cells readily branched in collagen gel and Matrigel while bcl-2 -/- UB cells did not undergo significant branching in either matrix. Re-expression of bcl-2 in bcl-2 -/- UB cells restored their ability to undergo branching morphogenesis in Matrigel. Consistent with our in vitro data, we show that in the absence of bcl-2, embryonic kidneys undergo decreased UB branching. We observed decreased numbers of UB branch points, UB branch tips and a decreased distance to the first UB branch point in the absence of bcl-2. The alterations in bcl-2 -/- UB cell adhesion and migration was also associated with a significant alteration in expression of a number of extracellular matrix proteins. Bcl-2 -/- UB cells exhibited increased fibronectin expression and decreased thrombospondin-1 and osteopontin expression. Taken together, these data suggest that bcl-2 is required for the proper regulation of cell adhesive and migratory mechanisms, perhaps through modulation of the cellular microenvironment.

    Bcl-2 expression modulates cell adhesion and migration promoting branching of ureteric bud cells. Publishing Authors By Initials

    n sheibaniN Sheibani,ea scheefEA Scheef,ta dimaioTA Dimaio,y wangY Wang,s kondoS Kondo,cm sorensonCM Sorenson,

    For similar urogenital system: urinary tract: ureter research abstracts see: urogenital system: urinary tract: ureter research

    PUBMED ID PMID:

    MEDLINE DATE:

    Bcl-2 expression modulates cell adhesion and migration promoting branching of ureteric bud cells. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of cellular physiology

    VOLUME: 210

    Page Numbers: 616-25

    Journal Abbreviation: J. Cell. Physiol.

    ISSN: 0021-9541

    DAY: 3

    MONTH: Mar

    YEAR: 2007

    Bcl-2 expression modulates cell adhesion and migration promoting branching of ureteric bud cells. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 50222

    Bcl-2 expression modulates cell adhesion and migration promoting branching of ureteric bud cells. Keywords Mesh Terms:

    KEYWORDS: Ureter

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Bcl-2 expression modulates cell adhesion and migration promoting branching of ureteric bud cells. Information

    Substance Name: Collagen

    Registry Number: 9007-34-5

    Grant and Affiliation Information for Bcl-2 expression modulates cell adhesion and migration promoting branching of ureteric bud cells.

    AFFILIATION: Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NEI

    GRANT: EY13700

    ACRONYM: EY

    MEDLINETA: J Cell Physiol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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