Show simple item record

dc.contributor.authorFriman, Tomasen_US
dc.contributor.authorGustafsson, Renataen_US
dc.contributor.authorStuhr, Linda Elin Birkhaugen_US
dc.contributor.authorChidiac, Jeanen_US
dc.contributor.authorHeldin, Nils-Eriken_US
dc.contributor.authorReed, Rolf K.en_US
dc.contributor.authorOldberg, Åkeen_US
dc.contributor.authorRubin, Kristoferen_US
dc.PublishedPLoS ONE 7(3): e34082eng
dc.description.abstractStroma properties affect carcinoma physiology and direct malignant cell development. Here we present data showing that αVβ3 expressed by stromal cells is involved in the control of interstitial fluid pressure (IFP), extracellular volume (ECV) and collagen scaffold architecture in experimental murine carcinoma. IFP was elevated and ECV lowered in syngeneic CT26 colon and LM3 mammary carcinomas grown in integrin β3-deficient compared to wild-type BALB/c mice. Integrin β3-deficiency had no effect on carcinoma growth rate or on vascular morphology and function. Analyses by electron microscopy of carcinomas from integrin β3-deficient mice revealed a coarser and denser collagen network compared to carcinomas in wild-type littermates. Collagen fibers were built from heterogeneous and thicker collagen fibrils in carcinomas from integrin β3-deficient mice. The fibrotic extracellular matrix (ECM) did not correlate with increased macrophage infiltration in integrin β3-deficient mice bearing CT26 tumors, indicating that the fibrotic phenotype was not mediated by increased inflammation. In conclusion, we report that integrin β3-deficiency in tumor stroma led to an elevated IFP and lowered ECV that correlated with a more fibrotic ECM, underlining the role of the collagen network for carcinoma physiology.en_US
dc.publisherPublic Library of Scienceeng
dc.rightsAttribution CC BYeng
dc.titleIncreased Fibrosis and Interstitial Fluid Pressure in Two Different Types of Syngeneic Murine Carcinoma Grown in Integrin β3-Subunit Deficient Miceen_US
dc.typePeer reviewed
dc.typeJournal article
dc.rights.holderCopyright 2012 Friman et al.

Files in this item


This item appears in the following Collection(s)

Show simple item record

Attribution CC BY
Except where otherwise noted, this item's license is described as Attribution CC BY