The Iowa Homemaker vol.3, no.4-5

Table of Contents We “Do Over” Our Rooms by Irma Camp and Alice Dodge, page 1 The Mysteries of Amateur Make Up by Frederica Shattuck, page 2 Fall Time Is Pickling Time by Katherine Howells, page 4 Episodes Concerning Evolution of Home Economics by Ruth Elaine Wilson, page 5 Tea – Suggestive of the Rainbow by Esther Ellen Rayburn, page 6 Vary the Vegetable by Blanche Ingersoll, page 7 Constipation and Its Dangers by Anne Mundt, page 8 Graduate Credit Conference for Vocational Home Economics at Iowa State by Eleanor Murray, page 9 Fish That Is Appetizing by Maxine Smith, page 9 Economy, Or a Wrong Idea by Harriett Wallace, page 1

Cytokines regulate the affinity of soluble CD44 for hyaluronan

AbstractCD44, a receptor for the extracellular matrix glycosaminoglycan hyaluronan, has been implicated in many adhesion-dependent cellular processes including tumor growth and metastasis. Soluble CD44 has been identified in the serum of normal individuals. Furthermore, tumor progression is often associated with marked increases in plasma levels of soluble CD44. Release of soluble CD44 by proteolytic cleavage (shedding) of membrane-anchored CD44 is likely to alter cellular responses to the environment due to modification of the cell surface and the potential for soluble CD44 to influence CD44-mediated hyaluronan binding to cell surfaces. Cellular activation is typically required to induce hyaluronan binding to cell surface CD44 but the affinity of endogenous soluble CD44 for hyaluronan remains unknown. In this study, we demonstrate that oncostatin M and transforming growth factor β1 (TGF-β1) which stimulate hyaluronan binding to HTB58 lung epithelial-derived tumor cells, also induce the release of soluble CD44. Interestingly, soluble CD44 released by oncostatin M-treated cells retained the ligand-binding properties of the membrane-anchored receptor. In contrast, soluble CD44 released from TGF-β1-treated HTB58 cells differed in its hyaluronan-binding capacity from cell surface CD44 expressed on TGF-β1-stimulated cells. These data indicate that the mechanisms that regulate the generation of soluble CD44 may also govern the binding of the released receptor to hyaluronan and therefore determine the impact on CD44-dependent physiologic and pathologic processes