HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 293/4/C1272    most recent 00051.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Barac-Nieto, M. Articles by Spitzer, A. Search for Related Content PubMed PubMed Citation Articles by Barac-Nieto, M. Articles by Spitzer, A.

EXTRACELLULAR MATRIX, CELL INTERACTIONS

Cell-matrix interactions modulate transepithelial phosphate transport in P_i-deprived OK cells

¹Department of Physiology, Faculty of Medicine, Kuwait University, Kuwait; ²Department of Pediatrics, Albert Einstein College of Medicine, New York, New York; and ³Department of Medicine, University of Maryland, Baltimore, Maryland

Submitted 5 February 2006 ; accepted in final form 20 July 2007

In opossum kidney (OK) cells as well as in kidney proximal tubules, P_i depletion increases apical (A) and basolateral (B) Na⁺-dependent P_i cell influxes. In OK cells' monolayers in contrast to proximal tubules, there is no increase in transepithelial P_i transport. This limitation may be due to altered cell-matrix interactions. A and B cell ³²P_i uptakes and transepithelial ³²P_i and [¹⁴C]mannitol fluxes were measured in OK cells grown on uncoated or on Matrigel-coated filter inserts. Cells were exposed overnight to solution of either low (0.25 mM) or high (2.5 mM) P_i. When grown on Matrigel, immunofluorescence of apical NaPi4 (an isoform of the sodium-phosphate cotransporter) transporters increased and A and B ³²P_i uptakes into P_i depleted cells were five and threefold higher than in P_i replete cells (P < 0.001). P_i deprivation resulted in larger increase in A to B (4.6x, P < 0.001) than in B to A (3.5x, P < 0.001) P_i flux and net P_i transport from A to B increased 10-fold (P < 0.001). With P_i depletion increases in B to A (3.4x) and A to B (3.3x) paracellular [¹⁴C]mannitol fluxes were similar, and its net flux was opposite to that of P_i. In cells grown on uncoated filters, transepithelial and paracellular unidirectional and net P_i fluxes decreased or did not change with P_i depletion, despite twofold increases in apical and basolateral P_i cell influxes. In summary, Matrigel-OK cell interactions, particularly in P_i-depleted cells, led to enhanced expression of apical NaPi4 transporters resulting in higher P_i transport rates across cell boundaries; apical P_i readily entered the transcellular transport pool and paracellular fluxes were smaller fractions of transepithelial P_i fluxes. These Matrigel-induced changes led to an increase in net transepithelial apical to basolateral P_i transport.

renal; mineral; transport; paracellular; transcellular; cell compartments