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

2007 ◽  
Vol 293 (4) ◽  
pp. C1272-C1277 ◽  
Author(s):  
Mario Barac-Nieto ◽  
Edward J. Weinman ◽  
Adrian Spitzer
Keyword(s):  
Phosphate Transport ◽  
Proximal Tubules ◽  
Opossum Kidney ◽  
Ok Cells ◽  
Cell Matrix ◽  
Matrix Interactions ◽  
Enhanced Expression ◽  
Altered Cell ◽  
Cell Matrix Interactions ◽  
Induced Changes

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

scholarly journals Proximal Tubular Epithelial Cell Integrins Respond to High Glucose by Altered Cell-Matrix Interactions and Differentially Regulate Matrixin Expression

2002 ◽  
Vol 82 (8) ◽  
pp. 1081-1093 ◽  
Author(s):  
Panagiotis M Karamessinis ◽  
Athina K Tzinia ◽  
Paraskevi V Kitsiou ◽  
William G Stetler-Stevenson ◽  
Alfred F Michael ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
High Glucose ◽  
Tubular Epithelial Cell ◽  
Proximal Tubular Epithelial Cell ◽  
Cell Matrix ◽  
Matrix Interactions ◽  
Proximal Tubular ◽  
Altered Cell ◽  
Cell Matrix Interactions

scholarly journals Altered cell–cell and cell–matrix interactions in the development of systemic autoimmunity

Autoimmunity ◽  
2009 ◽  
Vol 42 (4) ◽  
pp. 278-281 ◽  
Author(s):  
Angelika Antoni ◽  
Lee H. Graham ◽  
Joyce Rauch ◽  
Jerrold S. Levine
Keyword(s):  
Cell Matrix ◽  
Systemic Autoimmunity ◽  
Matrix Interactions ◽  
Altered Cell ◽  
Cell Matrix Interactions ◽  
Cell Cell

Use of F9 teratocarcinoma STEM cells to study cell-matrix interactions in the early mouse embryo

1992 ◽  
Vol 50 (1) ◽  
pp. 602-603
Author(s):  
Marc Lenburg ◽  
Rulang Jiang ◽  
Lengya Cheng ◽  
Laura Grabel
Keyword(s):  
Mouse Embryo ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Cell Types ◽  
Embryoid Bodies ◽  
F9 Cells ◽  
Cell Matrix ◽  
Matrix Interactions ◽  
Cell Matrix Interactions ◽  
F9 Teratocarcinoma

We are interested in defining the cell-cell and cell-matrix interactions that help direct the differentiation of extraembryonic endoderm in the peri-implantation mouse embryo. At the blastocyst stage the mouse embryo consists of an outer layer of trophectoderm surrounding the fluid-filled blastocoel cavity and an eccentrically located inner cell mass. On the free surface of the inner cell mass, facing the blastocoel cavity, a layer of primitive endoderm forms. Primitive endoderm then generates two distinct cell types; parietal endoderm (PE) which migrates along the inner surface of the trophectoderm and secretes large amounts of basement membrane components as well as tissue-type plasminogen activator (tPA), and visceral endoderm (VE), a columnar epithelial layer characterized by tight junctions, microvilli, and the synthesis and secretion of α-fetoprotein. As these events occur after implantation, we have turned to the F9 teratocarcinoma system as an in vitro model for examining the differentiation of these cell types. When F9 cells are treated in monolayer with retinoic acid plus cyclic-AMP, they differentiate into PE. In contrast, when F9 cells are treated in suspension with retinoic acid, they form embryoid bodies (EBs) which consist of an outer layer of VE and an inner core of undifferentiated stem cells. In addition, we have established that when VE containing embryoid bodies are plated on a fibronectin coated substrate, PE migrates onto the matrix and this interaction is inhibited by RGDS as well as antibodies directed against the β1 integrin subunit. This transition is accompanied by a significant increase in the level of tPA in the PE cells. Thus, the outgrowth system provides a spatially appropriate model for studying the differentiation and migration of PE from a VE precursor.

Cell matrix interactions in asthma

1997 ◽  
Vol 27 (1) ◽  
pp. 22-27
Author(s):  
K. GOLDRING ◽  
J. A. WARNER
Keyword(s):  
Cell Matrix ◽  
Matrix Interactions ◽  
Cell Matrix Interactions

scholarly journals A computational framework for modeling cell–matrix interactions in soft biological tissues

2021 ◽  
Author(s):  
Jonas F. Eichinger ◽  
Maximilian J. Grill ◽  
Iman Davoodi Kermani ◽  
Roland C. Aydin ◽  
Wolfgang A. Wall ◽  
...  
Keyword(s):  
Soft Tissues ◽  
Three Dimensional ◽  
Biological Tissues ◽  
Computational Framework ◽  
Cell Matrix ◽  
Physiological Processes ◽  
Matrix Interactions ◽  
Mechanical Homeostasis ◽  
Cell Matrix Interactions ◽  
Short Time

AbstractLiving soft tissues appear to promote the development and maintenance of a preferred mechanical state within a defined tolerance around a so-called set point. This phenomenon is often referred to as mechanical homeostasis. In contradiction to the prominent role of mechanical homeostasis in various (patho)physiological processes, its underlying micromechanical mechanisms acting on the level of individual cells and fibers remain poorly understood, especially how these mechanisms on the microscale lead to what we macroscopically call mechanical homeostasis. Here, we present a novel computational framework based on the finite element method that is constructed bottom up, that is, it models key mechanobiological mechanisms such as actin cytoskeleton contraction and molecular clutch behavior of individual cells interacting with a reconstructed three-dimensional extracellular fiber matrix. The framework reproduces many experimental observations regarding mechanical homeostasis on short time scales (hours), in which the deposition and degradation of extracellular matrix can largely be neglected. This model can serve as a systematic tool for future in silico studies of the origin of the numerous still unexplained experimental observations about mechanical homeostasis.

Osteoblast-derived acetylcholinesterase: a novel mediator of cell-matrix interactions in bone?

Bone ◽  
1999 ◽  
Vol 24 (4) ◽  
pp. 297-303 ◽  
Author(s):  
P.G Genever ◽  
M.A Birch ◽  
E Brown ◽  
T.M Skerry
Keyword(s):  
Cell Matrix ◽  
Matrix Interactions ◽  
Cell Matrix Interactions

A dual mechanism for regulation of kidney phosphate transport by parathyroid hormone

1987 ◽  
Vol 253 (2) ◽  
pp. E221-E227 ◽  
Author(s):  
J. A. Cole ◽  
S. L. Eber ◽  
R. E. Poelling ◽  
P. K. Thorne ◽  
L. R. Forte
Keyword(s):  
Protein Kinase C ◽  
Parathyroid Hormone ◽  
Protein Kinase ◽  
Phorbol Esters ◽  
Rank Order ◽  
Phosphate Transport ◽  
Opossum Kidney ◽  
Ok Cells ◽  
Kinase C ◽  
Camp Formation

Regulation of phosphate transport by parathyroid hormone (PTH) was investigated in continuous lines of kidney cells. Phosphate transport was reduced by PTH-(1-34) at physiological concentrations (EC50 5 X 10(-11) M), whereas much higher concentrations were required to stimulate cAMP formation (EC50 1 X 10(-8) M) in opossum kidney (OK) cells. The PTH analogue [Nle]PTH-(3-34) also inhibited phosphate transport but did not enhance cAMP formation. Instead, [Nle]PTH-(3-34) was a competitive antagonist of PTH-(1-34) at cyclase-coupled receptors. PTH-(7-34) had no effect on phosphate transport or cAMP formation. Phorbol esters or mezerein were potent inhibitors of phosphate transport but did not affect cAMP synthesis. Their potencies paralleled the rank-order potency of these agents as activators of protein kinase c in other systems. Maximally effective concentrations of PTH-(1-34) and mezerein did not produce additive inhibition of phosphate transport in OK cells. Phorbol esters stimulated phosphate transport in JTC-12 cells, but PTH-(1-34) had no effect. We concluded that PTH regulates OK cell phosphate transport by interacting with two classes of receptors, and transmembrane-signaling mechanisms. Physiological levels of PTH-(1-34) may regulate phosphate transport by activation of protein kinase c, whereas higher concentrations appear to activate adenylate cyclase.

Sign in / Sign up

Export Citation Format

Share Document