Mononuclear Leukocytes Preferentially Bind via CD44 to Hyaluronan on Human Intestinal Mucosal Smooth Muscle Cells after Virus Infection or Treatment with Poly(I·C)

Motte, Carol A. de la; Hascall, Vincent C.; Calabro, Anthony; Yen‐Lieberman, Belinda; Strong, Scott A.

doi:10.1074/jbc.274.43.30747

Cited by 184 publications

(253 citation statements)

References 56 publications

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“…It has been suggested that this may be proinflammatory, with the cables acting as distress signals that might perpetuate chronic inflammation [45]. Others have suggested that the cables could be anti-inflammatory and control leukocyte activation by preventing adhesion through ICAM-1 [48], VCAM-1 or VLA-4 [49], or by preventing loss of matrix [32,47].…”

Section: Hyaluronan Crosslinkingmentioning

confidence: 99%

Hyaluronan-dependent pericellular matrix☆

Evanko¹,

Tammi²,

Tammi³

et al. 2007

Advanced Drug Delivery Reviews

259

238

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Hyaluronan is a multifunctional glycosaminoglycan that forms the structural basis of the pericellular matrix. Hyaluronan is extruded directly through the plasma membrane by one of three hyaluronan synthases and anchored to the cell surface by the synthase or cell surface receptors such as CD44 or RHAMM. Aggregating proteoglycans and other hyaluronan-binding proteins, contribute to the material and biological properties of the matrix and regulate cell and tissue function. The pericellular matrix plays multiple complex roles in cell adhesion/de-adhesion, and cell shape changes associated with proliferation and locomotion. Time-lapse studies show that pericellular matrix formation facilitates cell detachment and mitotic cell rounding. Hyaluronan crosslinking occurs through various proteins, such as tenascin, TSG-6, inter-alpha-trypsin inhibitor, pentraxin and TSP-1. This creates higher order levels of structured hyaluronan that may regulate inflammation and other biological processes. Microvillous or filopodial membrane protrusions are created by active hyaluronan synthesis, and form the scaffold of hyaluronan coats in certain cells. The importance of the pericellular matrix in cellular mechanotransduction and the response to mechanical strain are also discussed.

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Section: Hyaluronan Crosslinkingmentioning

confidence: 99%

Hyaluronan-dependent pericellular matrix☆

Evanko¹,

Tammi²,

Tammi³

et al. 2007

Advanced Drug Delivery Reviews

259

238

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“…Assay for Monocyte Adhesion (11,27)-RMCs in 6-well plates were treated up to 72 h with 10% FBS and concentrations of 5.6 -25.6 mM D-glucose. After washing gently three times with cold medium, U937 monocytes (1 ml, 5 ϫ 10 6 cells/ml) were added to the cultures and then incubated at 4°C for 1 h. The cultures were then washed by placing 1 ml of cold medium gently onto the cultures, followed by rocking 3-5 times and aspirating from the side.…”

Section: Establishment Of Rmc Cultures and Induction Of Diabetes In Rmentioning

confidence: 99%

“…Previously, we showed that monocytes preferentially bind, by means of a mechanism that involves CD44, to hyaluronan cable-like structures synthesized by smooth muscle cells isolated from human intestinal mucosa, after they have been treated with a virus or with the viral mimetic, poly I:C (a synthetic double-stranded RNA) (11,12). This indicates that structures based on hyaluronan can mediate the adhesion of monocytes to resident cells.…”

mentioning

confidence: 95%

Hyaluronan Structures Synthesized by Rat Mesangial Cells in Response to Hyperglycemia Induce Monocyte Adhesion

Ai-min

Hascall

2004

Journal of Biological Chemistry

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128

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Mesangial expansion, the principal glomerular lesion in diabetic nephropathy, is preceded by a phenotypic activation and transient proliferation of the glomerular mesangial cells and by a prominent glomerular infiltration of monocytes and macrophages. Because this infiltration seems to play a key role in the subsequent mesangial matrix expansion, we tested the response of cultures of rat mesangial cells (RMCs) for monocyte adhesion in response to hyperglycemia. Increasing the medium glucose concentration from 5.6 mM (normal) to 25.6 mM (hyperglycemic) significantly increased hyaluronan in the cell matrix, with a concurrent 3-to 4-fold increase in adhesion of U937 monocytic leukemic cells to cultures of near confluent RMCs. These responses were attributed directly to the high glucose concentration and not to increased extracellular osmolality. The monocytes primarily bind directly to hyaluronan-based structures in vitro. Abnormal deposits of hyaluronan were found in glomeruli of kidney sections from diabetic rats 1 week after streptozotocin treatment, often with closely associated monocytes/macrophages, suggesting that similar structures are relevant in vivo. The monocyte adhesion response to high glucose concentration required growth stimulation of RMCs by serum and activation of protein kinase C, and was inhibited by prior passage of the RMCs in the presence of heparin. These results suggest that the response may be cell growth state and protein kinase C-dependent. When incubated with the viral mimetic, poly I:C, in the presence of normal glucose, heparin-passaged RMCs still increased cell-associated hyaluronan and exhibited hyaluronan-mediated adhesion of monocytes, indicating that the two stimuli, high glucose and viral mimetic, induce the production of the hyaluronan structures that promote monocyte adhesion by distinctly different intracellular signaling mechanisms.Mesangial expansion, the principal glomerular lesion in diabetic nephropathy, reduces the area for filtration and leads eventually to sclerosis and renal failure (1, 2). However, the expansion of the mesangial extracellular matrix (ECM) 1 and the sclerosis that characterize diabetic nephropathy are preceded by a phenotypic activation and transient proliferation of the glomerular mesangial cells. This is followed by a prominent glomerular infiltration of monocytes and macrophages (3-5) that seems to play a key role in the subsequent mesangial matrix expansion, hypercellularity, and onset of proteinuria (6, 7). Nevertheless, the molecular mechanisms underlying glomerular infiltration by monocytes and macrophages are still unclear.The interaction of monocytes with mesangial cells in culture has been studied previously using U937 cells, a monocytic leukemic cell line that is a widely accepted model for monocyte adhesion (7,8), and mesangial cell cultures incubated in media with high glucose concentrations bind more U937 cells (7). Generally, the interactions between monocytes and resident cells involve: (i) monocyte cell surface proteins, including C...

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“…U937 cell adhesion was measured as described previously (24). Briefly, HK-2 cells were grown on 24-well culture plates until confluent.…”

Section: Assay For Leukocyte Adhesionmentioning

confidence: 99%

BMP-7 Modulates Hyaluronan-Mediated Proximal Tubular Cell-Monocyte Interaction

Selbi¹,

Motte²,

Hascall³

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Increased synthesis of hyaluronan (HA) in the renal corticointerstitium has been documented in renal injury, although the functional significance of this is unclear. The aim of the work presented in the current study was to examine the role of HA in monocyte binding by proximal tubular cells (PTC). Using the PTC line HK-2, the authors show that unstimulated cells formed pericellular HA cable-like structures that bound mononuclear leukocytes via their cell surface CD44. Stimulation with bone morphogenic protein-7 (BMP-7) led to increased formation of HA cable-like structures and also a dosedependent increase in CD44-dependent binding of radiolabeled

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Mononuclear Leukocytes Preferentially Bind via CD44 to Hyaluronan on Human Intestinal Mucosal Smooth Muscle Cells after Virus Infection or Treatment with Poly(I·C)

Cited by 184 publications

References 56 publications

Hyaluronan-dependent pericellular matrix☆

Hyaluronan-dependent pericellular matrix☆

Hyaluronan Structures Synthesized by Rat Mesangial Cells in Response to Hyperglycemia Induce Monocyte Adhesion

BMP-7 Modulates Hyaluronan-Mediated Proximal Tubular Cell-Monocyte Interaction

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