Real-time monitoring of cell migration, phagocytosis and cell surface receptor dynamics using a novel, live-cell opto-microfluidic technique

2015 ◽  
Vol 872 ◽  
pp. 95-99 ◽  
Author(s):  
Gregor S. Kijanka ◽  
Ivan K. Dimov ◽  
Robert Burger ◽  
Jens Ducrée
Keyword(s):  
Cell Migration ◽  
Cell Surface ◽  
Real Time ◽  
Live Cell ◽  
Cell Surface Receptor ◽  
Real Time Monitoring ◽  
Receptor Dynamics ◽  
Surface Receptor ◽  
Microfluidic Technique

Analysis of Cell-Surface Receptor Dynamics through Covalent Labeling by Catalyst-Tethered Antibody

2015 ◽  
Vol 137 (16) ◽  
pp. 5372-5380 ◽  
Author(s):  
Takahiro Hayashi ◽  
Yuki Yasueda ◽  
Tomonori Tamura ◽  
Yousuke Takaoka ◽  
Itaru Hamachi
Keyword(s):  
Cell Surface ◽  
Cell Surface Receptor ◽  
Covalent Labeling ◽  
Receptor Dynamics ◽  
Surface Receptor

scholarly journals Sphingosine 1-Phosphate Stimulates Cell Migration through a Gi-coupled Cell Surface Receptor

1999 ◽  
Vol 274 (50) ◽  
pp. 35343-35350 ◽  
Author(s):  
Fang Wang ◽  
James R. Van Brocklyn ◽  
John P. Hobson ◽  
Sharareh Movafagh ◽  
Zofia Zukowska-Grojec ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Surface ◽  
Cell Surface Receptor ◽  
Sphingosine 1 Phosphate ◽  
Surface Receptor

scholarly journals CD44H regulates tumor cell migration on hyaluronate-coated substrate.

1992 ◽  
Vol 118 (4) ◽  
pp. 971-977 ◽  
Author(s):  
L Thomas ◽  
H R Byers ◽  
J Vink ◽  
I Stamenkovic
Keyword(s):  
Cell Migration ◽  
Cell Surface ◽  
Binding Capacity ◽  
Surface Glycoprotein ◽  
Cell Surface Receptor ◽  
Cell Surface Glycoprotein ◽  
Tumor Cell Migration ◽  
Coated Substrate ◽  
Direct Demonstration ◽  
Surface Receptor

CD44 is a broadly distributed cell surface glycoprotein expressed in different isoforms in various tissues and cell lines. One of two recently characterized human isoforms, CD44H, is a cell surface receptor for hyaluronate, suggesting a role in the regulation of cell-cell and cell-substrate interactions as well as of cell migration. While CD44H has been shown to mediate cell adhesion, direct demonstration that CD44H expression promotes cell motility has been lacking. In this work we show that a human melanoma cell line, stably transfected with CD44H, displays enhanced motility on hyaluronate-coated surfaces while transfectants expressing an isoform that does not bind hyaluronate, CD44E, fail to do so. Migration of CD44H-expressing transfectants is observed to be blocked by a soluble CD44-immunoglobulin fusion protein as well as by anti-CD44 antibody, and to depend on the presence of the cytoplasmic domain of CD44. However, cells expressing CD44H cytoplasmic deletion mutants retain significant binding capacity to hyaluronate-coated substrate. Taken together, our results provide direct evidence that CD44H plays a major role in regulating cell migration on hyaluronate-coated substrate.

Altered cell surface receptor dynamics and circulatory occurrence of neutrophils in a small animal fracture model

2020 ◽  
Vol 216 (10) ◽  
pp. 153108
Author(s):  
Michel P.J. Teuben ◽  
Martijn Hofman ◽  
Johannes Greven ◽  
Alba Shehu ◽  
Henrik Teuber ◽  
...  
Keyword(s):  
Cell Surface ◽  
Small Animal ◽  
Cell Surface Receptor ◽  
Fracture Model ◽  
Receptor Dynamics ◽  
Surface Receptor ◽  
Altered Cell

scholarly journals Mitogenesis, cell migration, and loss of focal adhesions induced by tenascin-C interacting with its cell surface receptor, annexin II.

1996 ◽  
Vol 7 (6) ◽  
pp. 883-892 ◽  
Author(s):  
C Y Chung ◽  
J E Murphy-Ullrich ◽  
H P Erickson
Keyword(s):  
Endothelial Cells ◽  
Cell Migration ◽  
Cell Surface ◽  
Focal Adhesions ◽  
Cell Surface Receptor ◽  
Annexin Ii ◽  
Tenascin C ◽  
Subsequent Response ◽  
Surface Receptor ◽  
A Cell

In a previous study we demonstrated that the alternatively spliced region of tenascin-C, TNfnA-D, bound with high affinity to a cell surface receptor, annexin II. In the present study we demonstrate three changes in cellular activity that are produced by adding intact tenascin-C or TNfnA-D to cells, and we show that all three activities are blocked by antibodies against annexin II. 1) TNfnA-D added to confluent endothelial cells induced loss of focal adhesions. 2) TNfnA-D produced a mitogenic response of confluent, growth-arrested endothelial cells in 1% serum. TNfnA-D stimulated mitogenesis only when it was added to cells before or during exposure to other mitogens, such as basic fibroblast growth factor or serum. Thus the effect of TNfnA-D seems to be to facilitate the subsequent response to growth factors. 3) TNfnA-D enhanced cell migration in a cell culture wound assay. Antibodies to annexin II blocked all three cellular responses to TNfnA-D. These data show that annexin II receptors on endothelial cells mediate several cell regulatory functions attributed to tenascin-C, potentially through modulation of intracellular signalling pathways.

Expression, function, and localization of the REG cell surface receptor

2001 ◽  
Vol 120 (5) ◽  
pp. A18-A19
Author(s):  
B DIECKGRAEFE ◽  
C HOUCHEN ◽  
H ZHANG
Keyword(s):  
Cell Surface ◽  
Cell Surface Receptor ◽  
Surface Receptor

Inhibition of rat ventricular automaticity by adenosine

1985 ◽  
Vol 248 (6) ◽  
pp. H907-H913 ◽  
Author(s):  
L. J. Heller ◽  
R. A. Olsson
Keyword(s):  
Cell Surface ◽  
Cell Surface Receptor ◽  
Chronotropic Effect ◽  
Surface Receptors ◽  
Adenosine Concentration ◽  
Surface Receptor ◽  
Ventricular Automaticity ◽  
Beating Rate ◽  
Chronotropic Effects ◽  
Developed Pressure

This study was designed to characterize adenosine's negative chronotropic effect on ventricular pacemakers. The spontaneous beating rate of isolated, isovolumic rat ventricular preparations perfused with Krebs-Henseleit solution decreased as the adenosine concentration was increased [log M effective concentration 50% (EC50) = -5.22 +/- 0.17]. The lack of effect of propranolol or atropine on this adenosine response eliminates the involvement of endogenous neurotransmitters. Support for the involvement of an external cell surface receptor was provided by findings that theophylline and 8-(4-sulfophenyl)theophylline, an analogue thought to act solely at the cell surface, significantly increased the adenosine log M EC50 to -3.94 +/- 0.22 and -3.61 +/- 0.22, respectively. An increase in spontaneous beating rate induced by theophylline, but not by its analogue, was blocked by the addition of propranolol. The relative chronotropic potency of the adenosine analogues R-PIA, S-PIA, and NECA suggests that the cell surface receptors may be of the Ri type. The negative chronotropic effects of adenosine and its analogues occurred at concentrations that had no effect on the developed pressure of the paced preparation. Electrocardiographic evaluations indicate that at high agonist concentrations, there was an abrupt alteration in electrical properties of the preparation, which could be blocked by theophylline and its analogue.

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