scholarly journals Development of Inflammatory Angiogenesis by Local Stimulation of Fas In Vivo

1997 ◽  
Vol 186 (1) ◽  
pp. 147-152 ◽  
Author(s):  
Luigi Biancone ◽  
Antonella De Martino ◽  
Viviana Orlandi ◽  
Pier Giulio Conaldi ◽  
Antonio Toniolo ◽  
...  
Keyword(s):  
Fas Ligand ◽  
Surrounding Tissue ◽  
Apoptotic Cells ◽  
Lymphocyte Apoptosis ◽  
Ligand Interaction ◽  
Monocytes And Macrophages ◽  
Inflammatory Angiogenesis ◽  
Local Stimulation ◽  
Stimulation Of

Fas–Fas ligand interaction is thought to be a crucial mechanism in controlling lymphocyte expansion by inducing lymphocyte apoptosis. However, Fas is also broadly expressed on nonlymphoid cells, where its function in vivo remains to be determined. In this study, we describe the development of inflammatory angiogenesis induced by agonistic anti-Fas mAb Jo2 in a murine model where Matrigel is used as a vehicle for the delivery of mediators. The subcutaneous implants in mice of Matrigel containing mAb Jo2 became rapidly infiltrated by endothelial cells and by scattered monocytes and macrophages. After formation and canalization of new vessels, marked intravascular accumulation and extravasation of neutrophils were observed. Several mast cells were also detected in the inflammatory infiltrate. The phenomenon was dose and time dependent and required the presence of heparin. The dependency on activation of Fas is suggested by the observation that the inflammatory angiogenesis was restricted to the agonistic anti-Fas mAb and it was absent in lpr Fas-mutant mice. Apoptotic cells were not detectable at any time inside the implant or in the surrounding tissue, suggesting that angiogenesis and cell infiltration did not result from recruitment of phagocytes by apoptotic cells but rather by a stimulatory signal through Fas-engagement. These findings suggest a role for Fas–Fas ligand interaction in promoting local angiogenesis and inflammation.

Role of macrophage CD44 in the disposal of inflammatory cell corpses*

2002 ◽  
Vol 103 (5) ◽  
pp. 441-449 ◽  
Author(s):  
Sharon VIVERS ◽  
Ian DRANSFIELD ◽  
Simon P. HART
Keyword(s):  
Molecular Mechanisms ◽  
Inflammatory Diseases ◽  
Surrounding Tissue ◽  
Human Macrophage ◽  
Neutrophil Granulocytes ◽  
Apoptotic Cells ◽  
Tissue Destruction

Understanding the cellular and molecular mechanisms that determine whether inflammation resolves or progresses to scarring and tissue destruction should lead to the development of effective therapeutic strategies for inflammatory diseases. Apoptosis of neutrophil granulocytes is an important determinant of the resolution of inflammation, providing a mechanism for down-regulation of function and triggering clearance by macrophages without inducing a pro-inflammatory response. However, if the rate of cell death by apoptosis is such that the macrophage clearance capacity is exceeded, apoptotic cells may progress to secondary necrosis, resulting in the release of harmful cellular contents and in damage to the surrounding tissue. There are many possible ways in which the rate and capacity of the macrophage-mediated clearance of apoptotic cells may be enhanced or suppressed. Ligation of human macrophage surface CD44 by bivalent monoclonal antibodies rapidly and profoundly augments the capacity of macrophages to phagocytose apoptotic neutrophils in vitro. The molecular mechanism behind this effect and its potential significance in vivo is a current focus of research.

scholarly journals Local stimulation of the adenosine A2Breceptors induces an increased release of IL-6 in mouse striatum: an in vivo microdialysis study

2008 ◽  
Vol 105 (3) ◽  
pp. 904-909 ◽  
Author(s):  
Juan Francisco Vazquez ◽  
Hans-Willi Clement ◽  
Olaf Sommer ◽  
Eberhard Schulz ◽  
Dietrich van Calker
Keyword(s):  
In Vivo Microdialysis ◽  
Mouse Striatum ◽  
Microdialysis Study ◽  
Local Stimulation ◽  
Stimulation Of

A physiological role for α2-HS glycoprotein: stimulation of macrophage uptake of apoptotic cells

2003 ◽  
Vol 105 (3) ◽  
pp. 267-268 ◽  
Author(s):  
Janet M. LORD
Keyword(s):  
Physiological Role ◽  
Clinical Science ◽  
Apoptotic Cells ◽  
Science Reporting ◽  
Serum Glycoprotein ◽  
Macrophage Uptake ◽  
Stimulation Of

This comment describes the study by Jersmann and co-workers in this issue of Clinical Science reporting the results of a study of the role of the serum glycoprotein fetuin in the uptake of apoptotic cells by macrophages. They show that fetuin is able to stimulate the macropinocytosis of apoptotic cells in vivo, which would be therapeutically useful following chemotherapy when the increased numbers of apoptotic cells could exceed the capacity of the macrophage network.

scholarly journals Peripheral T cells undergoing superantigen-induced apoptosis in vivo express B220 and upregulate Fas and Fas ligand.

1996 ◽  
Vol 183 (2) ◽  
pp. 431-437 ◽  
Author(s):  
T Renno ◽  
M Hahne ◽  
J Tschopp ◽  
H R MacDonald
Keyword(s):  
T Cells ◽  
Fas Ligand ◽  
Apoptotic Cell ◽  
Initial Increase ◽  
Apoptotic Cells ◽  
Peripheral T Cells ◽  
Fas L ◽  
Induced Apoptosis

Staphylococcal enterotoxin B (SEB) is a bacterial superantigen (SAg) that predominantly interacts with V(beta)8+ T cells. In vivo treatment of mice with SEB leads to an initial increase in the percentage of V(beta)8+ T cells, followed by a decrease in the numbers of these cells, eventually reaching lower levels than those found before treatment with the SAg. This decrease is due to apoptosis of the SEB-responding cells. In the present study, we use the distinct light scattering characteristics of apoptotic cells to characterize T cells that are being deleted in response to SEB in vivo. We show that dying, SEB-reactive T cells express high levels of Fas and Fas ligand (Fas-L), which are implicated in apoptotic cell death. In addition, the B cell marker B220 is upregulated on apoptotic cells. Moreover, we show that the generation of cells with an apoptotic phenotype is severely impaired in response to SEB in functional Fas-L-deficient mutant gld mice, confirming the role of the Fas pathway in SAg mediated peripheral deletion in vivo.

Limbic Gamma Rhythms. I. Phase-Locked Oscillations in Hippocampal CA1 and Subiculum

1998 ◽  
Vol 80 (1) ◽  
pp. 155-161 ◽  
Author(s):  
Simon B. Colling ◽  
Ian M. Stanford ◽  
Roger D. Traub ◽  
John G. R. Jefferys
Keyword(s):  
Receptor Antagonist ◽  
Hippocampal Slices ◽  
Gamma Oscillations ◽  
Surrounding Tissue ◽  
Tetanic Stimulation ◽  
Hippocampal Ca1 ◽  
Epileptic Discharges ◽  
Gamma Rhythms ◽  
Local Stimulation ◽  
Stimulation Of

Colling, Simon B., Ian M. Stanford, Roger D. Traub, and John G. R. Jefferys. Limbic gamma rhythms. I. Phase-locked oscillations in hippocampal CA1 and subiculum. J. Neurophysiol. 80: 155–161, 1998. Gamma oscillations (∼40 Hz) were induced in transverse hippocampal slices by tetanic stimulation of CA1 and/or subiculum. Tetanic stimulation of each site elicited population gamma oscillations in the surrounding tissue <400 μm away. Stimulation of CA1 alone could evoke activity at both CA1 and subiculum. Subicular stimulation, however, did not transmit to CA1. When the rostral end of CA1 was stimulated, gamma oscillations transmitted across <1.5 mm of silent CA1 before reappearing in the subiculum. Tetanic stimulation of CA1 increased [K+]o to 8.2 ± 1.5 mM (mean ± SE). The location of the peak increase corresponded to the site of local gamma generation. Silent areas of CA1 experienced smaller [K+]o increases, to 4.9 ± 0.7 mM. The subiculum, which generated gamma, remained at the baseline 3.0 mM. Although fluctuations in [K+]o may have an impact on the generation of gamma rhythms, they are not necessary for them. Gamma oscillations had similar frequencies in CA1 and subiculum (40.4 ± 2.9 and 43.9 ± 3.1 Hz, respectively). When present in both, the oscillations typically were phase locked with the subiculum lagging by 5.4 ± 1.8 ms. When both CA1 and subiculum were stimulated the lag decreased by 28%. These delays approximate those expected for the conduction velocity of axons between the two regions, here estimated at 0.52 ± 0.07 m/s. Transmission of gamma oscillations from CA1 to subiculum was blocked by the focal addition of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-receptor antagonist, 6-nitro-7-sulfamoylbenzo[f]quinoxaline-2,3-dione, to the subiculum. Oscillations induced in CA1 by local tetanic stimulation were blocked by focal application of the γ-aminobutyric acid-A (GABAA) receptor antagonist, bicuculline, to CA1. Focal application of bicuculline to the subiculum blocked gamma due to subicular stimulation but not that due to CA1 stimulation. Bath-applied bicuculline disrupted subicular gamma evoked by subicular stimulation and led to a transient period of epileptiform responses before completely blocking responses. The further addition of the GABAB receptor antagonist, CGP 55845A, reversed this block, restoring the epileptic discharges evoked by tetanic stimulation. This suggests that the subiculum differs from hippocampal CA3 and neocortex, in having a powerful GABAB receptor-dependent mechanism to prevent epileptic discharges. The subiculum generates gamma rhythms both in response to local stimulation and to gamma rhythms evoked in CA1. Subicular gamma differs from that in CA1 in the presence of population spike doublets rather than singlets on many cycles. In both areas, generation of gamma by local stimulation depends on GABAA receptors, suggesting that the subiculum shares the interneuronal network mechanism we proposed for CA1.

Stimulation of ovarian progesterone secretion by oxytocin in vivo

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S199-S200
Author(s):  
E. DIETRICH ◽  
K. RENTELMANN ◽  
W. WUTTKE
Keyword(s):  
Progesterone Secretion ◽  
Stimulation Of

Nanorobots Sense Local Physiochemical Heterogeneities of Tumor Matrisome

2020 ◽  
Author(s):  
Debayan Dasgupta ◽  
Dharma Pally ◽  
Deepak K. Saini ◽  
Ramray Bhat ◽  
Ambarish Ghosh
Keyword(s):  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Adhesive Force ◽  
Surrounding Tissue ◽  
Quantitative Measurements ◽  
Malignant Breast Tumor ◽  
Malignant Breast ◽  
Cancer Dissemination

The dissemination of cancer is brought about by continuous interaction of malignant cells with their surrounding tissue microenvironment. Understanding and quantifying the remodeling of local extracellular matrix (ECM) by invading cells can therefore provide fundamental insights into the dynamics of cancer dissemination. In this paper, we use an active and untethered nanomechanical tool, realized as magnetically driven nanorobots, to locally probe a 3D tissue culture microenvironment consisting of cancerous and non-cancerous epithelia, embedded within reconstituted basement membrane (rBM) matrix. Our assay is designed to mimic the in vivo histopathological milieu of a malignant breast tumor. We find that nanorobots preferentially adhere to the ECM near cancer cells: this is due to the distinct charge conditions of the cancer-remodeled ECM. Surprisingly, quantitative measurements estimate that the adhesive force increases with the metastatic ability of cancer cell lines, while the spatial extent of the remodeled ECM was measured to be approximately 40 μm for all cancer cell lines studied here. We hypothesized and experimentally confirmed that specific sialic acid linkages specific to cancer-secreted ECM may be a major contributing factor in determining this adhesive behavior. The findings reported here can lead to promising applications in cancer diagnosis, quantification of cancer aggression, in vivo drug delivery applications, and establishes the tremendous potential of magnetic nanorobots for fundamental studies of cancer biomechanics.

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