scholarly journals The morphofunctional changes in the skin after long influence of low-scale ionizing radiation

2002 ◽  
Vol 1 (4) ◽  
pp. 32-37
Author(s):  
Ja. V. Porovsky ◽  
F. F. Tetenev

We researched musculocutaneous samples in two experimental groups, including 19 Chernobyl liquidation participants and 27 residents of the Siberian chemical combine zone, to trace the changes, which had happened in their skin after a long period of constant small-scale ionizing radiation influence. The analysis showed that the greatest changes had taken place in the epidermis of both groups in the form of thickening of horny and cellular layers and inflammatory infiltration of lymphocytes provided with the productive panvasculitis in the majority of arterioles. It is supposed, that after the long small-scale irradiation influence, in the skin develops two forms of reaction: defense reaction in the form of proliferative hyperkeratosis and immunopathological reaction, which is a consequence of activation in the cellular layer of epidermis combined with the appearance of effector section of immune answer, which stimulates the interaction of epidermal T-lymphocytes with the endothelial cells of derma vessels and participation of blood vessels of microcircular channel.

Nature ◽  
1978 ◽  
Vol 271 (5642) ◽  
pp. 246-248 ◽  
Author(s):  
H. R. CARNE ◽  
ELEANOR O. ONON

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Maria I. Alvarez-Vergara ◽  
Alicia E. Rosales-Nieves ◽  
Rosana March-Diaz ◽  
Guiomar Rodriguez-Perinan ◽  
Nieves Lara-Ureña ◽  
...  

AbstractThe human Alzheimer’s disease (AD) brain accumulates angiogenic markers but paradoxically, the cerebral microvasculature is reduced around Aß plaques. Here we demonstrate that angiogenesis is started near Aß plaques in both AD mouse models and human AD samples. However, endothelial cells express the molecular signature of non-productive angiogenesis (NPA) and accumulate, around Aß plaques, a tip cell marker and IB4 reactive vascular anomalies with reduced NOTCH activity. Notably, NPA induction by endothelial loss of presenilin, whose mutations cause familial AD and which activity has been shown to decrease with age, produced a similar vascular phenotype in the absence of Aß pathology. We also show that Aß plaque-associated NPA locally disassembles blood vessels, leaving behind vascular scars, and that microglial phagocytosis contributes to the local loss of endothelial cells. These results define the role of NPA and microglia in local blood vessel disassembly and highlight the vascular component of presenilin loss of function in AD.


1993 ◽  
Vol 43 (1-2) ◽  
pp. 23-30 ◽  
Author(s):  
R.M. McCarron ◽  
L. Wang ◽  
M.K. Racke ◽  
D.E. McFarlin ◽  
M. Spatz

2013 ◽  
Vol 90 (1) ◽  
pp. 71-80 ◽  
Author(s):  
Kwang Seok Kim ◽  
Jung Eun Kim ◽  
Kyu Jin Choi ◽  
Sangwoo Bae ◽  
Dong Ho Kim

2016 ◽  
Vol 56 (8) ◽  
pp. 1052-1059 ◽  
Author(s):  
P. V. Strekalova ◽  
Yu. A. Nagovitsyn ◽  
A. Riehokainen ◽  
V. V. Smirnova

2016 ◽  
Vol 124 (6) ◽  
pp. 1780-1787 ◽  
Author(s):  
Zhenjun Zhao ◽  
Michael S. Johnson ◽  
Biyi Chen ◽  
Michael Grace ◽  
Jaysree Ukath ◽  
...  

OBJECT Stereotactic radiosurgery (SRS) is an established intervention for brain arteriovenous malformations (AVMs). The processes of AVM vessel occlusion after SRS are poorly understood. To improve SRS efficacy, it is important to understand the cellular response of blood vessels to radiation. The molecular changes on the surface of AVM endothelial cells after irradiation may also be used for vascular targeting. This study investigates radiation-induced externalization of phosphatidylserine (PS) on endothelial cells using live-cell imaging. METHODS An immortalized cell line generated from mouse brain endothelium, bEnd.3 cells, was cultured and irradiated at different radiation doses using a linear accelerator. PS externalization in the cells was subsequently visualized using polarity-sensitive indicator of viability and apoptosis (pSIVA)-IANBD, a polarity-sensitive probe. Live-cell imaging was used to monitor PS externalization in real time. The effects of radiation on the cell cycle of bEnd.3 cells were also examined by flow cytometry. RESULTS Ionizing radiation effects are dose dependent. Reduction in the cell proliferation rate was observed after exposure to 5 Gy radiation, whereas higher radiation doses (15 Gy and 25 Gy) totally inhibited proliferation. In comparison with cells treated with sham radiation, the irradiated cells showed distinct pseudopodial elongation with little or no spreading of the cell body. The percentages of pSIVA-positive cells were significantly higher (p = 0.04) 24 hours after treatment in the cultures that received 25- and 15-Gy doses of radiation. This effect was sustained until the end of the experiment (3 days). Radiation at 5 Gy did not induce significant PS externalization compared with the sham-radiation controls at any time points (p > 0.15). Flow cytometric analysis data indicate that irradiation induced growth arrest of bEnd.3 cells, with cells accumulating in the G2 phase of the cell cycle. CONCLUSIONS Ionizing radiation causes remarkable cellular changes in endothelial cells. Significant PS externalization is induced by radiation at doses of 15 Gy or higher, concomitant with a block in the cell cycle. Radiation-induced markers/targets may have high discriminating power to be harnessed in vascular targeting for AVM treatment.


1988 ◽  
Vol 117 (1) ◽  
pp. 111-126 ◽  
Author(s):  
Druie E. Cavender ◽  
Dorian O. Haskard ◽  
Dominic Maliakkal ◽  
Morris Ziff

RSC Advances ◽  
2017 ◽  
Vol 7 (60) ◽  
pp. 37612-37626 ◽  
Author(s):  
Vishal Nemaysh ◽  
Pratibha Mehta Luthra

Platelet-derived growth factor receptor-beta (PDGFR-β) is expressed by endothelial cells (ECs) of tumor-associated blood vessels and regulates primarily early hematopoiesis.


2001 ◽  
Vol 125 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Mark W. Lingen

Abstract The basic signs and symptoms of inflammation and wound healing have been appreciated for thousands of years. However, the specific cells involved and their roles in this complex environment are still being elucidated today. In 1926, the origin of the phagocytic mononuclear ameboid wandering cell (macrophage) had not been determined. One popular theory was that the cells were differentiated from the endothelial cells of the nearby blood vessels, whereas others believed that the cells came from the peripheral blood or resting wandering cells. The purpose of this article is to review the seminal article published by Lang regarding this topic nearly 75 years ago. In addition, this article will review what is now known with regard to the role of the macrophage and endothelial cells in the development of angiogenesis, which is arguably the most critical component of successful inflammatory process or wound healing.


1990 ◽  
Vol 110 (5) ◽  
pp. 1757-1766 ◽  
Author(s):  
W Risau ◽  
B Engelhardt ◽  
H Wekerle

The endothelial blood-brain barrier (BBB) has a critical role in controlling lymphocyte traffic into the central nervous system (CNS), both in physiological immunosurveillance, and in its pathological aberrations. The intercellular signals that possibly could induce lymphocytes to cross the BBB include immunogenic presentation of protein (auto-)antigens by BBB endothelia to circulating T lymphocytes. This concept has raised much, though controversial, attention. We approached this problem by analyzing in vitro immunospecific interactions between clonal rat T lymphocyte lines with syngeneic, stringently purified endothelial monolayer cultures from adult brain micro-vessels. The rat brain endothelia (RBE) were established from rat brain capillaries using double collagenase digestion, density gradient fractionation and selective cytolysis of contaminating pericytes by anti-Thy 1.1 antibodies and complement. Incubation with interferon-gamma in most of the brain-derived endothelial cells induced Ia-antigens in the cytoplasm and on the cell surface in some of the cells. Before the treatment, the cells were completely Ia-negative. Pericytes were unresponsive to IFN-gamma treatment. When confronted with syngeneic T cell lines specific for protein (auto-)antigens (e.g., ovalbumin and myelin basic protein, MBP), RBE were completely unable to induce antigen-specific proliferation of syngeneic T lymphocytes irrespective of pretreatment with IFN-gamma and of cell density. RBE were inert towards the T cells, and did not suppress T cell activation induced by other "professional" antigen presenting cells (APC) such as thymus-derived dendritic cells or macrophages. IFN-gamma-treated RBE were, however, susceptible to immunospecific T cell killing. They were lysed by MBP-specific T cells in the presence of the specific antigen or Con A. Antigen dependent lysis was restricted by the appropriate (MHC) class II product. We conclude that the interaction of brain endothelial cells with encephalitogenic T lymphocytes may involve recognition of antigen in the molecular context of relevant MHC products, but that this interaction per se is insufficient to initiate the full T cell activation program.


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