Inhibition of a Radiation-Induced Senescence-Like Phenotype: A Possible Mechanism for Potentially Lethal Damage Repair in Vascular Endothelial Cells

2008 ◽  
Vol 170 (4) ◽  
pp. 534-539 ◽  
Author(s):  
Kaori Igarashi ◽  
Masahiko Miura
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Lethal Damage ◽  
Damage Repair ◽  
Radiation Induced

scholarly journals Stromal Cell-Derived Factor 1 Protects Brain Vascular Endothelial Cells from Radiation-Induced Brain Damage

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1230 ◽  
Author(s):  
Heo ◽  
Kim ◽  
Woo ◽  
Kim ◽  
Choi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Stromal Cell ◽  
Radiation Treatment ◽  
Vascular Endothelial Cells ◽  
Critical Role ◽  
Vascular Endothelial ◽  
Brain Endothelial Cells ◽  
Endothelial Cell Function ◽  
Radiation Induced ◽  
Stromal Cell Derived Factor

Stromal cell-derived factor 1 (SDF-1) and its main receptor, CXC chemokine receptor 4 (CXCR4), play a critical role in endothelial cell function regulation during cardiogenesis, angiogenesis, and reendothelialization after injury. The expression of CXCR4 and SDF-1 in brain endothelial cells decreases due to ionizing radiation treatment and aging. SDF-1 protein treatment in the senescent and radiation-damaged cells reduced several senescence phenotypes, such as decreased cell proliferation, upregulated p53 and p21 expression, and increased senescence-associated beta-galactosidase (SA-β-gal) activity, through CXCR4-dependent signaling. By inhibiting extracellular signal-regulated kinase (ERK) and signal transducer and activator of transcription protein 3 (STAT3), we confirmed that activation of both is important in recovery by SDF-1-related mechanisms. A CXCR4 agonist, ATI2341, protected brain endothelial cells from radiation-induced damage. In irradiation-damaged tissue, ATI2341 treatment inhibited cell death in the villi of the small intestine and decreased SA-β-gal activity in arterial tissue. An ischemic injury experiment revealed no decrease in blood flow by irradiation in ATI2341-administrated mice. ATI2341 treatment specifically affected CXCR4 action in mouse brain vessels and partially restored normal cognitive ability in irradiated mice. These results demonstrate that SDF-1 and ATI2341 may offer potential therapeutic approaches to recover tissues damaged during chemotherapy or radiotherapy, particularly by protecting vascular endothelial cells.

scholarly journals Celecoxib Alleviates Radiation-Induced Brain Injury in Rats by Maintaining the Integrity of Blood-Brain Barrier

Dose-Response ◽  
2021 ◽  
Vol 19 (2) ◽  
pp. 155932582110243
Author(s):  
Xiaoting Xu ◽  
Hao Huang ◽  
Yu Tu ◽  
Jiaxing Sun ◽  
Yaozu Xiong ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Brain Injury ◽  
Protective Effect ◽  
Blood Brain Barrier ◽  
Vascular Endothelial Cells ◽  
Brain Barrier ◽  
Vascular Endothelial ◽  
Blood Brain ◽  
Radiation Induced ◽  
Cox 2

The underlying mechanisms of radiation-induced brain injury are poorly understood, although COX-2 inhibitors have been shown to reduce brain injury after irradiation. In the present study, the effect of celecoxib (a selective COX-2 inhibitor) pretreatment on radiation-induced injury to rat brain was studied by means of histopathological staining, evaluation of integrity of blood-brain barrier and detection of the expressions of inflammation-associated genes. The protective effect of celecoxib on human brain microvascular endothelial cells (HBMECs) against irradiation was examined and the potential mechanisms were explored. Colony formation assay and apoptosis assay were undertaken to evaluate the effect of celecoxib on the radiosensitivity of the HBMECs. ELISA was used to measure 6-keto-prostaglandin F1α (6-keto-PGF1α) and thromboxane B2 (TXB2) secretion. Western blot was employed to examine apoptosis-related proteins expressions. It was found that celecoxib protected rat from radiation-induced brain injury by maintaining the integrity of the blood-brain barrier and reducing inflammation in rat brain tissues. In addition, celecoxib showed a significant protective effect on HBMECs against irradiation, which involves inhibited apoptosis and decreased TXB2/6-keto-PGF1α ratio in brain vascular endothelial cells. In conclusion, celecoxib could alleviate radiation-induced brain injury in rats, which may be partially due to the protective effect on brain vascular endothelial cells from radiation-induced apoptosis.

Roles of ROS and PKC-βII in ionizing radiation-induced eNOS activation in human vascular endothelial cells

2015 ◽  
Vol 70 ◽  
pp. 55-65 ◽  
Author(s):  
Kimimasa Sakata ◽  
Takashi Kondo ◽  
Natsumi Mizuno ◽  
Miki Shoji ◽  
Hironobu Yasui ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ionizing Radiation ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Radiation Induced

scholarly journals Enhanced Adhesion of Early Endothelial Progenitor Cells to Radiation-induced Senescence-like Vascular Endothelial Cells in vitro

2009 ◽  
Vol 50 (5) ◽  
pp. 469-475 ◽  
Author(s):  
Nuttawut SERMSATHANASAWADI ◽  
Hideto ISHII ◽  
Kaori IGARASHI ◽  
Masahiko MIURA ◽  
Masayuki YOSHIDA ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Endothelial Progenitor ◽  
Radiation Induced

Radiation-induced senescence-like phenotype in proliferating and plateau-phase vascular endothelial cells

2007 ◽  
Vol 313 (15) ◽  
pp. 3326-3336 ◽  
Author(s):  
Kaori Igarashi ◽  
Ippei Sakimoto ◽  
Keiko Kataoka ◽  
Keisuke Ohta ◽  
Masahiko Miura
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Plateau Phase ◽  
Radiation Induced

scholarly journals Protective effect of polydatin on radiation-induced injury of intestinal epithelial and endothelial cells

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Li Li ◽  
Ke Zhang ◽  
Ji Zhang ◽  
Ya-Nan Zeng ◽  
Feng Lai ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Small Intestine ◽  
Vascular Endothelial Cells ◽  
Tissue Sample ◽  
Proliferative Potential ◽  
Vascular Endothelial ◽  
Intestinal Epithelial ◽  
Intestinal Villi ◽  
Radiation Induced ◽  
Hematoxylin And Eosin

This study aimed to examine the radioprotective effect of polydatin (PD) on crypt and endothelial cells of the small intestines of C57BL/6 mice that received abdominal irradiation (IR). Mice were treated with 6 MV X-ray (20 Gy) abdominal IR at a dose rate of 200 cGy/min. Thirty minutes before or after IR, mice were intraperitoneally injected with PD. The rate of survival of the mice at 30 days after IR was determined. The duodenum (upper small intestine), jejunum (middle small intestine), and ileum (lower small intestine) were collected and subjected to hematoxylin and eosin staining. Tissue sample sections were analyzed through light microscopy, and the lengths of at least 20 intestinal villi were measured in each group; the average number of crypts was obtained from 10 intestinal samples in each group. Microvessel density was assessed using CD31-positive (brown) vascular endothelial cells/cell clusters. FHs74Int cell proliferation was measured using the CCK-8 assay. PD administration (25 mg/kg) before IR was the most effective in prolonging the survival of C57BL/6 mice. PD reduced radiation-induced injury of intestinal villi, prevented loss of crypts, increased intestinal crypt growth, protected against IR-induced intestinal injury, and enhanced the proliferative potential and reduced the apoptosis of FHs74Int cells after IR. Moreover, PD increased small intestinal MVD and reduced the apoptosis of intestinal microvascular endothelial cells in mice after IR. Therefore, PD was found to be able to protect the two types of cells from radiation damage and to thus alleviate radiation-induced injury of small intestine.

The Endothelial Cell and the Factor VIII Bypassing Activity of Prothrombin Complex Concentrate

1988 ◽  
Vol 60 (02) ◽  
pp. 226-229 ◽  
Author(s):  
Jerome M Teitel ◽  
Hong-Yu Ni ◽  
John J Freedman ◽  
M Bernadette Garvey
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Factor Viii ◽  
Prothrombin Complex Concentrate ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Monolayer Cultures ◽  
Coagulant Activity ◽  
Time Courses ◽  
Privileged Site

SummarySome classical hemophiliacs have a paradoxical hemostatic response to prothrombin complex concentrate (PCC). We hypothesized that vascular endothelial cells (EC) may contribute to this “factor VIII bypassing activity”. When PCC were incubated with suspensions or monolayer cultures of EC, they acquired the ability to partially bypass the defect of factor VIII deficient plasma. This factor VIII bypassing activity distributed with EC and not with the supernatant PCC, and was not a general property of intravascular cells. The effect of PCC was even more dramatic on fixed EC monolayers, which became procoagulant after incubation with PCC. The time courses of association and dissociation of the PCC-derived factor VIII bypassing activity of fixed and viable EC monolayers were both rapid. We conclude that EC may provide a privileged site for sequestration of constituents of PCC which express coagulant activity and which bypass the abnormality of factor VIII deficient plasma.

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