X射线照射对人脐静脉内皮细胞焦亡的影响

doi:10.3969/j.issn.1004-616x.2021.02.002

Abstract

Abstract: OBJECTIVE: To investigate the effects of X-ray irradiation on pyroptosis of human umbilical vein endothelial cells (HUVEC). METHODS: Pyroptosis is an inflammatory programmed cell death process. Cells were irradiated with a single dose of 10 Gy X-ray. In order to investigate the occurrence of X-ray induced pyroptosis,levels of IL-1 β,IL-6,TNF-α and IL-18 which were secreted by HUVEC cells from 0 to 72 h after the radiation were determined using the ELISA assay. Caspase-1 which is cleaved to the activated state is a key step of pyroptosis. Therefore,the activated levels of Caspase-1 were detected using Western blot at 6-48 h after the single dose of 10 Gy X-ray irradiation. Morphological changes of HUVECs were detected using transmission electron microscopy (TEM) at 72 h after the irradiation. Flow cytometry (FCM) was used to detect the changes of pyroptosis after a single dose and a small dose of multiple exposures (2.5 Gy/d×4 d). RESULTS: Compared with the control group,the levels of IL-1 β,IL-6,TNF-α and IL-18 in HUVEC cells 0-72 h after the radiation were significantly higher (P<0.05) and the levels of activated Caspase-1 at 6-48 h after the radiation was increased (P<0.05). The cell volumes were increased with swelling. The percentages of pyroptoti cells after the single and multiple exposures were significantly higher than that of the control group (P<0.01). In addition,the pyroptotic death rates after the single dose was twice as high as that after the multiple doses (P<0.01). CONCLUSION: X-ray exposure induced pyroptosis in HUVEC cells. Under the same total dose,the damage levels from the single dose exposure were significantly higher than that from the multiple exposures.

Key words: X-ray, HUVEC, pyroptosis, Caspase-1

CLC Number:

R994.6

LI Chen, TIAN Mei, QI Xuesong, WANG Chunyan, QU Gonglin, SHAO Shuai, WANG Chengfang, GOU Qiao. Induction of pyroptosis by X-rays in human umbilical vein endothelial cells[J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2021, 33(2): 89-94.

References

[1] DARBY S C, EWERTZ M, MCGALE P, et al. Risk of ischemic heart disease in women after radiotherapy for breast cancer[J]. N Engl J Med, 2013, 368(11):987-998.
[2] YUSUF S W, SAMI S, DAHER I N. Radiation-induced heart disease:a clinical update[J]. Cardiol Res Pract, 2011, 2011:317659.
[3] CUZICK J, STEWART H, RUTQVIST L, et al. Cause-specific mortality in long-term survivors of breast cancer who participated in trials of radiotherapy[J]. J Clin Oncol, 1994, 12(3):447-453.
[4] DARBY S C, EWERTZ M, HALL P. Ischemic heart disease after breast cancer radiotherapy[J]. N Engl J Med, 2013, 368(26):2527.
[5] RUSSELL N S, HOVING S, HEENEMAN S, et al. Novel insights into pathological changes in muscular arteries of radiotherapy patients[J]. Radiother Oncol, 2009, 92(3):477-483.
[6] MCGALE P, DARBY S C, HALL P, et al. Incidence of heart disease in 35, 000 women treated with radiotherapy for breast cancer in Denmark and Sweden[J]. Radiother Oncol, 2011, 100(2):167-175.
[7] MAN S M, KARKI R, KANNEGANTI T D. Molecular mechanisms and functions of pyroptosis, inflammatory caspases and inflammasomes in infectious diseases[J]. Immunol Rev, 2017, 277(1):61-75.
[8] FERNANDES-ALNEMRI T, WU J, YU J W, et al. The pyroptosome:a supramolecular assembly of ASC dimers mediating inflammatory cell death via caspase-1 activation[J]. Cell Death Differ, 2007, 14(9):1590-1604.
[9] BAROJA-MAZO A, MARTÍN-SÁNCHEZ F, GOMEZ A I, et al. The NLRP3 inflammasome is released as a particulate danger signal that amplifies the inflammatory response[J]. Nat Immunol, 2014, 15(8):738-748.
[10] FRANKLIN B S, BOSSALLER L, DE NARDO D, et al. The adaptor ASC has extracellular and ‘prionoid’ activities that propagate inflammation[J]. Nat Immunol, 2014, 15(8):727-737.
[11] VENKATESULU B P, MAHADEVAN L S, ALIRU M L, et al. Radiation-induced endothelial vascular injury:a review of possible mechanisms[J]. JACC Basic Transl Sci, 2018, 3(4):563-572.
[12] SLEZAK J, KURA B, RAVINGEROVÁ T, et al. Mechanisms of cardiac radiation injury and potential preventive approaches[J]. Can J Physiol Pharmacol, 2015, 93(9):737-753.
[13] RAFⅡ S, GINSBERG M, SCANDURA J, et al. Transplantation of endothelial cells to mitigate acute and chronic radiation injury to vital organs[J]. Radiat Res, 2016, 186(2):196-202.
[14] WU D M, HAN R, DENG S H, et al. Protective effects of flagellin A N/C against radiation-induced NLR pyrin domain containing 3 inflammasome-dependent pyroptosis in intestinal cells[J]. Int J Radiat Oncol Biol Phys, 2018, 101(1):107-117.
[15] LIAO H, WANG H X, RONG X M, et al. Mesenchymal stem cells attenuate radiation-induced brain injury by inhibiting microglia pyroptosis[J]. Biomed Res Int, 2017, 2017:1948985.
[16] LIU Y G, CHEN J K, ZHANG Z T, et al. NLRP3 inflammasome activation mediates radiation-induced pyroptosis in bone marrow-derived macrophages[J]. Cell Death Dis, 2017, 8(2):e2579.
[17] 陈艳芳. 不同分割方式对大鼠全脑照射后脑损伤程度的观察[D]. 天津:天津医科大学, 2007.
[18] 潘纯国, 刘智华, 王静怡, 等. 单次与分次剂量照射大鼠放射性肺损伤模型的建立[J]. 实用癌症杂志, 2015, 30(10):1423-1425, 1429.

Induction of pyroptosis by X-rays in human umbilical vein endothelial cells

PDF (PC)

Knowledge

Abstract

Cite this article

share this article

References

Related Articles 9

Recommended Articles

Metrics

Comments

[1]	JIANG Shan, DU Feng, KANG Bingwen, YIN Caocao, ZHOU Jian, SHI Ying, WANG Yue, ZHOU Gengyao, QIN Xujun. Attenuation of D-galactose-induced senescence of human umbilical vein endothelial cells by isorhamnetin [J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2021, 33(2): 95-100.
[2]	LIU Jieyi, ZHANG Rui, XIA Dong, LI Rong, LI Xiaowen, CHEN Zixu, WEI Qing, ZHAO Zhiqiang, HE Yun. Combined toxicity of different PM_2.5 components in human umbilical vein endothelial cells [J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2021, 33(2): 116-123,128.
[3]	WU Qingsong, FU Zhongxue. Association between polymorphisms of XRCC1 Arg194Trp and susceptibility to colorectal cancer in Chinese: a Meta-analysis [J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2016, 28(2): 134-140.
[4]	DONG Xiaomei, WANG Zhi, ZHANG Guowei, DONG Jianyun, ZHOU Niya, LING Xi, LIU Jinyi, CAO Jia, ZHANG Lilong, AO Lin. Genotoxic effects of low dose ionizing radiation occupationally exposed in industrial flaw detection workers [J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2015, 27(2): 101-105.
[5]	HAN Xiao-yan，LIU Qing，GAO Li-ping，MA Jian-xiu，HUANG Chao-jie，ZHANG Hong. Role of NOX family in PC-3 cell damage induced by X-ray irradiation [J]. , 2012, 24(1): 30-34.
[6]	LIANG Xiao-fang，ZOU Yue，JIANG Qi-sheng，LI Feng-sheng，WANG Lu，ZHOU Xiang-yan. Effects of X-rays on the expression of Bmi-1 gene in human lung adenocarcinoma cell line A549 [J]. , 2011, 23(6): 456-459.
[7]	WU Cong-mei1,HUANG Tian-hua1,WU De-sheng1,XIE Qing-dong1,LI De-rui2,CHEN Xiu-ru2,XU Xiao-hu3. Experimental Study on Inhibition of pEgr-TNFα Gene Therapy Combined with Radiotherapy on Esophageal Cancer Cells [J]. , 2006, 18(1): 6-008.
[8]	WU Cong-mei 1,LI Xiu-yi 2. STUDY ON CONSTRUCTION OF pcEgr-IFNγ AND EXPRESSION PROPERTY OF X-RAYINDUCTION IN VITRO [J]. , 2003, 15(1): 1-4.
[9]	SUN Yuan-ming; LI Jin; WANG Qin; TANG Wei-sheng; WANG Zhi-quan. CYTOGENETIC EVALUATION OF LONG-TERM IRRADIATION EFFECT ON WORKERS EARLY EN-GAGED IN X-RAY MEDICINE IN CHINA BY FLUORESCENCE IN SI TU HYBRIDIZATION [J]. , 2002, 14(2): 75-079.