AI Chat Paper
Note: Please note that the following content is generated by AMiner AI. SciOpen does not take any responsibility related to this content.
{{lang === 'zh_CN' ? '文章概述' : 'Summary'}}
{{lang === 'en_US' ? '中' : 'Eng'}}
Chat more with AI
Powered by AMiner. Clicking this button will take you away from SciOpen.
Home Genes & Diseases Article
PDF (3.4 MB)
Cite
EndNote(RIS) BibTeX
Collect
Submit Manuscript AI Chat Paper
Show Outline
Outline
Show full outline
Hide outline
Outline
Show full outline
Hide outline
Full Length Article | Open Access

Anti-endothelial cell antibody rich sera from rheumatic heart disease patients induces proinflammatory phenotype and methylation alteration in endothelial cells

Mukul Rastogia, Subendu Sarkara, Ankita Makola, Rana Sandip Singhb, Uma Nahar Saikiac, Dibyajyoti Banerjeea, Seema Choprad, Anuradha Chakrabortia,( )
Department of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India
Department of Cardiothoracic and Vascular Surgery, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India
Department of Histopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India
Department of Obstetrics and Gynaecology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India

Peer review under responsibility of Chongqing Medical University.

Show Author Information

Abstract

Rheumatic heart disease (RHD) is a major cause of cardiovascular morbidity and mortality in developing nations like India. RHD commonly affects the mitral valve which is lined by a single layer of endothelial cells (ECs). The role of ECs in mitral valve damage during RHD is not well elucidated. In here, anti-endothelial cell antibody from RHD patients has been used to stimulate the ECs (HUVECs and HMVECs). ECs proinflammatory phenotype with increased expression of TNFα, IL-6, IL-8, IFNγ, IL-1β, ICAM1, VCAM1, E-selectin, laminin B, and vimentin was documented in both ECs. The promoter hypomethylation of various key inflammatory cytokines (TNFα, IL-6, and IL-8), integrin (ICAM1) associated with leukocyte transendothelial migration, and extracellular matrix genes (vimentin, and laminin) were also observed. Further, the in-vitro data was in accordance with ex-vivo observations which correlated significantly with the etiological factors such as smoking, socioeconomic status, and housing. Thus, the study sheds light on the role of ECs in RHD which is a step forward in the elucidation of disease pathogenesis.

Keywords

InflammationDNA methylationEndothelial cellsAnti-Endothelial cell antibodiesRheumatic heart disease

References

1

Watkins DA, Johnson CO, Colquhoun SM, et al. Global, regional, and national burden of rheumatic heart disease, 1990-2015. N Engl J Med. 2017;377:713–722.
Crossref Google Scholar
2

Sarkar S, Chopra S, Rohit MK, Banerjee D, Chakraborti A. Vitamin D regulates the production of vascular endothelial growth factor: a triggering cause in the pathogenesis of rheumatic heart disease? Med Hypotheses. 2016;95:62–66.
Crossref Google Scholar
3

Sarkar S, Rastogi M, Kumar R, Chakraborti A. Killer cell immunoglobulin like receptors (KIR) gene variations in rheumatic fever and rheumatic heart disease patients from North India. J Clin Infect Dis Pract. 2016;1:105.
Crossref Google Scholar
4

Sarkar S, Rastogi M, Chaudhary P, et al. Association of rheumatic fever & rheumatic heart disease with plausible early & late-stage disease markers. Indian J Med Res. 2017;145:758–766.
Crossref Google Scholar
5

Cunningham MW. Streptococcus and rheumatic fever. Curr Opin Rheumatol. 2012;24:408–416.
Crossref Google Scholar
6

Dinkla K, Nitsche-Schmitz DP, Barroso V, et al. Identification of a streptococcal octapeptide motif involved in acute rheumatic fever. J Biol Chem. 2007;282:18686–18693.
Crossref Google Scholar
7

Scalzi V, Hadi HA, Alessandri C, et al. Anti-endothelial cell antibodies in rheumatic heart disease. Clin Exp Immunol. 2010;161:570–575.
Crossref Google Scholar
8

Okello E, Kakande B, Sebatta E, et al. Socioeconomic and environmental risk factors among rheumatic heart disease patients in Uganda. PLoS One. 2012;7. e43917.
Crossref Google Scholar
9

Bierne H, Hamon M, Cossart P. Epigenetics and bacterial infections. Cold Spring Harb Perspect Med. 2012;2:a010272.
Crossref Google Scholar
10

Gomez-Diaz E, Jorda M, Peinado MA, Rivero A. Epigenetics of host-pathogen interactions: the road ahead and the road behind. PLoS Pathog. 2012;8. e1003007.
Crossref Google Scholar
11

Kubota T, Miyake K, Hirasawa T. Epigenetic understanding of gene-environment interactions in psychiatric disorders: a new concept of clinical genetics. Clin Epigenetics. 2012;4:1.
Crossref Google Scholar
12

Shen K, Liu H, Jing R, Yi J, Zhou X. DNA methylation dysregulations in rheumatic heart valve disease. BMC Cardiovasc Disord. 2017;17:159.
Crossref Google Scholar
13

Zheng D, Chen X, Li N, et al. Differentially methylated regions in patients with rheumatic heart disease and secondary pulmonary arterial hypertension. Exp Ther Med. 2017;14:1367–1372.
Crossref Google Scholar
14

Dunn J, Qiu H, Kim S, et al. Flow-dependent epigenetic DNA methylation regulates endothelial gene expression and atherosclerosis. J Clin Invest. 2014;124:3187–3199.
Crossref Google Scholar
15

Yang M, Chen P, Peng H, et al. Cigarette smoke extract induces aberrant cytochrome-c oxidase subunit Ⅱ methylation and apoptosis in human umbilical vascular endothelial cells. Am J Physiol Cell Physiol. 2015;308:C378-C384.
Crossref Google Scholar
16

Baudin B, Bruneel A, Bosselut N, Vaubourdolle M. A protocol for isolation and culture of human umbilical vein endothelial cells. Nat Protoc. 2007;2:481–485.
Crossref Google Scholar
17

Conti F, Alessandri C, Bompane D, et al. Autoantibody profile in systemic lupus erythematosus with psychiatric manifestations: a role for anti-endothelial-cell antibodies. Arthritis Res Ther. 2004;6:R366-R372.
Crossref Google Scholar
18

Sambrook J, Fritsch EF, Maniatis T. Molecular Cloning. New York: Cold spring harbor laboratory press; 1989.
19

Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods. 2001;25:402–408.
Crossref Google Scholar
20

Gardiner-Garden M, Frommer M. Transcripts and CpG islands associated with the pro-opiomelanocortin gene and other neurally expressed genes. J Mol Endocrinol. Jun 1994;12:365–382.
Crossref Google Scholar
21

van Dijk M, Visser A, Posthuma J, Poutsma A, Oudejans CB. Naturally occurring variation in trophoblast invasion as a source of novel (epigenetic) biomarkers. Front Genet. 2012;3:22.
Crossref Google Scholar
22

Martins Cde O, Santos KS, Ferreira FM, et al. Distinct mitral valve proteomic profiles in rheumatic heart disease and myxomatous degeneration. Clin Med Insights Cardiol. 2014;8:79–86.
Crossref Google Scholar
23

Oberoi SS. Updating income ranges for Kuppuswamy’s socio-economic status scale for the year 2014. Indian J Public Health. 2015;59:156–157.
Crossref Google Scholar
24

Woldu B, Bloomfield GS. Rheumatic heart disease in the twenty-first century. Curr Cardiol Rep. 2016;18:96.
Crossref Google Scholar
25

Sumpio BE, Riley JT, Dardik A. Cells in focus: endothelial cell. Int J Biochem Cell Biol. 2002;34:1508–1512.
Crossref Google Scholar
26

Nkomo VT, Gardin JM, Skelton TN, Gottdiener JS, Scott CG, Enriquez-Sarano M. Burden of valvular heart diseases: a population-based study. Lancet. 2006;368:1005–1011.
Crossref Google Scholar
27

Karayama M, Inui N, Suda T, Nakamura Y, Nakamura H, Chida K. Antiendothelial cell antibodies in patients with COPD. Chest. 2010;138:1303–1308.
Crossref Google Scholar
28

Nandi S, Kumar R, Ray P, Vohra H, Ganguly NK. Clinical score card for diagnosis of group A streptococcal sore throat. Indian J Pediatr. 2002;69:471–475.
Crossref Google Scholar
29

Meira ZM, Goulart EM, Colosimo EA, Mota CC. Long term follow up of rheumatic fever and predictors of severe rheumatic valvar disease in Brazilian children and adolescents. Heart. 2005;91:1019–1022.
Crossref Google Scholar
30

Azad MB, Lissitsyn Y, Miller GE, Becker AB, HayGlass KT, Kozyrskyj AL. Influence of socioeconomic status trajectories on innate immune responsiveness in children. PLoS One. 2012;7. e38669.
Crossref Google Scholar
31

Mukae H, Vincent R, Quinlan K, et al. The effect of repeated exposure to particulate air pollution (PM10) on the bone marrow. Am J Respir Crit Care Med. 2001;163:201–209.
Crossref Google Scholar
32

Swiston JR, Davidson W, Attridge S, Li GT, Brauer M, van Eeden SF. Wood smoke exposure induces a pulmonary and systemic inflammatory response in firefighters. Eur Respir J. 2008;32:129–138.
Crossref Google Scholar
33

Dutta A, Mukherjee B, Das D, Banerjee A, Ray MR. Hypertension with elevated levels of oxidized low-density lipoprotein and anticardiolipin antibody in the circulation of premenopausal Indian women chronically exposed to biomass smoke during cooking. Indoor Air. 2011;21:165–176.
Crossref Google Scholar
34

Bordron A, Dueymes M, Levy Y, et al. The binding of some human antiendothelial cell antibodies induces endothelial cell apoptosis. J Clin Invest. May 15 1998;101:2029–2035.
Crossref Google Scholar
35

Muhl H, Pfeilschifter J. Anti-inflammatory properties of pro-inflammatory interferon-gamma. Int Immunopharmacol. 2003;3:1247–1255.
Crossref Google Scholar
36

Huang YH, Yang HY, Huang SW, Ou G, Hsu YF, Hsu MJ. Interleukin-6 induces vascular endothelial growth Factor-C expression via Src-FAK-STAT3 signaling in lymphatic endothelial cells. PLoS One. 2016;11. e0158839.
Crossref Google Scholar
37

Sano M, Fukuda K, Kodama H, et al. Interleukin-6 family of cytokines mediate angiotensin Ⅱ-induced cardiac hypertrophy in rodent cardiomyocytes. J Biol Chem. 2000;275:29717–29723.
Crossref Google Scholar
38

Schrader LI, Kinzenbaw DA, Johnson AW, Faraci FM, Didion SP. IL-6 deficiency protects against angiotensin Ⅱ induced endothelial dysfunction and hypertrophy. Arterioscler Thromb Vasc Biol. 2007;27:2576–2581.
Crossref Google Scholar
39

Carvalho D, Savage CO, Isenberg D, Pearson JD. IgG anti-endothelial cell autoantibodies from patients with systemic lupus erythematosus or systemic vasculitis stimulate the release of two endothelial cell-derived mediators, which enhance adhesion molecule expression and leukocyte adhesion in an autocrine manner. Arthritis Rheum. 1999;42:631–640.
Crossref Google Scholar
40

Sumitran-Karuppan S, Tyden G, Reinholt F, Berg U, Moller E. Hyperacute rejections of two consecutive renal allografts and early loss of the third transplant caused by non-HLA antibodies specific for endothelial cells. Transpl Immunol. 1997;5:321–327.
Crossref Google Scholar
41

Tan PH, Chan C, Xue SA, et al. Phenotypic and functional differences between human saphenous vein (HSVEC) and umbilical vein (HUVEC) endothelial cells. Atherosclerosis. 2004;173:171–183.
Crossref Google Scholar
42

Shah B, Sharma M, Kumar R, Brahmadathan KN, Abraham VJ, Tandon R. Rheumatic heart disease: progress and challenges in India. Indian J Pediatr. 2013;80:S77-S86.
Crossref Google Scholar
43

Zhang MA, Rego D, Moshkova M, et al. Peroxisome proliferator-activated receptor (PPAR)alpha and -gamma regulate IFNgamma and IL-17A production by human T cells in a sex-specific way. Proc Natl Acad Sci U S A. 2012;109:9505–9510.
Crossref Google Scholar
44

Chrobak I, Lenna S, Stawski L, Trojanowska M. Interferon-gamma promotes vascular remodeling in human microvascular endothelial cells by upregulating endothelin (ET)-1 and transforming growth factor (TGF) beta2. J Cell Physiol. 2013;228:1774–1783.
Crossref Google Scholar
45

Levick SP, Goldspink PH. Could interferon-gamma be a therapeutic target for treating heart failure? Heart Fail Rev. 2014;19:227–236.
Crossref Google Scholar
46

Tollerud DJ, Clark JW, Brown LM, et al. The effects of cigarette smoking on T cell subsets. A population-based survey of healthy caucasians. Am Rev Respir Dis. 1989;139:1446–1451.
Crossref Google Scholar
47

Bidkar M, Vassallo R, Luckey D, Smart M, Mouapi K, Taneja V. Cigarette smoke induces immune responses to vimentin in both, arthritis-susceptible and -resistant humanized mice. PLoS One. 2016;11. e0162341.
Crossref Google Scholar
48

Costenbader KH, Karlson EW. Cigarette smoking and autoimmune disease: what can we learn from epidemiology? Lupus. 2006;15:737–745.
Crossref Google Scholar
49

Oberyszyn TM, Conti CJ, Ross MS, et al. Beta2 integrin/ICAM-1 adhesion molecule interactions in cutaneous inflammation and tumor promotion. Carcinogenesis. 1998;19:445–455.
Crossref Google Scholar
50

Dave JM, Bayless KJ. Vimentin as an integral regulator of cell adhesion and endothelial sprouting. Microcirculation. 2014;21:333–344.
Crossref Google Scholar
51

Hafez M, Yahia S, Eldars W, et al. Prediction of residual valvular lesions in rheumatic heart disease: role of adhesion molecules. Pediatr Cardiol. 2013;34:583–590.
Crossref Google Scholar
52

Mor-Vaknin N, Punturieri A, Sitwala K, Markovitz DM. Vimentin is secreted by activated macrophages. Nat Cell Biol. 2003;5:59–63.
Crossref Google Scholar
53

Yousif LF, Di Russo J, Sorokin L. Laminin isoforms in endothelial and perivascular basement membranes. Cell Adhes Migr. 2013;7:101–110.
Crossref Google Scholar
54

Berk BC, Fujiwara K, Lehoux S. ECM remodeling in hypertensive heart disease. J Clin Invest. 2007;117:568–575.
Crossref Google Scholar
Genes & Diseases
Volume 5 Issue 3,
September 2018
Pages 275-289
DOI: 10.1016/j.gendis.2018.02.002
Cite this article:
Rastogi M, Sarkar S, Makol A, et al. Anti-endothelial cell antibody rich sera from rheumatic heart disease patients induces proinflammatory phenotype and methylation alteration in endothelial cells. Genes & Diseases, 2018, 5(3): 275-289. https://doi.org/10.1016/j.gendis.2018.02.002

214

Views

1

Downloads

4

Crossref

N/A

Web of Science

4

Scopus

0

CSCD

Altmetrics
Received: 24 November 2017
Accepted: 05 February 2018
Published: 13 February 2018
© 2018, Chongqing Medical University.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Return