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Porcine coronary arteries: immunohistochemical profile of TNF-alpha, IL-1beta, TGF-beta1 and ICAM-1
- Department of Sensory Organs, Sapienza University of Rome, Italy
- Department of Anatomical, Histological, Forensic Medicine and Orthopaedics Sciences, Sapienza University of Rome, Italy
- Department of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Italy
- UOC of Pathology, Sandro Pertini Hospital, Rome, Italy, Italy
- Department of Human Neurosciences, Sapienza University of Rome, Italy
- Department of Motor Sciences and Wellness, University of Naples “Parthenope”, Naples, Italy
- Department of Emergency Medicine, Foundation of Policlinico Agostino Gemelli-IRCCS, Catholic University of Sacred Heart, Rome, Italy
- Department of Anaesthesia and Critical Care, AON SS Antonio e Biagio e Cesare Arrigo, Alessandria, Italy
- Foundation Ospedale Alba-Bra and Department of Anaesthesia, Critical Care and Emergency Medicine, Pietro and Michele Ferrero Hospital, Verduno, Italy
open access
Abstract
Background: In our study we used immunohistochemical technique to demonstrate the presence of the cytokines tumour necrosis factor alpha (TNF-α), interleukin 1beta (IL-1β), transforming growth factor beta1 (TGF-β1) and intercellular adhesion molecule-1 (ICAM-1) in porcine coronaries even in physiological conditions.
Materials and methods: Inflammatory cytokines are polypeptide mediators which act as a communication signal between immune system cells and other types of cellsin different organs and tissues, both in human and pig coronary circulation.
Results: Our results show that pro-inflammatory cytokines TNF-α, IL-1β, TGF-β1 and ICAM-1 are also present in the medium tunica of the coronary arteries under physiological conditions. These results may be compared with those found in coronary atherosclerosis, where the increase in TNF-α has a dramatic effect on the function of the left ventricle, and the high value of IL-1 correlates directly with the extent of myocardial necrosis. In our study we observe the damage and activation of endothelial cells; this induces endothelial dysfunction by accumulation and oxidation of low density lipoproteins (LDL). The formation of oxidized LDL could play a central role in the amplification of the inflammatory response causing an increased expression of pro-inflammatory cytokines which promotes leukocyte recruitment in the intimal layer. These leukocytes, after the adhesion to the endothelium, penetrate the intimate tunic.
Conclusions: Therefore inflammatory processes promote the onset and evolution of atheroma and the development of thrombotic complications.
Abstract
Background: In our study we used immunohistochemical technique to demonstrate the presence of the cytokines tumour necrosis factor alpha (TNF-α), interleukin 1beta (IL-1β), transforming growth factor beta1 (TGF-β1) and intercellular adhesion molecule-1 (ICAM-1) in porcine coronaries even in physiological conditions.
Materials and methods: Inflammatory cytokines are polypeptide mediators which act as a communication signal between immune system cells and other types of cellsin different organs and tissues, both in human and pig coronary circulation.
Results: Our results show that pro-inflammatory cytokines TNF-α, IL-1β, TGF-β1 and ICAM-1 are also present in the medium tunica of the coronary arteries under physiological conditions. These results may be compared with those found in coronary atherosclerosis, where the increase in TNF-α has a dramatic effect on the function of the left ventricle, and the high value of IL-1 correlates directly with the extent of myocardial necrosis. In our study we observe the damage and activation of endothelial cells; this induces endothelial dysfunction by accumulation and oxidation of low density lipoproteins (LDL). The formation of oxidized LDL could play a central role in the amplification of the inflammatory response causing an increased expression of pro-inflammatory cytokines which promotes leukocyte recruitment in the intimal layer. These leukocytes, after the adhesion to the endothelium, penetrate the intimate tunic.
Conclusions: Therefore inflammatory processes promote the onset and evolution of atheroma and the development of thrombotic complications.
Keywords
porcine coronary arteries, cytokines, IL-1beta, TNF-alpha, TGF-beta1, ICAM-1
Title
Porcine coronary arteries: immunohistochemical profile of TNF-alpha, IL-1beta, TGF-beta1 and ICAM-1
Journal
Issue
Article type
Original article
Pages
119-126
Published online
2021-12-16
Page views
3524
Article views/downloads
1115
DOI
Pubmed
Bibliographic record
Folia Morphol 2023;82(1):119-126.
Keywords
porcine coronary arteries
cytokines
IL-1beta
TNF-alpha
TGF-beta1
ICAM-1
Authors
S. Taurone
M. T. Santarelli
E. De Santis
C. Di Gioia
E. Pompili
F. Pellegrino
P. Familiari
V. Papa
C. Zanza
L. Coppola
G. Familiari
M. Artico
- Åkerblom A, James SK, Lakic TG, et al. Interleukin-18 in patients with acute coronary syndromes. Clin Cardiol. 2019; 42(12): 1202–1209.
- Alexander H, Sprague R, Khalil A. Inflammatory cytokines in vascular dysfunction and vascular disease. Biochem Pharmacol. 2009; 78(6): 539–552.
- Alexander MR, Owens GK. Epigenetic control of smooth muscle cell differentiation and phenotypic switching in vascular development and disease. Annu Rev Physiol. 2012; 74: 13–40.
- Apostolakis S, Vogiatzi K, Amanatidou V, et al. Interleukin 8 and cardiovascular disease. Cardiovasc Res. 2009; 84(3): 353–360.
- Ballou S, Lozanski G. Induction of inflammatory cytokine release from cultured human monocytes by C-reactive protein. Cytokine. 1992; 4(5): 361–368.
- Bianchi E, Artico M, Di Cristofano C, et al. Growth factors, their receptor expression and markers for proliferation of endothelial and neoplastic cells in human osteosarcoma. Int J Immunopathol Pharmacol. 2013; 26(3): 621–632.
- Bonomini F, Taurone S, Parnigotto P, et al. Role of parnaparin in atherosclerosis. Int J Exp Pathol. 2016; 97(6): 457–464.
- Camejo G, Hurt-Camejo E, Wiklund O, et al. Association of apo B lipoproteins with arterial proteoglycans: pathological significance and molecular basis. Atherosclerosis. 1998; 139(2): 205–222.
- De Bosscher K, Vanden Berghe W, Haegeman G. The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression. Endocr Rev. 2003; 24(4): 488–522.
- Devaraj S, Kumaresan PR, Jialal I. Effect of C-reactive protein on chemokine expression in human aortic endothelial cells. J Mol Cell Cardiol. 2004; 36(3): 405–410.
- Ding Z, Pothineni NV, Goel A, et al. Impact of hepatitis C seropositivity on the risk of coronary heart disease events. Am J Cardiol. 2014; 114(12): 1841–1845.
- Dong ZM, Chapman SM, Brown AA, et al. The combined role of P- and E-selectins in atherosclerosis. J Clin Invest. 1998; 102(1): 145–152.
- Gerdes N, Sukhova GK, Libby P, et al. Expression of interleukin (IL)-18 and functional IL-18 receptor on human vascular endothelial cells, smooth muscle cells, and macrophages: implications for atherogenesis. J Exp Med. 2002; 195(2): 245–257.
- Gu L, Okada Y, Clinton S, et al. Absence of monocyte chemoattractant protein-1 reduces atherosclerosis in low density lipoprotein receptor–deficient mice. Mol Cell. 1998; 2(2): 275–281.
- Hołda MK, Hołda J, Koziej M, et al. Porcine heart interatrial septum anatomy. Ann Anat. 2018; 217: 24–28.
- Ikeda U, Ohkawa F, Seino Y, et al. Serum interleukin 6 levels become elevated in acute myocardial infarction. J Mol Cell Cardiol. 1992; 24(6): 579–584.
- Kitagawa T, Yamamoto H, Horiguchi J, et al. Characterization of noncalcified coronary plaques and identification of culprit lesions in patients with acute coronary syndrome by 64-slice computed tomography. JACC Cardiovasc Imaging. 2009; 2(2): 153–160.
- Kukielka GL, Smith CW, LaRosa GJ, et al. Interleukin-8 gene induction in the myocardium after ischemia and reperfusion in vivo. J Clin Invest. 1995; 95(1): 89–103.
- Lavagno L, Gunella G, Bardelli C, et al. Anti-inflammatory drugs and tumor necrosis factor-alpha production from monocytes: role of transcription factor NF-kappa B and implication for rheumatoid arthritis therapy. Eur J Pharmacol. 2004; 501(1-3): 199–208.
- Lelovas PP, Kostomitsopoulos NG, Xanthos TT. A comparative anatomic and physiologic overview of the porcine heart. J Am Assoc Lab Anim Sci. 2014; 53(5): 432–438.
- Ley K, Huo Y. VCAM-1 is critical in atherosclerosis. J Clin Invest. 2001; 107(10): 1209–1210.
- Libby P. The vascular biology of atherosclerosis. Chapter in book: Braunwald’s Heart disease, 7Th Ed. Elsevier-Saunders, Philadeplhia 2005: 921–993.
- Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation. 2002; 105(9): 1135–1143.
- Liuzzo G, Crea F, Santamaria M, et al. Persistent activation of nuclear factor kappa-B signaling pathway in patients with unstable angina and elevated levels of c-reactive protein. J Am Coll Cardiol. 2007; 49(2): 185–194.
- Marie C, Cavaillon M. Negative feedback ininflammation. The role of anti-inflammatory cytokine. Bulletin de L Institute Pasteur. 1997; 95: 141–154.
- Martínez GJ, Robertson S, Barraclough J, et al. Colchicine acutely suppresses local cardiac production of inflammatory cytokines in patients with an acute coronary syndrome. J Am Heart Assoc. 2015; 4(8): e002128.
- Mitsumata M, Fishel RS, Nerem RM, et al. Fluid shear stress stimulates platelet-derived growth factor expression in endothelial cells. Am J Physiol. 1993; 265(1 Pt 2): H3–H8.
- Moulton KS, Heller E, Konerding MA, et al. Angiogenesis inhibitors endostatin or TNP-470 reduce intimal neovascularization and plaque growth in apolipoprotein E-deficient mice. Circulation. 1999; 99(13): 1726–1732.
- Mourouzis K, Oikonomou E, Siasos G, et al. Pro-inflammatory cytokines in acute coronary syndromes. Curr Pharm Des. 2020; 26(36): 4624–4647.
- Rafieian-Kopaei M, Setorki M, Doudi M, et al. Atherosclerosis: process, indicators, risk factors and new hopes. Int J Prev Med. 2014; 5(8): 927–946.
- Robertson S, Martínez GJ, Payet CA, et al. Colchicine therapy in acute coronary syndrome patients acts on caspase-1 to suppress NLRP3 inflammasome monocyte activation. Clin Sci (Lond). 2016; 130(14): 1237–1246.
- Rong JX, Rangaswamy S, Shen L, et al. Arterial injury by cholesterol oxidation products causes endothelial dysfunction and arterial wall cholesterol accumulation. Arterioscler Thromb Vasc Biol. 1998; 18(12): 1885–1894.
- Ross R. Atherosclerosis: an inflammatory disease. N Engl J Med. 1999; 340(2): 115–126.
- Russell DA, Abbott CR, Gough MJ. Vascular endothelial growth factor is associated with histological instability of carotid plaques. Br J Surg. 2008; 95(5): 576–581.
- Sabatine MS, Morrow DA, de Lemos JA, et al. Multimarker approach to risk stratification in non-ST elevation acute coronary syndromes: simultaneous assessment of troponin I, C-reactive protein, and B-type natriuretic peptide. Circulation. 2002; 105(15): 1760–1763.
- Sakaguchi H, Takeya M, Suzuki H, et al. Role of macrophage scavenger receptors in diet-induced atherosclerosis in mice. Lab Invest. 1998; 78(4): 423–434.
- Sean PD. Cellular and oxidative mechanisms associated with interleukin-6 signaling in the vasculature. Int J Mol Sci. 2017; 18(12).
- Sheth AR, Grewal US, Patel HP, et al. Possible mechanisms responsible for acute coronary events in COVID-19. Med Hypotheses. 2020; 143: 110125.
- Spoletini M, Taurone S, Tombolini M, et al. Trophic and neurotrophic factors in human pituitary adenomas (Review). Int J Oncol. 2017; 51(4): 1014–1024.
- Taurone S, Galli F, Signore A, et al. VEGF in nuclear medicine: Clinical application in cancer and future perspectives (Review). Int J Oncol. 2016; 49(2): 437–447.
- Ueland T, Aukrust P, Caidahl K. CCL21 and prognosis in acute coronary syndrome. Aging. 2019; 11(21): 9225–9226.
- Vaidya K, Martínez G, Patel S. The role of colchicine in acute coronary syndromes. Clin Ther. 2019; 41(1): 11–20.
- Yang Ke, Zhang XJ, Cao LiJ, et al. Toll-like receptor 4 mediates inflammatory cytokine secretion in smooth muscle cells induced by oxidized low-density lipoprotein. PLoS One. 2014; 9(4): e95935.
- Zohlnhöfer D, Richter T, Neumann FJ, et al. Transcriptome analysis reveals a role of interferon-γ in human neointima formation. Mol Cell. 2001; 7(5): 1059–1069.