open access

Vol 82, No 1 (2023)
Original article
Submitted: 2021-07-05
Accepted: 2021-11-27
Published online: 2021-12-16
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Porcine coronary arteries: immunohistochemical profile of TNF-alpha, IL-1beta, TGF-beta1 and ICAM-1

S. Taurone1, M. T. Santarelli1, E. De Santis2, C. Di Gioia3, E. Pompili2, F. Pellegrino4, P. Familiari5, V. Papa6, C. Zanza789, L. Coppola4, G. Familiari2, M. Artico1
·
Pubmed: 34966995
·
Folia Morphol 2023;82(1):119-126.
Affiliations
  1. Department of Sensory Organs, Sapienza University of Rome, Italy
  2. Department of Anatomical, Histological, Forensic Medicine and Orthopaedics Sciences, Sapienza University of Rome, Italy
  3. Department of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Italy
  4. UOC of Pathology, Sandro Pertini Hospital, Rome, Italy, Italy
  5. Department of Human Neurosciences, Sapienza University of Rome, Italy
  6. Department of Motor Sciences and Wellness, University of Naples “Parthenope”, Naples, Italy
  7. Department of Emergency Medicine, Foundation of Policlinico Agostino Gemelli-IRCCS, Catholic University of Sacred Heart, Rome, Italy
  8. Department of Anaesthesia and Critical Care, AON SS Antonio e Biagio e Cesare Arrigo, Alessandria, Italy
  9. Foundation Ospedale Alba-Bra and Department of Anaesthesia, Critical Care and Emergency Medicine, Pietro and Michele Ferrero Hospital, Verduno, Italy

open access

Vol 82, No 1 (2023)
ORIGINAL ARTICLES
Submitted: 2021-07-05
Accepted: 2021-11-27
Published online: 2021-12-16

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.

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Keywords

porcine coronary arteries, cytokines, IL-1beta, TNF-alpha, TGF-beta1, ICAM-1

About this article
Title

Porcine coronary arteries: immunohistochemical profile of TNF-alpha, IL-1beta, TGF-beta1 and ICAM-1

Journal

Folia Morphologica

Issue

Vol 82, No 1 (2023)

Article type

Original article

Pages

119-126

Published online

2021-12-16

Page views

3520

Article views/downloads

1111

DOI

10.5603/FM.a2021.0137

Pubmed

34966995

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

References (44)
  1. Åkerblom A, James SK, Lakic TG, et al. Interleukin-18 in patients with acute coronary syndromes. Clin Cardiol. 2019; 42(12): 1202–1209.
  2. Alexander H, Sprague R, Khalil A. Inflammatory cytokines in vascular dysfunction and vascular disease. Biochem Pharmacol. 2009; 78(6): 539–552.
  3. 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.
  4. Apostolakis S, Vogiatzi K, Amanatidou V, et al. Interleukin 8 and cardiovascular disease. Cardiovasc Res. 2009; 84(3): 353–360.
  5. Ballou S, Lozanski G. Induction of inflammatory cytokine release from cultured human monocytes by C-reactive protein. Cytokine. 1992; 4(5): 361–368.
  6. 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.
  7. Bonomini F, Taurone S, Parnigotto P, et al. Role of parnaparin in atherosclerosis. Int J Exp Pathol. 2016; 97(6): 457–464.
  8. 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.
  9. 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.
  10. 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.
  11. 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.
  12. 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.
  13. 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.
  14. 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.
  15. Hołda MK, Hołda J, Koziej M, et al. Porcine heart interatrial septum anatomy. Ann Anat. 2018; 217: 24–28.
  16. 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.
  17. 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.
  18. 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.
  19. 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.
  20. 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.
  21. Ley K, Huo Y. VCAM-1 is critical in atherosclerosis. J Clin Invest. 2001; 107(10): 1209–1210.
  22. Libby P. The vascular biology of atherosclerosis. Chapter in book: Braunwald’s Heart disease, 7Th Ed. Elsevier-Saunders, Philadeplhia 2005: 921–993.
  23. Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation. 2002; 105(9): 1135–1143.
  24. 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.
  25. Marie C, Cavaillon M. Negative feedback ininflammation. The role of anti-inflammatory cytokine. Bulletin de L Institute Pasteur. 1997; 95: 141–154.
  26. 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.
  27. 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.
  28. 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.
  29. Mourouzis K, Oikonomou E, Siasos G, et al. Pro-inflammatory cytokines in acute coronary syndromes. Curr Pharm Des. 2020; 26(36): 4624–4647.
  30. 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.
  31. 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.
  32. 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.
  33. Ross R. Atherosclerosis: an inflammatory disease. N Engl J Med. 1999; 340(2): 115–126.
  34. 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.
  35. 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.
  36. 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.
  37. Sean PD. Cellular and oxidative mechanisms associated with interleukin-6 signaling in the vasculature. Int J Mol Sci. 2017; 18(12).
  38. Sheth AR, Grewal US, Patel HP, et al. Possible mechanisms responsible for acute coronary events in COVID-19. Med Hypotheses. 2020; 143: 110125.
  39. 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.
  40. 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.
  41. Ueland T, Aukrust P, Caidahl K. CCL21 and prognosis in acute coronary syndrome. Aging. 2019; 11(21): 9225–9226.
  42. Vaidya K, Martínez G, Patel S. The role of colchicine in acute coronary syndromes. Clin Ther. 2019; 41(1): 11–20.
  43. 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.
  44. 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.

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