open access
Apoptosis biomarkers (Apaf-1, sFa s, sFa s-L, and caspase-9), albumin, and fetuin-A levels in pulmonary thromboembolic patients
, 2, 2, 1, 2
Affiliations- Sivas Cumhuriyet University, Faculty of Medicine, Department of Biochemistry, Sivas, Turkey
- Sivas Cumhuriyet University, Faculty of Medicine, Department of Emergency Medicine, Sivas, Turkey
open access
Abstract
INTRODUCTION: Pulmonary thromboembolism (PE) is the third most common medical emergency with mortality due to ischemia and reperfusion lung injury. Lung ischaemia-reperfusion injury. Lung reperfusion damage is believed to cause cellular damage and apoptosis. The aim of the present study was to evaluate the levels of fetuin-A, albumin, and apoptosis biomarkers (Apaf-1, sFas, and sFasL) among pulmonary thromboembolic patients.
MATERIAL AND METHODS: Blood samples were collected from 45 volunteer patients and 40 healthy control volunteers. Human apoptosis biomarkers (Apaf-1, sFas, sFasL, and caspase-9) and fetuin-A values were measured by ELISA device. Student’s t-test or Mann-Whitney U test were used for continuous variables, and categorical variables were compared with the chi-square test to assess the significance of intergroup differences. The mean values of apoptosis biomarkers and acute phase reactants between dead and survival patients were also compared.
RESULTS: While the apoptosis mean values of Apaf-1, sFas, sFasL, and caspase-9 for the control group were 0.12 ± 0.01, 332.1 ± 28.0, 130.4 ± 34.6, and 74.3 ± 2.6, for the patient group they were 0.14 ± 0.02, 509.1 ± 67.6, 139.9 ± 23.7, and 79.4 ± 2.8, respectively. The group differences were significant for all the biomarkers (p = 0.01, p = 0.001, p = 0.19, and p = 0.01, respectively). The negative acute phase fetuin- A and albumin levels decreased significantly in the patient groups (p = 0.01 and p = 0.01, respectively).
CONCLUSİONS: Intrinsic and extrinsic apoptosis pathways are stimulated during pulmonary embolism, and negative acute phase reactants are decreased. There was a correlation with the mortality and Apaf-1, sFas, caspase-9, fetuin, and albumin levels.
Abstract
INTRODUCTION: Pulmonary thromboembolism (PE) is the third most common medical emergency with mortality due to ischemia and reperfusion lung injury. Lung ischaemia-reperfusion injury. Lung reperfusion damage is believed to cause cellular damage and apoptosis. The aim of the present study was to evaluate the levels of fetuin-A, albumin, and apoptosis biomarkers (Apaf-1, sFas, and sFasL) among pulmonary thromboembolic patients.
MATERIAL AND METHODS: Blood samples were collected from 45 volunteer patients and 40 healthy control volunteers. Human apoptosis biomarkers (Apaf-1, sFas, sFasL, and caspase-9) and fetuin-A values were measured by ELISA device. Student’s t-test or Mann-Whitney U test were used for continuous variables, and categorical variables were compared with the chi-square test to assess the significance of intergroup differences. The mean values of apoptosis biomarkers and acute phase reactants between dead and survival patients were also compared.
RESULTS: While the apoptosis mean values of Apaf-1, sFas, sFasL, and caspase-9 for the control group were 0.12 ± 0.01, 332.1 ± 28.0, 130.4 ± 34.6, and 74.3 ± 2.6, for the patient group they were 0.14 ± 0.02, 509.1 ± 67.6, 139.9 ± 23.7, and 79.4 ± 2.8, respectively. The group differences were significant for all the biomarkers (p = 0.01, p = 0.001, p = 0.19, and p = 0.01, respectively). The negative acute phase fetuin- A and albumin levels decreased significantly in the patient groups (p = 0.01 and p = 0.01, respectively).
CONCLUSİONS: Intrinsic and extrinsic apoptosis pathways are stimulated during pulmonary embolism, and negative acute phase reactants are decreased. There was a correlation with the mortality and Apaf-1, sFas, caspase-9, fetuin, and albumin levels.
Keywords
apoptosis; pulmonary thromboembolism; sFas, sFasL; caspase-9; Apaf-1
About this articleTitle
Apoptosis biomarkers (Apaf-1, sFa s, sFa s-L, and caspase-9), albumin, and fetuin-A levels in pulmonary thromboembolic patients
Journal
Disaster and Emergency Medicine Journal
Issue
Article type
Research paper
Pages
1-6
Published online
2020-02-07
Page views
898
Article views/downloads
608
DOI
Bibliographic record
Disaster Emerg Med J 2020;5(1):1-6.
Keywords
apoptosis
pulmonary thromboembolism
sFas
sFasL
caspase-9
Apaf-1
Authors
Hüseyin Aydın
Yusuf Kenan Tekin
İlhan Korkmaz
Zeynep Eker
Erdal Demirtaş
References (29)- Stein PD, Hull RD, Ghali WA, et al. Tracking the uptake of evidence: two decades of hospital practice trends for diagnosing deep vein thrombosis and pulmonary embolism. Arch Intern Med. 2003; 163(10): 1213–1219.
- Ng CSH, Wan S, Yim APC. Pulmonary ischaemia-reperfusion injury: role of apoptosis. Eur Respir J. 2005; 25(2): 356–363.
- Damico R, Zulueta JJ, Hassoun PM. Pulmonary endothelial cell NOX. Am J Respir Cell Mol Biol. 2012; 47(2): 129–139.
- Gu S, Zhao Y, Guo J, et al. High expression of APAF-1 elevates erythroid apoptosis in iron overload myelodysplastic syndrome. Tumour Biol. 2014; 35(3): 2211–2218.
- Kerr JF, Wyllie AH, Currie AR. Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics. Br J Cancer. 1972; 26(4): 239–257.
- Wu CC, Bratton SB. Regulation of the intrinsic apoptosis pathway by reactive oxygen species. Antioxid Redox Signal. 2013; 19(6): 546–558.
- Verbrugge I, Johnstone RW, Smyth MJ. SnapShot: Extrinsic apoptosis pathways. Cell. 2010; 143(7): 1192, 1192.e1–2.
- Bratton SB, Salvesen GS. Regulation of the Apaf-1-caspase-9 apoptosome. J Cell Sci. 2010; 123(Pt 19): 3209–3214.
- Argüelles S, Guerrero-Castilla A, Cano M, et al. Advantages and disadvantages of apoptosis in the aging process. Ann N Y Acad Sci. 2019; 1443(1): 20–33.
- Chen Q, Pandi SP, Kerrigan L, et al. Cystic fibrosis epithelial cells are primed for apoptosis as a result of increased Fas (CD95). J Cyst Fibros. 2018; 17(5): 616–623.
- Minas M, Mystridou P, Georgoulias P, et al. Fetuin-A is associated with disease severity and exacerbation frequency in patients with COPD. COPD. 2013; 10(1): 28–34.
- Galembeck F, Cann J. Fetuin as a trypsin inhibitor. Archives of Biochemistry and Biophysics. 1974; 164(1): 326–331.
- Bilgir O, Kebapcilar L, Bilgir F, et al. Decreased Serum Fetuin-A Levels are Associated with Coronary Artery Diseases. Internal Medicine. 2010; 49(13): 1281–1285.
- Majno G, Joris I. Apoptosis, oncosis, and necrosis. An overview of cell death. Am J Pathol. 1995; 146(1): 3–15.
- Fischer S, Cassivi SD, Xavier AM, et al. Cell death in human lung transplantation: apoptosis induction in human lungs during ischemia and after transplantation. Ann Surg. 2000; 231(3): 424–431.
- Kannan K, Jain S. Oxidative stress and apoptosis. Pathophysiology. 2000; 7(3): 153–163.
- Carden D, Granger D. Pathophysiology of ischaemia-reperfusion injury. The Journal of Pathology. 2000; 190(3): 255–266, doi: 10.1002/(sici)1096-9896(200002)190:3<255::aid-path526>3.0.co;2-6.
- Arnalich F, Maldifassi MC, Ciria E, et al. Plasma levels of mitochondrial and nuclear DNA in patients with massive pulmonary embolism in the emergency department: a prospective cohort study. Crit Care. 2013; 17(3): R90.
- Bauer MK, Vogt M, Los M, et al. Role of reactive oxygen intermediates in activation-induced CD95 (APO-1/Fas) ligand expression. J Biol Chem. 1998; 273(14): 8048–8055.
- Suzuki M, Aoshiba K, Nagai A. Oxidative stress increases Fas ligand expression in endothelial cells. J Inflamm (Lond). 2006; 3: 11.
- Adly AA, Ismail EA, Andrawes NG, et al. Soluble Fas/FasL ratio as a marker of vasculopathy in children and adolescents with sickle cell disease. Cytokine. 2016; 79: 52–58.
- Cardinal H, Brophy JM, Bogaty P, et al. Usefulness of soluble fas levels for improving diagnostic accuracy and prognosis for acute coronary syndromes. Am J Cardiol. 2010; 105(6): 797–803.
- Forgiarini LA, Grün G, Kretzmann NA, et al. When is injury potentially reversible in a lung ischemia-reperfusion model? J Surg Res. 2013; 179(1): 168–174.
- Wang Y, Zhang Q, Zhong L, et al. Apoptotic Protease Activating Factor-1 Inhibitor Mitigates Myocardial Ischemia Injury via Disturbing Procaspase-9 Recruitment by Apaf-1. Oxid Med Cell Longev. 2017; 2017: 9747296.
- Mukhopadhyay S, Mondal SA, Kumar M, et al. Proinflammatory and antiinflammatory attributes of fetuin-a: a novel hepatokine modulating cardiovascular and glycemic outcomes in metabolic syndrome. Endocr Pract. 2014; 20(12): 1345–1351.
- Stefan N, Fritsche A, Weikert C, et al. Plasma fetuin-A levels and the risk of type 2 diabetes. Diabetes. 2008; 57(10): 2762–2767.
- Ma P, Feng Yc. Decreased serum fetuin-A levels and active inflammatory bowel disease. Am J Med Sci. 2014; 348(1): 47–51.
- Parlak ES, Alisik M, Karalezli A, et al. Are the thiol/disulfide redox status and HDL cholesterol levels associated with pulmonary embolism?: Thiol/disulfide redox status in pulmonary embolism. Clin Biochem. 2017; 50(18): 1020–1024.
- Hayıroğlu Mİ, Keskin M, Keskin T, et al. A Novel Independent Survival Predictor in Pulmonary Embolism: Prognostic Nutritional Index. Clin Appl Thromb Hemost. 2018; 24(4): 633–639.