Cathepsin B Is Implicated in Triglyceride (TG)-Induced Cell Death of Macrophage
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Macrophage cell death contributes to the formation of plaque, leading to the development of atherosclerosis. The accumulation of triglyceride (TG) is also associated with the pathogenesis of atherosclerosis. A previous study reported that TG induces the cell death of macrophages. This study examined whether the cytoplasmic release of cathepsin B from lysosome is associated with the TG-induced cell death of macrophage. The release of cathepsin B was increased in the TG-treated THP-1 macrophages, but the TG treatment did not affect cathepsin B expression. Furthermore, the inhibition of cathepsin B by its inhibitor, CA-074 Me, partially inhibited the TG-induced cell death of macrophage. TG-triggered macrophage cell death is mediated by the activation of caspase-1, -2, and apoptotic caspases. Therefore, this study investigated whether cathepsin B is implicated in the activation of these caspases. The inhibition of cathepsin B blocked the activation of caspase-7, -8, and -1 but did not affect the activity of caspase-3, -9, and -2. Overall, these results suggest that TG-induced cytoplasmic cathepsin B causes THP-1 macrophage cell death by activating caspase-1, leading to subsequent activation of the extrinsic apoptotic pathway.
Abstract
Macrophage cell death contributes to the formation of plaque, leading to the development of atherosclerosis. The accumulation of triglyceride (TG) is also associated with the pathogenesis of atherosclerosis. A previous study reported that TG induces the cell death of macrophages. This study examined whether the cytoplasmic release of cathepsin B from lysosome is associated with the TG-induced cell death of macrophage. The release of cathepsin B was increased in the TG-treated THP-1 macrophages, but the TG treatment did not affect cathepsin B expression. Furthermore, the inhibition of cathepsin B by its inhibitor, CA-074 Me, partially inhibited the TG-induced cell death of macrophage. TG-triggered macrophage cell death is mediated by the activation of caspase-1, -2, and apoptotic caspases. Therefore, this study investigated whether cathepsin B is implicated in the activation of these caspases. The inhibition of cathepsin B blocked the activation of caspase-7, -8, and -1 but did not affect the activity of caspase-3, -9, and -2. Overall, these results suggest that TG-induced cytoplasmic cathepsin B causes THP-1 macrophage cell death by activating caspase-1, leading to subsequent activation of the extrinsic apoptotic pathway.
참고문헌 (28)
- Ndrepepa G, "Atherosclerosis and ischaemic heart disease : Here to stay or gone tomorrow", Indian J Med Res, 146, pp.293~297 (2017)[DOI]
- Hyungtae Kim, "Prevalence and incidence of atherosclerotic cardiovascular disease and its risk factors in Korea: a nationwide population-based study", BMC Public Health, 19(1), pp.1112~ (2019), Springer Science and Business Media LLC[DOI]
- Moore KJ, "Macrophages in atherosclerosis : A dynamic balance", Nat Rev Immunol, 13, pp.709~721 (2013)[DOI]
- Daniel J. Rader, "Lipoproteins, macrophage function, and atherosclerosis: Beyond the foam cell?", Cell Metabolism, 1(4), pp.223~230 (2005), Elsevier BV[DOI]
- I Tabas, "Apoptosis and plaque destabilization in atherosclerosis: the role of macrophage apoptosis induced by cholesterol", Cell Death & Differentiation, 11(S1), pp.S12~S16 (2004), Springer Science and Business Media LLC[DOI]
- Sin Jee Son, "Triglyceride-Induced Macrophage Cell Death Is Triggered by Caspase-1", Biological and Pharmaceutical Bulletin, 36(1), pp.108~113 (2013), Pharmaceutical Society of Japan[DOI]
- 임재원, "Caspase-2 mediates triglyceride (TG)-induced macrophage cell death", BMB Reports, 50(10), pp.510~515 (2017), 생화학분자생물학회
- Milica Perišić Nanut, "Cysteine Cathepsins as Regulators of the Cytotoxicity of NK and T Cells", Frontiers in Immunology, 5, pp.616~ (2014), Frontiers Media SA[DOI]
- Cong-Lin Liu, "Cysteine protease cathepsins in cardiovascular disease: from basic research to clinical trials", Nature Reviews Cardiology, 15(6), pp.351~370 (2018), Springer Science and Business Media LLC[DOI]
- Jiqiu Chen, "In Vivo Imaging of Proteolytic Activity in Atherosclerosis", Circulation, 105(23), pp.2766~2771 (2002), Ovid Technologies (Wolters Kluwer Health)[DOI]
- Zhao CF, "The function of cathepsins B, D, and X in atherosclerosis", Am J Cardiovasc Dis, 6, pp.163~170 (2016)
- Angélique Chevriaux, "Cathepsin B Is Required for NLRP3 Inflammasome Activation in Macrophages, Through NLRP3 Interaction", Frontiers in Cell and Developmental Biology, 8, pp.167~ (2020), Frontiers Media SA[DOI]
- Anna Aronis, "Lipotoxic effects of triacylglycerols in J774.2 macrophages", Nutrition, 24(2), pp.167~176 (2008), Elsevier BV[DOI]
- Tsuchiya S, "Induction of maturation in cultured human monocytic leukemia cells by a phorbol diester", Cancer Res, 42, pp.1530~1536 (1982)
- J. Auwerx, "The human leukemia cell line, THP-1: A multifacetted model for the study of monocyte-macrophage differentiation", Experientia, 47(1), pp.22~31 (1991), Springer Science and Business Media LLC[DOI]
- Ivan Dimauro, "A simple protocol for the subcellular fractionation of skeletal muscle cells and tissue", BMC Research Notes, 5(1), pp.513~ (2012), Springer Science and Business Media LLC[DOI]
- 조효상, "Protective effects of Tat-NQO1 against oxidative stress-induced HT-22 cell damage, and ischemic injury in animals", BMB Reports, 49(11), pp.617~622 (2016), 생화학분자생물학회
- 주동현, "Biphasic activation of extracellular signal-regulated kinase (ERK) 1", 2 in epidermal growth factor (EGF)-stimulated SW480 colorectal cancer cells, 2016, pp.49(4), 220~225[DOI]
- Maria Eugenia Guicciardi, "Lysosomes in cell death", Oncogene, 23(16), pp.2881~2890 (2004), Springer Science and Business Media LLC[DOI]
- Mélanie Bruchard, "Chemotherapy-triggered cathepsin B release in myeloid-derived suppressor cells activates the Nlrp3 inflammasome and promotes tumor growth", Nature Medicine, 19(1), pp.57~64 (2013), Springer Science and Business Media LLC[DOI]
- 고광곤, "Hypertriglyceridemia and Cardiovascular Diseases: Revisited", Korean Circulation Journal, 46(2), pp.135~144 (2016), 대한심장학회[DOI]
- Jonas Wuopio, "Cathepsin B and S as markers for cardiovascular risk and all-cause mortality in patients with stable coronary heart disease during 10 years: a CLARICOR trial sub-study", Atherosclerosis, 278, pp.97~102 (2018), Elsevier BV[DOI]
- Ira Tabas, "Macrophage Apoptosis in Atherosclerosis: Consequences on Plaque Progression and the Role of Endoplasmic Reticulum Stress", Antioxidants & Redox Signaling, 11(9), pp.2333~2339 (2009), Mary Ann Liebert Inc[DOI]
- Aleš Premzl, "Intracellular proteolytic activity of cathepsin B is associated with capillary-like tube formation by endothelial cells in vitro", Journal of Cellular Biochemistry, 97(6), pp.1230~1240 (2006), Wiley[DOI]
- WEI LI, "Increased Expression and Translocation of Lysosomal Cathepsins Contribute to Macrophage Apoptosis in Atherogenesis", Annals of the New York Academy of Sciences, 1030(1), pp.427~433 (2004), Wiley[DOI]
- H Hentze, "Critical role for cathepsin B in mediating caspase-1-dependent interleukin-18 maturation and caspase-1-independent necrosis triggered by the microbial toxin nigericin", Cell Death & Differentiation, 10(9), pp.956~968 (2003), Springer Science and Business Media LLC[DOI]
- 임재원, "Triglyceride enhances susceptibility to TNF-a-induced cell death in THP-1 cells", Genes & Genomics, 36(1), pp.87~93 (2014), 한국유전학회[DOI]
- Lasse Foghsgaard, "Cathepsin B Acts as a Dominant Execution Protease in Tumor Cell Apoptosis Induced by Tumor Necrosis Factor", Journal of Cell Biology, 153(5), pp.999~1010 (2001), Rockefeller University Press[DOI]
