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The Immunology of Phospholipid-Binding Antibodies in the Anti-Phospholipid Syndrome and Related Disorders
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
E. Nigel Harris, Genesio Balestrieri, Angela Tincani, Azzudin E. Gharavi
Mary Pangborn first demonstrated that antibodies of syphilis were specific for a phospholipid obtained from beef heart tissue.25 Subsequently, she showed that the target phospholipid, which she called cardiolipin,26 was a complex acidic phospholipid.27-28 The structure of cardiolipin was eventually worked out by Faure and Coulon-Morelec,29,30 and by MacFarlane and Gray.31-32 They showed that this compound was a diphosphatidylglycerol with a free median (3-hydroxyl group and phosphatidyl groups at the a and y positions (Figure 1). Cardiolipin is a constituent of the mitochondrial membrane and can be extracted from a number of natural sources such as ox liver, ox heart, rat liver and several plants.33 In 1965, de Haas and Van Deenen were able to synthesize the compound and they showed that binding of syphilis sera to this synthetic product was little different to binding of cardiolipin obtained from natural sources.34
Nature, Function, and Biosynthesis of Surfactant Lipids
Published in Jacques R. Bourbon, Pulmonary Surfactant: Biochemical, Functional, Regulatory, and Clinical Concepts, 2019
The other minor phospholipids of lung surfactant are phosphatidylinositol (PI, about the same proportion as in membranes), phosphatidylethanolamine (five to seven times less than in membranes), sphingomyelin and phosphatidylserine (both five to ten times less than in membranes), and lysophosphatidylcholine. Cardiolipin is undetectable.
Mitochondrial Dysfunction and Allergic Disease
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Kritika Khanna, Anurag Agrawal
Cardiolipin is a unique phospholipid present only in the inner mitochondrial membrane in the eukaryotic cell (Daum 1985). Mitochondrial dysfunction can lead to extrusion of cardiolipin outside of the cells where it can act as a mito-DAMP and activate NLRP3 inflammasome (Iyer et al. 2013). Cardiolipin has also been shown to inhibit the anti-inflammatory pathways by blocking the production of IL-10 (Chakraborty et al. 2017).
Improved pharmacokinetics of HIV-neutralizing VRC01-class antibodies achieved by reduction of net positive charge on variable domain
Published in mAbs, 2023
Young D. Kwon, Amarendra Pegu, Eun Sung Yang, Baoshan Zhang, Michael F. Bender, Mangaiarkarasi Asokan, Qingbo Liu, Krisha McKee, Bob C. Lin, Tracy Liu, Mark K. Louder, Reda Rawi, Mateo Reveiz, Andrew J. Schaub, Chen-Hsiang Shen, Nicole A. Doria-Rose, Paolo Lusso, John R. Mascola, Peter D. Kwong
Polyreactivity was determined by ANA HEp−2 Staining Analysis (ZEUS Scientific Cat. No: FA2400) and anticardiolipin ELISA (Inova Diagnostics Cat. No.: 708625). For the HEp−2 assay all antibodies were tested at 25 and 50 μg/mL per manufacturer’s protocol and imaged on a Nikon Ts2R microscope for 500 ms. Scores from 0 to 3 were defined with four control antibodies VRC01-LS 4E10 VRC07-523LS and VRC07-G54W. Test antibodies were scored by visual estimation of staining intensity compared to the control antibodies. Scores equal to or greater than 1 at 25 μg/mL were classified as polyreactive and between 0 and 1 as mildly polyreactive. In the cardiolipin, ELISA antibodies were tested at a starting concentration of 100 μg/mL followed by 3-fold dilutions. IgG phospholipid (GPL) units were calculated from the standard curve. GPL score < 20 was considered as not reactive 20–80 as low positive and > 80 as high positive.
Improving mitochondrial function in preclinical models of heart failure: therapeutic targets for future clinical therapies?
Published in Expert Opinion on Therapeutic Targets, 2023
Anna Gorący, Jakub Rosik, Joanna Szostak, Bartosz Szostak, Szymon Retfiński, Filip Machaj, Andrzej Pawlik
Currently, the greatest challenge is to develop new research models that could simultaneously cover multiple points of drug action, restoring disrupted metabolic processes in the mitochondria as comprehensively as possible. Only the development of therapies that focus on improving as many dysregulated mitochondrial processes as possible in patients with HF will be able to bring the expected clinical improvement along with inhibition of disease progression. Major therapeutic targets for future clinical therapies should include the search for compounds that increase ATP synthesis and energy delivery, as well as inhibit ROS formation. In addition, regulation of the mitochondrial electron transport chain, improved removal of toxic metabolites from the cell and normalization of altered ionic homeostasis, especially calcium metabolism, appear to be promising therapeutic targets. It is also necessary to search for new compounds that will stimulate the nitric oxide and superoxide dismutase pathways to increase ATP production and enhance free radical uptake. Modulation of cardiolipins can result in improved mitochondrial inner membrane function. The search for compounds that affect ketone metabolism also seems promising. This could prevent pathological remodeling and cardiac hypertrophy. In addition, new therapies may aim to restore normal autophagy and mitophagy, which could improve cardiomyocyte function and prevent the development of HF.
Effect of chronic alcohol consumption on myocardial apoptosis in the rat model of isoproterenol-induced myocardial injury and investigation on the cardioprotective role of calpain inhibitor 1
Published in Drug and Chemical Toxicology, 2022
Aysegul Oglakci-Ilhan, Kevser Kusat-Ol, Kubilay Uzuner, Onur Uysal, Ibrahim Sogut, Ferruh Yucel, Gungor Kanbak
Cardiolipin is located in the inner membrane of mitochondria and when mitochondrial cardiolipins are peroxidized, there is a decrease in mitochondrial cardiolipin content. Figure 4 shows the mitochondrial cardiolipin results that we measured from fresh tissue in our experimental groups. Cardiolipin contents in the alcohol, MI, alcohol + MI, alcohol + MI + calpain inhibitor 1, and DMSO groups were statistically significantly lower than the control group (p < 0.001). Moreover, this decrease was higher in the alcohol + MI group than the other groups and cardiolipin contents in the alcohol + MI group was statistically significant compared with the alcohol and MI groups (p < 0.001, p < 0.001 respectively). Cardiolipin contents in the alcohol + MI + calpain inhibitor 1, and DMSO groups were found to be statistically significantly higher than the alcohol and alcohol + MI groups (p < 0.05, p < 0.001, respectively).