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Journal articles on the topic 'ApolipoproteinA-I Milano'

Author: Grafiati

Published: 14 March 2023

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1

Shah, P. K., J. Nilsson, S. Kaul, J. Yano, J. Zhu, A. Hamsten, and B. Cercek. "Inhibition of aortic atherosclerosis in apolipoprotein E-deficient mice by recombinant apolipoprotein A-I Milano." Journal of the American College of Cardiology 31 (February 1998): 390. http://dx.doi.org/10.1016/s0735-1097(98)80043-0.

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2

Shah, P. "Inhibition of Aortic Atherosclerosis in Apolipoprotein E-deficient Mice by Recombinant Apolipoprotein A-I Milano." Journal of the American College of Cardiology 31, no. 2 (February 1998): 390A. http://dx.doi.org/10.1016/s0735-1097(97)85397-1.

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3

Bhat, Shaila, Mary G. Sorci-Thomas, Laura Calabresi, Michael P. Samuel, and Michael J. Thomas. "Conformation of Dimeric Apolipoprotein A-I Milano on Recombinant Lipoprotein Particles." Biochemistry 49, no. 25 (June 29, 2010): 5213–24. http://dx.doi.org/10.1021/bi1003734.

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4

Klon, Anthony E., Martin K. Jones, Jere P. Segrest, and Stephen C. Harvey. "Molecular Belt Models for the Apolipoprotein A-I Paris and Milano Mutations." Biophysical Journal 79, no. 3 (September 2000): 1679–85. http://dx.doi.org/10.1016/s0006-3495(00)76417-4.

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5

Bielicki, John K., Mark R. McCall, Lori J. Stoltzfus, Amir Ravandi, Arnis Kuksis, Edward M. Rubin, and Trudy M. Forte. "Evidence That Apolipoprotein A-I Milano Has Reduced Capacity, Compared With Wild-Type Apolipoprotein A-I, to Recruit Membrane Cholesterol." Arteriosclerosis, Thrombosis, and Vascular Biology 17, no. 9 (September 1997): 1637–43. http://dx.doi.org/10.1161/01.atv.17.9.1637.

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6

Coin, B. D., P. K. Shah, J. Yano, M. D. Molloy, B. Cercek, and S. Kaul. "Reversal of impaired endothelium-dependent vasodilatation in apolipoprotein E-deficient mice by recombinant apolipoprotein A-I Milano." Journal of the American College of Cardiology 31 (1998): 60–61. http://dx.doi.org/10.1016/s0735-1097(98)80909-1.

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7

Bielicki, J. K., T. M. Forte, M. R. McCall, L. J. Stoltzfus, G. Chiesa, C. R. Sirtori, G. Franceschini, and E. M. Rubin. "High density lipoprotein particle size restriction in apolipoprotein A-I(Milano) transgenic mice." Journal of Lipid Research 38, no. 11 (November 1997): 2314–21. http://dx.doi.org/10.1016/s0022-2275(20)34945-2.

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8

Coin, B. D., P. K. Shah, J. Yano, M. D. Molloy, B. Cercek, and S. Kaul. "Recombinant apolipoprotein A-I Millano protects against lysophosphatidylcholine-induced endothelial dysfunction." Journal of the American College of Cardiology 31 (1998): 148. http://dx.doi.org/10.1016/s0735-1097(98)81288-6.

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9

Alexander, Eric T., Masafumi Tanaka, Momoe Kono, Hiroyuki Saito, Daniel J. Rader, and Michael C. Phillips. "Structural and functional consequences of the Milano mutation (R173C) in human apolipoprotein A-I." Journal of Lipid Research 50, no. 7 (March 24, 2009): 1409–19. http://dx.doi.org/10.1194/jlr.m800578-jlr200.

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10

Ameli, S., A. Hultgardh-Nilsson, B. Cercek, P. K. Shah, J. S. Forrester, H. Ageland, and J. Nilsson. "Recombinant apolipoprotein A-I Milano reduces intimal thickening after balloon injury in hypercholesterolemic rabbits." Circulation 90, no. 4 (October 1994): 1935–41. http://dx.doi.org/10.1161/01.cir.90.4.1935.

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11

Ma, Cheng-I. J., Jennifer A. Beckstead, Airlia Thompson, Anouar Hafiane, Rui Hao Leo Wang, Robert O. Ryan, and Robert S. Kiss. "Tweaking the cholesterol efflux capacity of reconstituted HDL." Biochemistry and Cell Biology 90, no. 5 (October 2012): 636–45. http://dx.doi.org/10.1139/o2012-015.

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Mechanisms to increase plasma high-density lipoprotein (HDL) or to promote egress of cholesterol from cholesterol-loaded cells (e.g., foam cells from atherosclerotic lesions) remain an important target to regress heart disease. Reconstituted HDL (rHDL) serves as a valuable vehicle to promote cellular cholesterol efflux in vitro and in vivo. rHDL were prepared with wild type apolipoprotein (apo) A-I and the rare variant, apoA-I Milano (M), and each apolipoprotein was reconstituted with phosphatidylcholine (PC) or sphingomyelin (SM). The four distinct rHDL generated were incubated with CHO cells, J774 macrophages, and BHK cells in cellular cholesterol efflux assays. In each cell type, apoA-I(M) SM-rHDL promoted the greatest cholesterol efflux. In BHK cells, the cholesterol efflux capacities of all four distinct rHDL were greatly enhanced by increased expression of ABCG1. Efflux to PC-containing rHDL was stimulated by transfection of a nonfunctional ABCA1 mutant (W590S), suggesting that binding to ABCA1 represents a competing interaction. This interpretation was confirmed by binding experiments. The data show that cholesterol efflux activity is dependent upon the apoA-I protein employed, as well as the phospholipid constituent of the rHDL. Future studies designed to optimize the efflux capacity of therapeutic rHDL may improve the value of this emerging intervention strategy.

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12

Bruckert, Eric, Arnold von Eckardstein, Harald Funke, Isabel Beucler, Heiko Wiebusch, Gérard Turpin, and Gerd Assmann. "The replacement of arginine by cysteine at residue 151 in Apolipoprotein A-I produces a phenotype similar to that of Apolipoprotein A-I Milano." Atherosclerosis 128, no. 1 (January 1997): 121–28. http://dx.doi.org/10.1016/s0021-9150(96)05982-5.

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13

Wang, Lai, Behrooz G. Sharifi, Theresa Pan, Lei Song, Ada Yukht, and Prediman K. Shah. "Bone Marrow Transplantation Shows Superior Atheroprotective Effects of Gene Therapy With Apolipoprotein A-I Milano Compared With Wild-Type Apolipoprotein A-I in Hyperlipidemic Mice." Journal of the American College of Cardiology 48, no. 7 (October 2006): 1459–68. http://dx.doi.org/10.1016/j.jacc.2006.07.040.

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14

Nicholls, Stephen J., E. Murat Tuzcu, Ilke Sipahi, Paul Schoenhagen, Tim Crowe, Samir Kapadia, and Steven E. Nissen. "Relationship Between Atheroma Regression and Change in Lumen Size After Infusion of Apolipoprotein A-I Milano." Journal of the American College of Cardiology 47, no. 5 (March 2006): 992–97. http://dx.doi.org/10.1016/j.jacc.2005.11.040.

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15

Cimmino, Giovanni, Walter S. Speidl, Sammy Elmariah, Borja Ibanez, Randolph Hutter, Valentin Fuster, and Juan Jose Badimon. "RECOMBINANT APOLIPOPROTEIN A-I MILANO DECREASES LEAFLET INFLAMMATION AND CALCIFICATION IN EXPERIMENTAL MODELS OF AORTIC STENOSIS." Journal of the American College of Cardiology 55, no. 10 (March 2010): A152.E1426. http://dx.doi.org/10.1016/s0735-1097(10)61427-1.

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16

Rocco, Alessandro Guerini, Cristina Sensi, Elisabetta Gianazza, Laura Calabresi, Guido Franceschini, Cesare R. Sirtori, and Ivano Eberini. "Structural and dynamic features of apolipoprotein A-I cysteine mutants, Milano and Paris, in synthetic HDL." Journal of Molecular Graphics and Modelling 29, no. 3 (November 2010): 406–14. http://dx.doi.org/10.1016/j.jmgm.2010.08.002.

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17

Bekaert, ED, P. Alaupovic, CS Knight-Gibson, G. Franceschini, and CR Sirtori. "Apolipoprotein A-I Milano: sex-related differences in the concentration and composition of apoA-I- and apoB-containing lipoprotein particles." Journal of Lipid Research 34, no. 1 (January 1993): 111–23. http://dx.doi.org/10.1016/s0022-2275(20)41325-2.

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18

Guerini Rocco, A., L. Mollica, E. Gianazza, L. Calabresi, C. R. Sirtori, and I. Eberini. "Tu-W16:8 A structural model for apolipoprotein A-I Milano (A-IM) in its heterodimeric form with apolipoprotein A-II (A-II)." Atherosclerosis Supplements 7, no. 3 (January 2006): 154. http://dx.doi.org/10.1016/s1567-5688(06)80604-5.

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19

Speidl, W. S., G. Cimmino, B. Ibanez, S. Elmariah, R. Hutter, M. J. Garcia, V. Fuster, M. E. Goldman, and J. J. Badimon. "Recombinant apolipoprotein A-I Milano rapidly reverses aortic valve stenosis and decreases leaflet inflammation in an experimental rabbit model." European Heart Journal 31, no. 16 (March 19, 2010): 2049–57. http://dx.doi.org/10.1093/eurheartj/ehq064.

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20

Nicholls, Stephen J., Rishi Puri, Christie M. Ballantyne, J. Wouter Jukema, John J. P. Kastelein, Wolfgang Koenig, R. Scott Wright, et al. "Effect of Infusion of High-Density Lipoprotein Mimetic Containing Recombinant Apolipoprotein A-I Milano on Coronary Disease in Patients With an Acute Coronary Syndrome in the MILANO-PILOT Trial." JAMA Cardiology 3, no. 9 (September 1, 2018): 806. http://dx.doi.org/10.1001/jamacardio.2018.2112.

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21

Kaul, Sanjay, Vladimir Rukshin, Raul Santos, Babak Azarbal, Charles L. Bisgaier, Jan Johansson, Vivian T. Tsang, et al. "Intramural Delivery of Recombinant Apolipoprotein A-I Milano /Phospholipid Complex (ETC-216) Inhibits In-Stent Stenosis in Porcine Coronary Arteries." Circulation 107, no. 20 (May 27, 2003): 2551–54. http://dx.doi.org/10.1161/01.cir.0000074042.19447.b1.

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22

Gomaraschi, Monica, Damiano Baldassarre, Mauro Amato, Sonia Eligini, Paola Conca, Cesare R. Sirtori, Guido Franceschini, and Laura Calabresi. "Normal Vascular Function Despite Low Levels of High-Density Lipoprotein Cholesterol in Carriers of the Apolipoprotein A-I Milano Mutant." Circulation 116, no. 19 (November 6, 2007): 2165–72. http://dx.doi.org/10.1161/circulationaha.107.705657.

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23

Chetty, Palaniappan Sevugan, Maki Ohshiro, Hiroyuki Saito, Padmaja Dhanasekaran, Sissel Lund-Katz, Leland Mayne, Walter Englander, and Michael C. Phillips. "Effects of the Iowa and Milano Mutations on Apolipoprotein A-I Structure and Dynamics Determined by Hydrogen Exchange and Mass Spectrometry." Biochemistry 51, no. 44 (October 24, 2012): 8993–9001. http://dx.doi.org/10.1021/bi300926j.

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24

Yan, Ying, Shulai Lu, Shaoyou Jia, Qingzhe Dong, Lei Wang, and Yunlong Wang. "Function of different proportions of apolipoprotein A-I cysteine mutants and apolipoprotein A-V on recombinant high-density lipoproteins in vitro." Bioscience Reports 39, no. 5 (May 2019). http://dx.doi.org/10.1042/bsr20190547.

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Abstract To explore the anti-atherosclerotic effects of recombinant high-density lipoproteins (rHDL) of apolipoprotein AI wild-type (apoA-Iwt), apolipoprotein AI Milano (apoA-IM), apolipoprotein AI (N74C) (apoA-I (N74C) )and apolipoprotein AV (apoA-V). We constructed rHDL liposomes (rHDLs), which included apoA-Iwt, apoA-IM, and apoA-I (N74C), followed by the synthesis of rHDLs, with the indicated ratios of apoA-Iwt, apoA-IM, apoA-I (N74C) and apoA-V. We investigated the anti-atherosclerotic effects by experiments including the DMPC clearance assay and experiments that assessed the in vitro antioxidation against low-density lipoprotein, the cellular uptake of oxidized low-density lipoprotein (oxLDL) and the in vitro intracellular lipid accumulation. Electron microscopy results revealed that as more apoA-V was present in rHDLs, the particle size of rHDLs was larger. The DMPC clearance assay subsequently showed that rHDL protein mixtures could promote DMPC turbidity clearance when more apoA-V was included in the reaction mixtures, with apoAV-rHDL showing the strongest turbidity clearance ability (P<0.05 vs AI-rHDL). In vitro antioxidation against low-density lipoprotein assays indicated that rHDLs containing apoA-V had increasing oxidation resistance against low-density lipoprotein (LDL) with higher apoA-V contents. Finally, cellular uptake of oxLDL and intracellular lipids suggested an apparent oxidation resistance to LDL oxidation in vitro and a reduced intracellular lipid accumulation in THP-1-derived macrophages, with AIM-rHDL demonstrating the greatest ability to decrease intracellular lipid accumulation. Different proportions of apolipoprotein A-I cysteine mutants and apolipoprotein A-V of rHDL changed the lipid binding capacity, particle size, and antioxidant capacity. These changes may show a beneficial effect of rHDL on atherosclerosis.

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25

Kalayci, Arzu, C. Michael Gibson, Paul M. Ridker, Samuel D. Wright, Bronwyn A. Kingwell, Serge Korjian, Gerald Chi, et al. "ApoA-I Infusion Therapies Following Acute Coronary Syndrome: Past, Present, and Future." Current Atherosclerosis Reports, May 7, 2022. http://dx.doi.org/10.1007/s11883-022-01025-7.

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Abstract Purpose of Review The elevated adverse cardiovascular event rate among patients with low high-density lipoprotein cholesterol (HDL-C) formed the basis for the hypothesis that elevating HDL-C would reduce those events. Attempts to raise endogenous HDL-C levels, however, have consistently failed to show improvements in cardiovascular outcomes. However, steady-state HDL-C concentration does not reflect the function of this complex family of particles. Indeed, HDL functions correlate only weakly with serum HDL-C concentration. Thus, the field has pivoted from simply raising the quantity of HDL-C to a focus on improving the putative anti-atherosclerotic functions of HDL particles. Such functions include the ability of HDL to promote the efflux of cholesterol from cholesterol-laden macrophages. Apolipoprotein A-I (apoA-I), the signature apoprotein of HDL, may facilitate the removal of cholesterol from atherosclerotic plaque, reduce the lesional lipid content and might thus stabilize vulnerable plaques, thereby reducing the risk of cardiac events. Infusion of preparations of apoA-I may improve cholesterol efflux capacity (CEC). This review summarizes the development of apoA-I therapies, compares their structural and functional properties and discusses the findings of previous studies including their limitations, and how CSL112, currently being tested in a phase III trial, may overcome these challenges. Recent Findings Three major ApoA-I-based approaches (MDCO-216, CER-001, and CSL111/CSL112) have aimed to enhance reverse cholesterol transport. These three therapies differ considerably in both lipid and protein composition. MDCO-216 contains recombinant ApoA-I Milano, CER-001 contains recombinant wild-type human ApoA-I, and CSL111/CSL112 contains native ApoA-I isolated from human plasma. Two of the three agents studied to date (apoA-1 Milano and CER-001) have undergone evaluation by intravascular ultrasound imaging, a technique that gauges lesion volume well but does not assess other important variables that may relate to clinical outcomes. ApoA-1 Milano and CER-001 reduce lecithin-cholesterol acyltransferase (LCAT) activity, potentially impairing the function of HDL in reverse cholesterol transport. Furthermore, apoA-I Milano can compete with and alter the function of the recipient’s endogenous apoA-I. In contrast to these agents, CSL112, a particle formulated using human plasma apoA-I and phosphatidylcholine, increases LCAT activity and does not lead to the malfunction of endogenous apoA-I. CSL112 robustly increases cholesterol efflux, promotes reverse cholesterol transport, and now is being tested in a phase III clinical trial. Summary Phase II-b studies of MDCO-216 and CER-001 failed to produce a significant reduction in coronary plaque volume as assessed by IVUS. However, the investigation to determine whether the direct infusion of a reconstituted apoA-I reduces post-myocardial infarction coronary events is being tested using CSL112, which is dosed at a higher level than MDCO-216 and CER-001 and has more favorable pharmacodynamics.

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26

Bellibas, S. Eralp, David Kallend, Alain Bobillier, Herman Kempen, and Peter L. Wijngaard. "Abstract 13324: Single Ascending Dose Pharmacokinetics and Pharmacodynamics of MDCO-216 (ApoA-I Milano/POPC) in Healthy Volunteers." Circulation 130, suppl_2 (November 25, 2014). http://dx.doi.org/10.1161/circ.130.suppl_2.13324.

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Introduction: MDCO-216, a complex of dimeric recombinant apolipoprotein A-I Milano (apoA-I M) and a phospholipid (POPC), is currently under development to improve cardiovascular outcomes by reducing plaque burden in patients with atherosclerotic disease. An earlier version of MDCO-216 has been shown to reduce atherosclerotic plaque burden in animal models and in patients with ACS. The purpose of this study was to assess the pharmacokinetics (PK), pharmacodynamics (PD), safety and tolerability of newly manufactured MDCO-216 first time in healthy volunteers. Methods: 24 healthy volunteers received a single dose of MDCO-216 (5, 10, 20, 30 or 40 mg/kg) or placebo (in 2:1 ratio) as a 2 hour IV infusion in a double-blind, randomised design. Serial blood samples were collected for PK and anti-drug Ab (ADA) analysis. An ex-vivo cholesterol efflux assay was used as one of several exploratory PD biomarkers for MDCO-216 activity. Results: No ADA was detected with any dose at any time point. Plasma mean T 1/2 of MDCO-216 ranged from 48 to 61 hours (56 hr. in average) and median T max ranged between 2 to 4 hours. No obvious difference in CL was observed with increases in dose and ranged from 0.62 to 0.98 mL/hr/kg. Exposure parameters increased with dose in a slightly less than dose-proportional manner with a range of 138 to 794 μg/mL for C max and 3391 to 20788 μg.hr/mL for AUC 0-48 . Dose-dependent increases in ABCA1-mediated efflux capacity of up to 4-fold above baseline and smaller increases of SRB1-mediated efflux capacity occurred rapidly after infusion at all doses. The dose-response analysis for ABCA1-mediated efflux best fitted into a sigmoid E max (maximum effect) PD model and predicts an E max of 15.6% which saturates around a 30 mg/kg dose of MDCO-216. Conclusions: This data demonstrate that MDCO-216 can profoundly stimulate the first step of reverse cholesterol transport at clinically achievable doses with a predictable PK/PD profile.

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27

Bellibas, S. Eralp, David Kallend, Alain Bobillier, Herman Kempen, and Peter L. Wijngaard. "Abstract 13357: MDCO-216 (ApoA-I Milano/POPC) Induces Reverse Cholesterol Transport in Stable Coronary Artery Disease Patients with a Dose Proportional Pharmacokinetics after Single Ascending Doses." Circulation 130, suppl_2 (November 25, 2014). http://dx.doi.org/10.1161/circ.130.suppl_2.13357.

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Introduction: MDCO-216, a complex of dimeric recombinant apolipoprotein A-I Milano (apoA-I M) and a phospholipid (POPC), is currently under development to improve cardiovascular outcomes by reducing plaque burden in patients with atherosclerotic disease. An earlier version of MDCO-216 has been shown effective in animal models and in patients with ACS. The purpose of this study was to assess the pharmacokinetics (PK), pharmacodynamics (PD) and safety of MDCO-216, manufactured by an improved process, first time in stable coronary artery disease (CAD) patients. Methods: 24 patients with known stable CAD received a single dose of MDCO-216 (10, 20, 30 or 40 mg/kg) or placebo (in 2:1 ratio) as a 2 hour IV infusion in a double-blind, randomised design. Blood samples were collected for PK and anti-drug Antibody (ADA) analysis. Ex-vivo cholesterol efflux assays were used as exploratory PD biomarkers for MDCO-216 activity. Results: Plasma mean T 1/2 of MDCO-216 ranged from 45 to 59 hours (53 hr. in average) and median T max ranged between 2 to 3 hours. No obvious difference in CL was observed with increases in dose and this ranged from 0.7 to 0.8 mL/hr/kg. Exposure parameters (C max and AUC) increased with dose in a dose-proportional manner. No ADA was detected with any dose at any time point. Dose-dependent increases in ABCA1-mediated efflux (up to 4-fold above baseline) and smaller increases of SRB1-mediated efflux occurred rapidly after infusion. The dose-response analysis for ABCA1-mediated efflux best fitted into a sigmoid E max (maximum effect) PD model and predicts an E max of 12.7% which saturates around a 16 mg/kg dose (see figure). Conclusions: This data is consistent with the findings of the previous IVUS study in ACS patients with MDCO-216 where maximum regression of atherosclerotic plaque burden was seen at a dose of 15 mg/kg; and support further development of this agent as a potential treatment for atherosclerotic disease.

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