دورية أكاديمية

Quantitative contributions of processes by which polyanion drugs reduce intracellular bioavailability and transfection efficiency of cationic siRNA lipoplex.

التفاصيل البيبلوغرافية
العنوان: Quantitative contributions of processes by which polyanion drugs reduce intracellular bioavailability and transfection efficiency of cationic siRNA lipoplex.
المؤلفون: Jaiprasart P; Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73117, United States., Yeung BZ; Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73117, United States; Optimum Therapeutics LLC, Carlsbad, CA 92008, United States., Lu Z; Optimum Therapeutics LLC, Carlsbad, CA 92008, United States; Institute of Quantitative Systems Pharmacology, Carlsbad, CA 92008, United States., Wientjes MG; Optimum Therapeutics LLC, Carlsbad, CA 92008, United States; Institute of Quantitative Systems Pharmacology, Carlsbad, CA 92008, United States., Cui M; Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73117, United States; Optimum Therapeutics LLC, Carlsbad, CA 92008, United States; Institute of Quantitative Systems Pharmacology, Carlsbad, CA 92008, United States., Hsieh CM; College of Pharmacy, Taipei Medical University, Taipei, Taiwan, ROC., Woo S; Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73117, United States., Au JL; Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73117, United States; Optimum Therapeutics LLC, Carlsbad, CA 92008, United States; Institute of Quantitative Systems Pharmacology, Carlsbad, CA 92008, United States; College of Pharmacy, Taipei Medical University, Taipei, Taiwan, ROC. Electronic address: jau@optimumtx.com.
المصدر: Journal of controlled release : official journal of the Controlled Release Society [J Control Release] 2018 Jan 28; Vol. 270, pp. 101-113. Date of Electronic Publication: 2017 Dec 22.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Elsevier Science Publishers Country of Publication: Netherlands NLM ID: 8607908 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-4995 (Electronic) Linking ISSN: 01683659 NLM ISO Abbreviation: J Control Release Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Amsterdam : Elsevier Science Publishers, 1984-
مواضيع طبية MeSH: Heparin/*administration & dosage , RNA, Small Interfering/*administration & dosage , Suramin/*administration & dosage , Survivin/*genetics, Biological Availability ; Gene Silencing ; HT29 Cells ; Humans ; Liposomes ; Transfection
مستخلص: RNA Interference (RNAi) is a potentially useful tool to correct the detrimental effects of faulty genes; several RNAi are undergoing clinical evaluation in various diseases. The present study identified the relative contributions of three mechanisms by which polyanion drugs reduced the gene silencing activity of Lipoplex, a complex of small interfering RNA (siRNA) and cationic liposomes. The study used a siRNA against the chemoresistance gene survivin and two model polyanion drugs (suramin, heparin). Products of Lipoplex destabilization were separated, identified, and/or quantified using ultrafiltration, gel electrophoresis, and RT-qPCR (quantitative reverse transcription polymerase chain reaction). Cell binding and endocytosis of fluorescence-labeled Lipoplex and the amount of siRNA at its site of action RISC (RNA-induced silencing complex) were evaluated using endocytosis markers, confocal microscopy, quantitative image analysis, immunoprecipitation, and RT-qPCR. The results show suramin and heparin exerted multiple concentration-dependent effects. First, these agents altered several Lipoplex properties (i.e., reduced particle size, changed surface charge, modified composition of protein biocorona). Second, both caused Lipoplex destabilization to release double- and single-strand siRNA and/or smaller siRNA-lipid complexes with reduced siRNA cargo. Third, both prevented the cell surface binding and internalization of Lipoplex, diminished the siRNA concentration in RISC, and retarded the mRNA knockdown. Suramin and heparin yielded qualitatively and quantitatively different results. Analysis of the experimental results of suramin using quantitative pharmacology (QP) modeling indicated the major cause of gene silencing activity loss depended on drug concentration, changing from inhibition of endocytosis at lower concentration (accounting for 60% loss at ~9μM) to inhibition of cell surface binding and loss of siRNA cargo at higher concentrations (accounting for 64% and 27%, respectively, at 70μM). In summary, the present study demonstrates the complex and dynamic interactions between polyanions and Lipoplex, and the use of QP modeling to delineate the contributions of three mechanisms to the eventual loss of gene silencing activity.
(Copyright © 2017 Elsevier B.V. All rights reserved.)
References: J R Soc Interface. 2015 Sep 6;12(110):0589. (PMID: 26289657)
Biochim Biophys Acta. 2010 Mar;1798(3):536-43. (PMID: 19917267)
Top Curr Chem. 2010;296:51-93. (PMID: 21504100)
Nature. 2004 Nov 11;432(7014):173-8. (PMID: 15538359)
AAPS J. 2010 Dec;12(4):492-503. (PMID: 20544328)
Arterioscler Thromb Vasc Biol. 2004 Sep;24(9):1549-57. (PMID: 15231514)
J Cell Biochem. 1985;29(3):265-73. (PMID: 4077932)
Cancer Res. 2010 Feb 15;70(4):1277-80. (PMID: 20124473)
Nat Rev Genet. 2011 May;12(5):329-40. (PMID: 21499294)
Cancer Res. 2001 Aug 15;61(16):6145-50. (PMID: 11507065)
ACS Nano. 2012 Nov 27;6(11):9447-54. (PMID: 23036046)
Biochim Biophys Acta. 1999 Jan 8;1415(2):331-41. (PMID: 9889391)
Methods. 2001 Dec;25(4):402-8. (PMID: 11846609)
J Control Release. 2010 Jan 4;141(1):38-41. (PMID: 19737587)
Adv Colloid Interface Sci. 2014 Mar;205:230-9. (PMID: 24529969)
Cancer Res. 1990 May 15;50(10):3036-42. (PMID: 1692253)
RNA. 2010 Dec;16(12):2553-63. (PMID: 20940339)
Nat Biotechnol. 2013 Jul;31(7):653-8. (PMID: 23792629)
Nat Biotechnol. 2017 Mar;35(3):222-229. (PMID: 28244992)
Biochemistry. 1996 May 7;35(18):5616-23. (PMID: 8639519)
Langmuir. 2011 Jun 7;27(11):6615-21. (PMID: 21528933)
Nat Nanotechnol. 2013 Oct;8(10):772-81. (PMID: 24056901)
Iran J Basic Med Sci. 2013 Feb;16(2):150-6. (PMID: 24298383)
Nature. 2009 Jan 22;457(7228):426-33. (PMID: 19158789)
AAPS J. 2015 Nov;17(6):1475-82. (PMID: 26286676)
RNA. 2004 May;10(5):766-71. (PMID: 15100431)
J Biol Chem. 2009 Jul 3;284(27):17897-901. (PMID: 19342379)
Proc Natl Acad Sci U S A. 2011 Oct 11;108(41):16968-73. (PMID: 21969544)
J Biol Chem. 1993 Mar 15;268(8):5985-9. (PMID: 8383683)
J Control Release. 2014 Mar 28;178:79-85. (PMID: 24462901)
ACS Chem Biol. 2012 Feb 17;7(2):403-10. (PMID: 22026461)
J Clin Oncol. 1989 Apr;7(4):499-508. (PMID: 2926472)
J Control Release. 2008 Feb 18;126(1):67-76. (PMID: 18068258)
Cancer Chemother Pharmacol. 2010 Nov;66(6):1019-29. (PMID: 20107799)
Cell Mol Life Sci. 2009 Sep;66(17):2873-96. (PMID: 19499185)
Nat Rev Drug Discov. 2009 Feb;8(2):129-38. (PMID: 19180106)
Mol Cell Biol. 1999 Jun;19(6):3989-97. (PMID: 10330139)
J Cell Biol. 1971 Sep;50(3):746-61. (PMID: 4398631)
Immunol Rev. 2007 Oct;219:17-36. (PMID: 17850479)
Eur Urol. 2014 Mar;65(3):516-20. (PMID: 24246407)
Traffic. 2011 Dec;12(12):1911-22. (PMID: 21910808)
Acc Chem Res. 2014 Aug 19;47(8):2651-9. (PMID: 25014679)
Exp Cell Res. 1999 Jul 10;250(1):231-40. (PMID: 10388537)
J Cell Biol. 1989 Feb;108(2):377-87. (PMID: 2918022)
Cancer Res. 2014 Mar 1;74(5):1307-10. (PMID: 24413533)
Subcell Biochem. 2002;36:39-60. (PMID: 12037989)
AAPS J. 2011 Dec;13(4):585-97. (PMID: 21904966)
Nat Rev Drug Discov. 2005 Jul;4(7):581-93. (PMID: 16052241)
Int J Mol Sci. 2016 Jan 26;17 (2):null. (PMID: 26821018)
Arch Biochem Biophys. 1993 Jun;303(2):474-82. (PMID: 8390225)
Eur J Pharm Sci. 2010 Jun 14;40(3):159-70. (PMID: 20359532)
Proc Natl Acad Sci U S A. 1996 Oct 29;93(22):12349-54. (PMID: 8901584)
Adv Drug Deliv Rev. 2016 Feb 1;97:280-301. (PMID: 26686425)
Pharmacol Rev. 2006 Mar;58(1):32-45. (PMID: 16507881)
J Cell Sci. 2009 Sep 15;122(Pt 18):3250-61. (PMID: 19690049)
J Urol. 2005 Jul;174(1):322-7. (PMID: 15947683)
Hum Mol Genet. 2011 Apr 15;20(R1):R79-86. (PMID: 21422098)
J Control Release. 2001 Sep 11;76(1-2):169-81. (PMID: 11532322)
Biomacromolecules. 2014 May 12;15(5):1612-24. (PMID: 24611467)
Gene Ther. 1999 Apr;6(4):585-94. (PMID: 10476218)
Nat Biotechnol. 2017 Mar;35(3):230-237. (PMID: 28244996)
Int J Med Sci. 2013 Nov 25;10(13):1888-98. (PMID: 24324366)
معلومات مُعتمدة: P20 GM103639 United States GM NIGMS NIH HHS; R01 EB015253 United States EB NIBIB NIH HHS; R01 GM100487 United States GM NIGMS NIH HHS; P30 CA225520 United States CA NCI NIH HHS; R01 CA163015 United States CA NCI NIH HHS; R01 CA158300 United States CA NCI NIH HHS
فهرسة مساهمة: Keywords: Anionic drug; Binding; Biocorona; Destabilization; Internalization; siRNA lipoplex
المشرفين على المادة: 0 (Liposomes)
0 (RNA, Small Interfering)
0 (Survivin)
6032D45BEM (Suramin)
9005-49-6 (Heparin)
تواريخ الأحداث: Date Created: 20171206 Date Completed: 20190128 Latest Revision: 20220326
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC5808856
DOI: 10.1016/j.jconrel.2017.12.001
PMID: 29203416
قاعدة البيانات: MEDLINE
الوصف
تدمد:1873-4995
DOI:10.1016/j.jconrel.2017.12.001