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Dual mechanisms of Bcl-2 regulation in IP3-receptor-mediated Ca2+ release: A computational study |
| Hong Qi(祁宏)1,2,†, Zhi-Qiang Shi(史志强)1,3, Zhi-Chao Li(李智超)1,3, Chang-Jun Sun(孙长君)1,3, Shi-Miao Wang(王世苗)3, Xiang Li(李翔)4,5, and Jian-Wei Shuai(帅建伟)4,5,‡ |
1 Complex Systems Research Center, Shanxi University, Taiyuan 030006, China;
2 Shanxi Key Laboratory of Mathematical Techniques and Big Data Analysis on Disease Control and Prevention, Shanxi University, Taiyuan 030006, China;
3 School of Mathematical Sciences, Shanxi University, Taiyuan 030006, China;
4 Department of Physics and Fujian Provincial Key Laboratory for Soft Functional Materials Research, Xiamen University, Xiamen 361005, China;
5 State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, and National Institute for Data Science in Health and Medicine, Xiamen University, Xiamen 361005, China |
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Abstract Inositol 1,4,5-trisphosphate receptors (IP3R)-mediated calcium ion (Ca2+) release plays a central role in the regulation of cell survival and death. Bcl-2 limits the Ca2+ release function of the IP3R through a direct or indirect mechanism. However, the two mechanisms are overwhelmingly complex and not completely understood. Here, we convert the mechanisms into a set of ordinary differential equations. We firstly simulate the time evolution of Ca2+ concentration under two different levels of Bcl-2 for the direct and indirect mechanism models and compare them with experimental results available in the literature. Secondly, we employ one- and two-parameter bifurcation analysis to demonstrate that Bcl-2 can suppress Ca2+ signal from a global point of view both in the direct and indirect mechanism models. We then use mathematical analysis to clarify that the indirect mechanism is more efficient than the direct mechanism in repressing Ca2+ signal. Lastly, we predict that the two mechanisms restrict Ca2+ signal synergistically. Together, our study provides theoretical insights into Bcl-2 regulation in IP3R-mediated Ca2+ release, which may be instrumental for the successful development of therapies to target Bcl-2 for cancer treatment.
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Received: 26 April 2021
Revised: 01 August 2021
Accepted manuscript online: 17 August 2021
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PACS:
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87.16.Vy
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(Ion channels)
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87.17.Aa
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(Modeling, computer simulation of cell processes)
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87.18.Vf
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(Systems biology)
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| Fund: Project supported by Shanxi Province Science Foundation for Youths (Grant No. 201901D211159) and the National Natural Science Foundation of China (Grant Nos. 11504214, 11874310, and 12090052). |
Corresponding Authors:
Hong Qi, Jian-Wei Shuai
E-mail: hongqi@sxu.edu.cn;jianweishuai@xmu.edu.cn
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Cite this article:
Hong Qi(祁宏), Zhi-Qiang Shi(史志强), Zhi-Chao Li(李智超), Chang-Jun Sun(孙长君), Shi-Miao Wang(王世苗), Xiang Li(李翔), and Jian-Wei Shuai(帅建伟) Dual mechanisms of Bcl-2 regulation in IP3-receptor-mediated Ca2+ release: A computational study 2021 Chin. Phys. B 30 108704
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[1] Berridge M J, Bootman M D and Roderick H L 2003 Nat. Rev. Mol. Cell Biol. 4 517
[2] Orrenius S, Zhivotovsky B and Nicotera P 2003 Nat. Rev. Mol. Cell Biol. 4 552
[3] Qi H, Li X, Jin Z, Simmen T and Shuai J 2020 iScience 23 101671
[4] Chong S J F, Marchi S, Petroni G, Kroemer G, Galluzzi L and Pervaiz S 2020 Trends Cell Biol. 30 537
[5] Distelhorst C W 2018 BBA-Mol. Cell Res. 1865 1795
[6] Bezprozvanny I, Watras J and Ehrlich B E 1991 Nature 351 751
[7] Alzayady K J, Wang L, Chandrasekhar R, Wagner L E, Van Petegem F and Yule D I 2016 Sci. Signal. 9 ra35
[8] Boehning D, Patterson R L, Sedaghat L, Glebova N O, Kurosaki T and Snyder S H 2003 Nat. Cell Biol. 5 1051
[9] Yin Z, Qi H, Liu L and Jin Z 2017 BioSystems 162 44
[10] Bonneau B, Prudent J, Popgeorgiev N and Gillet G 2013 BBA-Mol. Cell Res. 1833 1755
[11] Parys J B 2014 Sci. Signal. 7 pe4
[12] Rong Y, Bultynck G, Aromolaran A S, Zhong F, Parys J B, De Smedt H, Mignery G A, Roderick H L, Bootman M D and Distelhorst C W 2009 Proc. Natl. Acad. Sci. USA 106 14397
[13] Monaco G, Decrock E, Akl H, Ponsaerts R, Vervliet T, Luyten T, De Maeyer M, Missiaen L, Distelhorst C and De Smedt H 2012 Cell Death Differ. 19 295
[14] Ivanova H, Luyten T, Decrock E, Vervliet T, Leybaert L, Parys J B and Bultynck G 2017 Cell Calcium 62 41
[15] Monaco G, La Rovere R, Karamanou S, Welkenhuyzen K, Ivanova H, Vandermarliere E, Di Martile M, Del Bufalo D, De Smedt H, Parys J B, Economou A and Bultynck G 2018 FEBS J. 285 127
[16] Chang M, Zhong F, Lavik A R, Parys J B, Berridge M J and Distelhorst C W 2014 Proc. Natl. Acad. Sci. USA 111 1186
[17] Li X, Zhong J, Gao X, Wu Y, Shuai J and Qi H 2017 Chin. Phys. B 26 128703
[18] Qi H, Jiang Y, Yin Z, Jiang K, Li L and Shuai J 2018 Phys. Chem. Chem. Phys. 20 1964
[19] Qi H, Xu G, Peng X, Li X, Shuai J and Xu R 2020 Phys. Rev. E 102 062422
[20] Li X, Zhong C, Wu R, Xu X, Yang Z, Cai S, Wu X, Chen X, Yin Z, He Q, Li D, Xu F, Yan Y, Qi H, Xie C, Shuai J and Han J 2021 Protein & Cell 2021 1
[21] Niu S, Shuai J and Qi H 2017 Acta Phys. Sin. 66 238701 (in Chinese)
[22] De Young G W and Keizer J 1992 Proc. Natl. Acad. Sci. USA 89 9895
[23] Wagner L E, Li W and Yule D I 2003 J. Biol. Chem. 278 45811
[24] Tang T, Tu H, Wang Z and Bezprozvanny I 2003 J. Neurosci. 23 403
[25] Ferrell J E and Ha S H 2014 Trends Biochem. Sci. 39 496
[26] Li H, Rao A and Hogan P G 2011 Trends Cell Biol. 21 91
[27] Parys J and Bezprozvanny I 1995 Cell Calcium 18 353
[28] Svenningsson P, Nishi A, Fisone G, Girault J A, Nairn A C and Greengard P 2004 Annu. Rev. Pharmacol. Toxicol. 44 269
[29] Shin S Y, Choo S M, Kim D, Baek S J, Wolkenhauer O and Cho K H 2006 FEBS Lett. 580 5965
[30] Neves S R, Tsokas P, Sarkar A, Grace E A, Rangamani P, Taubenfeld S M, Alberini C M, Schaff J C, Blitzer R D and Moraru I I and Iyengar R 2008 Cell 133 666
[31] Tyson J J, Chen K C and Novak B 2003 Curr. Opin. Cell Biol. 15 221
[32] Shuai J, Yang D, Pearson J and Rüdiger S 2009 Chaos 19 037105
[33] Cai X, Li X, Qi H, Wei F, Chen J and Shuai J 2016 Phys. Biol. 13 056005
[34] Lindner A U, Prehn J H M and Huber H J 2013 Mol. Biosyst. 9 2359
[35] Liu Y and Zhao H 2016 Bioinformatics 32 3782
[36] Ivanova H, Vervliet T, Monaco G, Terry L E, Rosa N, Baker M R, Parys J B, Serysheva I I, Yule D I and Bultynck G 2019 CSH Perspect. Biol. 12 a035089
[37] Greenberg E F, Lavik A R and Distelhorst C W 2014 BBA-Mol. Cell Res. 1843 2205
[38] Monteith G R, Prevarskaya N and Roberts-Thomson S J 2017 Nat. Rev. Cancer 17 373
[39] Vervloessem T, Kerkhofs M, La Rovere R M, Sneyers F, Parys J B and Bultynck G 2018 Cell Calcium 70 102
[40] Singh R, Letai A and Sarosiek K 2019 Nat. Rev. Mol. Cell Biol. 20 175
[41] Yang J, Vais H, Gu W and Foskett J K 2016 Proc. Natl. Acad. Sci. USA 113 E1953
[42] Carpio M A, Means R E, Brill A L, Sainz A, Ehrlich B E and Katz S G 2021 Cell Rep. 34 108827 |
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