外源性H_2O_2对小鼠骨骼肌细胞MG53膜修复作用的影响
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摘要
目的:研究不同浓度外源性H_2O_2干预对骨骼肌细胞MG53(Mitsugumin 53)膜修复作用的影响,探讨H_2O_2与MG53的关系。方法:培养C2C12细胞,不同浓度外源性H_2O_2干预后检测MG53蛋白表达;培养MG53基因敲除(MG53 KO)小鼠原代骨骼肌细胞,转染绿色荧光蛋白(Green fluorescent protein, GFP)-MG53质粒后用不同浓度外源性H_2O_2干预,活细胞成像系统观察细胞膜损伤后MG53的修复过程,用荧光相对改变量ΔF/F0表示MG53修复能力。结果:①外源性H_2O_2能显著促进MG53蛋白表达升高;②高浓度的H_2O_2能显著增强MG53的膜修复作用。结论:H_2O_2能促进MG53蛋白表达并增强其修复作用。
引文
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[31] Liu Y, Shi QF, Ye YC, et al. Activated O2-·and H2O2mediated cell survival in SU11274-treated non-small-cell lung cancer A549 cells via c-Met-PI3K-Akt and c-Met-Grb2/SOS-Ras-p38 pathways[J]. J Pharmacol Sci, 2012, 119(2):150—159.
[32] Zhang Y, Wu HK, Lv FX, et al. MG53 is a double-edged sword for human diseases[J]. Acta Physiologica Sinica,2016, 68(4):505—516.
[33] Zhang Y, Lv F, Jin L, et al. MG53 participates in ischaemic postconditioning through the RISK signaling pathway[J]. Cardiovascular Res, 2011, 91:108—115.
[34] Cao CM, Zhang Y, Weisleder N, et al. MG53 constitutes a primary determinant of cardiac ischemic preconditioning[J]. Circulation, 2010, 121:2565—2574.
[2] Wang X, Xie W, Zhang Y, et al. Cardioprotection of ischemia/reperfusion injury by cholesterol dependent MG53-mediated membrane repair[J]. Circ Res, 2010, 107(1):76—83.
[3] He B, Tang RH, Weisleder N, et al. Enhancing muscle membrane repair by gene delivery of MG53 amelio-rates muscular dystrophy and heart failure in delta-Sarcogly-can-deficient hamsters[J]. Mol Ther, 2012, 20(4):727—735.
[4] Li H, Duann P, Lin PH, et al. Modulation of wound healing and scar formation by MG53 protein-mediated cell membrane repair[J]. J Biol Chem, 2015, 290(40):24592—24603.
[5] Kim SC, Kellett T, Wang S, et al. TRIM72 is required for effective repair of alveolar epithelial cell wounding[J]. Am J Physiol Lung Cell Mol Physiol, 2014, 307(6):L449—L459.
[6] Jia Y, Chen K, Lin P, et al. Treatment of acute lung injury by targeting MG53-me-diated cell membrane repair[J]. Nat Commun, 2014, 5:4387.
[7] Duann P, Li H, Lin P, et al. MG53-mediated cell membrane repair protects against acute kidney injury[J]. Sci Transl Med, 2015, 7(279):279ra236.
[8]吴迎,伊木清,曾凡星. MG53基因敲除对小鼠延迟性肌肉酸痛期骨骼肌损伤的影响[J].中国康复医学杂志, 2017, 32(6):636—642.
[9] Saxena I, Srikanth S, Chen Z. Cross talk between H2O2and interacting signal molecules under plant stress response[J].Front Plant Sci, 2016, 7:570.
[10] Dorfman J, Duong M, Zibaitis A, et al. Myocardial tissue engineering with autolog-ous myoblast implantation[J]. J Thorac Cardiovasc Surg, 1998, 116(5):744—751.
[11] Miyamoto K, Yamashita T, Tsukiyama T, et al. Reversible membrane permeabilization of mammalian cells treated with digitonin and its use for inducing nuclear reprogramming by Xenopus egg extracts[J]. Cloning Stem Cells,2008, 10(4):535—542.
[12] Draeger A, Schoenauer R, Atanassoff AP, et al. Dealing with damage:Plasma membrane repair mechanisms[J]. Biochimie, 2014, 107:66—72.
[13] Reddy A, Caler EV, Andrews NW. Plasma membrane repair is mediated by Ca2+-regulated exocytosis of lysosomes[J]. Cell, 2001, 106:157—169.
[14] Horn A, Van der Meulen JH, Defour A, et al. Mitochondrial redox signaling enables repair of injured skeletal muscle cells[J]. Sci Signal, 2017, 495(10):1—11.
[15] Jensen TE, Schjerling P, Viollet B, et al. AMPKα1 activation is required for stimulation of glucose uptake by twitch contraction, but not by H2O2,in mouse skeletal muscle[J].Plos One, 2008, 3(5):e2102.
[16] Finkel T, Holbrook NJ. Oxidants, oxidative stress and the biology of ageing[J]. Nature, 2000, 408:239—247.
[17] Hu Y, Kang C, Philp RJ. PKC delta phosphorylates p52ShcA at Ser29 to regulate ERK activation in response to H2O2[J]. Cell Signal, 2007, 19(2):410—418.
[18] Kim YK, Bae GU, Kang JK. Cooperation of H2O2-mediated ERK activation with Smad pathway in TGF-beta 1 induction of p21(WAF1/Cip1)[J]. Cell Signal, 2006, 18(2):236—243.
[19] Maryam, Rasoul, Asadollah, et al. Time course study of JNK activation in response to H2O2induced oxidative stress[J]. Alzheimer’s and Dementia, 2014, 10:493.
[20] Sen P, Chakraborty PK, Raha S, et al. p38 mitogen-activated protein kinase(p38MAPK)upregulates catalase levels in response to low dose H2O2treatment through enhancement of mRNA stability[J]. FEBS Lett, 2005, 579(20):4402—4406.
[21] Hensley, Robinson, Stewart, et al. Modulation of p38 kinase activation by IL1 beta, H2O2and antioxidants in primary glial cell culture[J]. Faseb Journal, 1998, 12(8):1403.
[22] Duan X, Chan KT, Lee KK, et al. Oxidative stress and plasma membrane repair in single myoblasts after femtosecond laser photoporation[J]. Ann Biomed Eng, 2015, 43(11):2735—2744.
[23] Yao Y, Xiao Z, Wong S, et al. The effects of oxidative stress on the compressive damage thresholds of C2C12mouse myoblasts:implications for deep tissue injury[J].Ann Biomed Eng, 2015, 43(2):287—296.
[24] Sablina AA, Budanov AV, Llynskaya GV, et al. The antioxidant function of the P53 tumor suppressor[J]. Nat Med,2005, 11:1306—1313.
[25] Zhu H, Lin P, De G, et al. Polymerase transcriptase release factor(PTRF)anchors MG53 protein to cell injury site for initiation of membrane repair[J]. J Biol Chem,2011, 286(15):12820—12824.
[26] Nguyen N, Yi JS, Park H, et al. Mitsugumin53(MG53)ligase ubiquitinates focal adhesion kinase during skeletal myogenesis[J]. J Biol Chem, 2014, 289(6):3209—3216.
[27] Samuel H, Xingming S, Maribeth H, et al. Stromal cell-derived factor-1βmediates cell survival through enhancing autophagy in bone marrow-derived mesenchymal stem cells[J]. PLoS One, 2013, 8(3):e58207.
[28] Philip L, Shivakumar K. cIAP-2 protects cardiac fibroblasts from oxidative damage:an obligate regulatory role for ERK1/2 MAPK and NF-kappaB[J]. J Mol Cell Cardiol,2013, 62:217—226.
[29] Yu M, Zhi J, Cui Y, et al. Role of the JAK-STAT pathway in protection of hydrogen peroxide preconditioning against apoptosis induced by oxidative stress in PC12 cells[J]. Apoptosis, 2006, 11:931—941.
[30] Ma Y, Wu D, Ding X, et al. CD38 plays key roles in both antioxidation and cell survival of H2O2-treated primary rodent astrocytes[J]. Int J Physiol Pathophysiol Pharmacol,2014, 6(2):102—108.
[31] Liu Y, Shi QF, Ye YC, et al. Activated O2-·and H2O2mediated cell survival in SU11274-treated non-small-cell lung cancer A549 cells via c-Met-PI3K-Akt and c-Met-Grb2/SOS-Ras-p38 pathways[J]. J Pharmacol Sci, 2012, 119(2):150—159.
[32] Zhang Y, Wu HK, Lv FX, et al. MG53 is a double-edged sword for human diseases[J]. Acta Physiologica Sinica,2016, 68(4):505—516.
[33] Zhang Y, Lv F, Jin L, et al. MG53 participates in ischaemic postconditioning through the RISK signaling pathway[J]. Cardiovascular Res, 2011, 91:108—115.
[34] Cao CM, Zhang Y, Weisleder N, et al. MG53 constitutes a primary determinant of cardiac ischemic preconditioning[J]. Circulation, 2010, 121:2565—2574.