Cellular polyploidy in organ homeostasis and regeneration

被引:9
作者
Fang, Juntao [1 ]
de Bruin, Alain [2 ,3 ]
Villunger, Andreas [4 ,5 ,6 ]
Schiffelers, Raymond [7 ]
Lei, Zhiyong [1 ,7 ]
Sluijter, Joost P. G. [1 ]
机构
[1] Univ Med Ctr Utrecht, Dept Expt Cardiol, Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands
[2] Univ Groningen, Dept Pediat, POB 30-001, NL-9700 RB Groningen, Netherlands
[3] Univ Utrecht, Dutch Mol Pathol Ctr, Dept Pathobiol, Yalelaan1, NL-3584 CL Utrecht, Netherlands
[4] Med Univ Innsbruck, Inst Dev Immunol, Bioctr, Innrain 80, A-6020 Innsbruck, Austria
[5] Ludwig Boltzmann Inst Rare & Undiagnosed Dis, Lazarettgasse 14,AKH BT 25-3 C-O CeMM Res Bldg,Hau, A-1090 Vienna, Austria
[6] CeMM Res Ctr Mol Med Austrian Acad Sci, Lazarettgasse 14,AKH BT 25-3, A-1090 Vienna, Austria
[7] Univ Med Ctr Utrecht, CDL Res, Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands
基金
欧洲研究理事会;
关键词
cellular polyploidy; tissue regeneration; cardiac regeneration; liver regeneration; MEDIATED ABSCISSION CHECKPOINT; POSTNATAL LIVER DEVELOPMENT; CARDIOMYOCYTE DNA-SYNTHESIS; TROPHOBLAST STEM-CELLS; IN-VIVO; HEPATOCYTE PLOIDY; CARDIAC MYOCYTES; PARTIAL-HEPATECTOMY; HEART REGENERATION; MAMMALIAN HEART;
D O I
10.1093/procel/pwac064
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Polyploid cells, which contain more than one set of chromosome pairs, are very common in nature. Polyploidy can provide cells with several potential benefits over their diploid counterparts, including an increase in cell size, contributing to organ growth and tissue homeostasis, and improving cellular robustness via increased tolerance to genomic stress and apoptotic signals. Here, we focus on why polyploidy in the cell occurs and which stress responses and molecular signals trigger cells to become polyploid. Moreover, we discuss its crucial roles in cell growth and tissue regeneration in the heart, liver, and other tissues.
引用
收藏
页码:560 / 578
页数:19
相关论文
共 257 条
[1]   MYOCARDIAL DNA CONTENT, PLOIDY LEVEL AND CELL NUMBER IN GERIATRIC HEARTS - POSTMORTEM EXAMINATIONS OF HUMAN MYOCARDIUM IN OLD-AGE [J].
ADLER, CP ;
FRIEDBURG, H .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1986, 18 (01) :39-53
[2]  
Adler CP, 1996, VIRCHOWS ARCH, V429, P159
[3]   Probing the role of septins in cardiomyocytes [J].
Ahuja, Preeti ;
Perriard, Evelyne ;
Trimble, William ;
Perriard, Jean-Claude ;
Ehler, Elisabeth .
EXPERIMENTAL CELL RESEARCH, 2006, 312 (09) :1598-1609
[4]   Postnatal telomere dysfunction induces cardiomyocyte cell-cycle arrest through p21 activation [J].
Aix, Esther ;
Gutierrez-Gutierrez, Oscar ;
Sanchez-Ferrer, Carlota ;
Aguado, Tania ;
Flores, Ignacio .
JOURNAL OF CELL BIOLOGY, 2016, 213 (05) :571-583
[5]  
Al-Hussaini H, 2008, MOL VIS, V14, P1784
[6]   Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice [J].
Ali, Shah R. ;
Hippenmeyer, Simon ;
Saadat, Lily V. ;
Luo, Liqun ;
Weissman, Irving L. ;
Ardehali, Reza .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2014, 111 (24) :8850-8855
[7]   Genome multiplication as adaptation to tissue survival: Evidence from gene expression in mammalian heart and liver [J].
Anatskaya, Olga V. ;
Vinogradov, Alexander E. .
GENOMICS, 2007, 89 (01) :70-80
[8]   Paraoxical relationship between protein content and nucleolar activity in mammalian cardiomyocytes [J].
Anatskaya, OV ;
Vinogradov, AE .
GENOME, 2004, 47 (03) :565-578
[9]   HEPATOCYTE POLYPLOIDY AND METABOLISM LIFE-HISTORY TRAITS - HYPOTHESES TESTING [J].
ANATSKAYA, OV ;
VINOGRADOV, AE ;
KUDRYAVTSEV, BN .
JOURNAL OF THEORETICAL BIOLOGY, 1994, 168 (02) :191-199
[10]  
Anatskaya OV, 2001, J EXP ZOOL, V289, P48, DOI 10.1002/1097-010X(20010101/31)289:1<48::AID-JEZ5>3.0.CO