The 4th Dimension and Adult Stem Cells: Can Timing Be Everything?

被引:27
作者
Gimble, Jeffrey M. [1 ]
Floyd, Z. Elizabeth [2 ]
Bunnell, Bruce A. [3 ,4 ,5 ]
机构
[1] Pennington Biomed Res Ctr, Stem Cell Biol Lab, Baton Rouge, LA 70808 USA
[2] Pennington Biomed Res Ctr, Ubiquitin Lab, Baton Rouge, LA 70808 USA
[3] Tulane Univ, Sch Med, Dept Pharmacol, New Orleans, LA 70112 USA
[4] Tulane Univ, Sch Med, Ctr Gene Therapy, New Orleans, LA 70112 USA
[5] Tulane Natl Primate Res Ctr, Div Gene Therapy, Covington, LA 70433 USA
关键词
ADIPOSE-DERIVED STEM CELL; BONE MARROW-DERIVED MESENCHYMAL STEM CELL; CANCER STEM CELL; CIRCADIAN; HEMATOPOIETIC STEM CELL; REV-ERB-ALPHA; CIRCADIAN GENE-EXPRESSION; HUMAN BONE-MARROW; GLYCOGEN-SYNTHASE KINASE-3; COLONY-STIMULATING FACTOR; CLOCK GENES; MOLECULAR CLOCK; IN-VITRO; SEASONAL-VARIATIONS; SIGNALING PATHWAYS;
D O I
10.1002/jcb.22153
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The rotation of the earth on its axis influences the physiology of all organisms. A highly conserved set of genes encoding the core circadian regulatory proteins (CCRP) has evolved across species. The CCRP acts through transcriptional and post-transcriptional mechanisms to direct the oscillatory expression of genes essential for key metabolic events. In addition to the light:dark cycle, the CCRP expression can be entrained by changes in feeding and physical activity patterns. While mammalian CCRP were originally associated with the central clock located within the suprachiasmatic nucleus of the brain, there is a growing body of evidence documenting the presence of the CCRP in peripheral tissues. It is now evident that the CCRP play a role in regulating the proliferation, differentiation, and function of adult stem cells in multiple organs. This concise review highlights findings concerning the role of the CCRP in modulating the adult stem cell activities. Although the manuscript focuses on hematopoietic stem cells (HSCs), bone marrow-derived mesenchymal stem cells (BMSCs), adipose-derived stem cells (ASCs) and cancer stem cells, it is likely that the contribution of the CCRP merits consideration and evaluation in all stem cell pathways. J. Cell. Biochem. 107: 569-578, 2009. (C) 2009 Wiley-Liss, Inc.
引用
收藏
页码:569 / 578
页数:10
相关论文
共 123 条
[1]  
AARDAL NP, 1984, EXP HEMATOL, V12, P61
[2]  
AARDAL NP, 1983, EXP HEMATOL, V11, P792
[3]   Circadian rhythm of granulocyte-macrophage colony-stimulating factor in normal subjects and neutropenic hospitalised patients [J].
Abdelaal, MA ;
Hashim, IA ;
Zawawi, TH ;
Felimban, SK ;
Sobhi, EM ;
Jeje, O ;
Oni, GA .
IRISH JOURNAL OF MEDICAL SCIENCE, 2000, 169 (01) :55-57
[4]  
Abrahamsen JF, 1997, EUR J HAEMATOL, V58, P333
[5]   The orphan nuclear receptor RORα regulates circadian transcription of the mammalian core-clock Bmal1 [J].
Akashi, M ;
Takumi, T .
NATURE STRUCTURAL & MOLECULAR BIOLOGY, 2005, 12 (05) :441-448
[6]   Control of intracellular dynamics of mammalian period proteins by casein kinase I ε (CKIε) and CKIδ in cultured cells [J].
Akashi, M ;
Tsuchiya, Y ;
Yoshino, T ;
Nishida, E .
MOLECULAR AND CELLULAR BIOLOGY, 2002, 22 (06) :1693-1703
[7]   Nuclear receptor corepressor and histone deacetylase 3 govern circadian metabolic physiology [J].
Alenghat, Theresa ;
Meyers, Katherine ;
Mullican, Shannon E. ;
Leitner, Kirstin ;
Adeniji-Adele, Adetoun ;
Avila, Jacqueline ;
Bucan, Maja ;
Ahima, Rexford S. ;
Kaestner, Klaus H. ;
Lazar, Mitchell A. .
NATURE, 2008, 456 (7224) :997-U88
[8]   Rhythmic messenger ribonucleic acid expression of clock genes and adipocytokines in mouse visceral adipose tissue [J].
Ando, H ;
Yanagihara, H ;
Hayashi, Y ;
Obi, Y ;
Tsuruoka, S ;
Takamura, T ;
Kaneko, S ;
Fujimura, A .
ENDOCRINOLOGY, 2005, 146 (12) :5631-5636
[9]   Disruption of the circadian clock due to the Clock mutation has discrete effects on aging and carcinogenesis [J].
Antoch, Marina P. ;
Gorbacheva, Victoria Y. ;
Vykhovanets, Olena ;
Toshkov, Illia A. ;
Kondratov, Roman V. ;
Kondratova, Anna A. ;
Lee, Choogon ;
Nikitin, Alexander Yu .
CELL CYCLE, 2008, 7 (09) :1197-1204
[10]   LITHIUM ION REVERSIBLY INHIBITS INDUCER-STIMULATED ADIPOSE CONVERSION OF 3T3-LL CELLS [J].
ARATANI, Y ;
SUGIMOTO, E ;
KITAGAWA, Y .
FEBS LETTERS, 1987, 218 (01) :47-51