PMID- 24209617
OWN - NLM
STAT- MEDLINE
DCOM- 20140123
LR  - 20220318
IS  - 1097-4172 (Electronic)
IS  - 0092-8674 (Print)
IS  - 0092-8674 (Linking)
VI  - 155
IP  - 4
DP  - 2013 Nov 7
TI  - Lin28 enhances tissue repair by reprogramming cellular metabolism.
PG  - 778-92
LID - S0092-8674(13)01278-6 [pii]
LID - 10.1016/j.cell.2013.09.059 [doi]
AB  - Regeneration capacity declines with age, but why juvenile organisms show enhanced 
      tissue repair remains unexplained. Lin28a, a highly conserved RNA-binding protein 
      expressed during embryogenesis, plays roles in development, pluripotency, and 
      metabolism. To determine whether Lin28a might influence tissue repair in adults, 
      we engineered the reactivation of Lin28a expression in several models of tissue 
      injury. Lin28a reactivation improved hair regrowth by promoting anagen in hair 
      follicles and accelerated regrowth of cartilage, bone, and mesenchyme after ear 
      and digit injuries. Lin28a inhibits let-7 microRNA biogenesis; however, let-7 
      repression was necessary but insufficient to enhance repair. Lin28a bound to and 
      enhanced the translation of mRNAs for several metabolic enzymes, thereby 
      increasing glycolysis and oxidative phosphorylation (OxPhos). Lin28a-mediated 
      enhancement of tissue repair was negated by OxPhos inhibition, whereas a 
      pharmacologically induced increase in OxPhos enhanced repair. Thus, Lin28a 
      enhances tissue repair in some adult tissues by reprogramming cellular 
      bioenergetics. PAPERCLIP:
CI  - Copyright (c) 2013 Elsevier Inc. All rights reserved.
FAU - Shyh-Chang, Ng
AU  - Shyh-Chang N
AD  - Stem Cell Transplantation Program, Division of Pediatric Hematology/Oncology, 
      Boston Children's Hospital and Dana-Farber Cancer Institute, Boston, MA 02115, 
      USA; Department of Biological Chemistry and Molecular Pharmacology, Harvard 
      Medical School, Boston, MA 02115, USA; Harvard Stem Cell Institute, Boston, MA 
      02115, USA; Manton Center for Orphan Disease Research, Boston, MA 02115, USA; 
      Howard Hughes Medical Institute, Boston, MA 02115, USA; Department of Medicine, 
      Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, MA 
      02115, USA.
FAU - Zhu, Hao
AU  - Zhu H
FAU - Yvanka de Soysa, T
AU  - Yvanka de Soysa T
FAU - Shinoda, Gen
AU  - Shinoda G
FAU - Seligson, Marc T
AU  - Seligson MT
FAU - Tsanov, Kaloyan M
AU  - Tsanov KM
FAU - Nguyen, Liem
AU  - Nguyen L
FAU - Asara, John M
AU  - Asara JM
FAU - Cantley, Lewis C
AU  - Cantley LC
FAU - Daley, George Q
AU  - Daley GQ
LA  - eng
GR  - HHMI/Howard Hughes Medical Institute/United States
GR  - K08 CA157727/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cell
JT  - Cell
JID - 0413066
RN  - 0 (Lin-28 protein, mouse)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA-Binding Proteins)
RN  - 0 (mirnlet7 microRNA, mouse)
SB  - IM
CIN - Cell. 2013 Nov 7;155(4):738-9. PMID: 24209612
CIN - Nat Rev Mol Cell Biol. 2014 Jan;15(1):4. PMID: 24281190
CIN - EMBO J. 2014 Jan 7;33(1):5-6. PMID: 24357531
MH  - Animals
MH  - Embryo, Mammalian/metabolism
MH  - Energy Metabolism
MH  - Extremities/physiology
MH  - Hair Follicle/physiology
MH  - Humans
MH  - Mice
MH  - Mice, Transgenic
MH  - MicroRNAs/metabolism
MH  - RNA-Binding Proteins/*metabolism
MH  - Regeneration
MH  - *Wound Healing
PMC - PMC3917449
MID - NIHMS540675
EDAT- 2013/11/12 06:00
MHDA- 2014/01/24 06:00
PMCR- 2014/11/07
CRDT- 2013/11/12 06:00
PHST- 2013/02/12 00:00 [received]
PHST- 2013/07/23 00:00 [revised]
PHST- 2013/09/27 00:00 [accepted]
PHST- 2013/11/12 06:00 [entrez]
PHST- 2013/11/12 06:00 [pubmed]
PHST- 2014/01/24 06:00 [medline]
PHST- 2014/11/07 00:00 [pmc-release]
AID - S0092-8674(13)01278-6 [pii]
AID - 10.1016/j.cell.2013.09.059 [doi]
PST - ppublish
SO  - Cell. 2013 Nov 7;155(4):778-92. doi: 10.1016/j.cell.2013.09.059.