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Heart repair by reprogramming non-myocytes with cardiac transcription factors.
Song K, Nam YJ, Luo X, Qi X, Tan W, Huang GN, Acharya A, Smith CL, Tallquist MD, Neilson EG, Hill JA, Bassel-Duby R, Olson EN
(2012) Nature 485: 599-604
MeSH Terms: Animals, Basic Helix-Loop-Helix Transcription Factors, Cell Lineage, Cell Transdifferentiation, Cellular Reprogramming, Fibroblasts, Heart, Mice, Myocardial Infarction, Myocardium, Myocytes, Cardiac, Phenotype, Regenerative Medicine, S100 Calcium-Binding Protein A4, S100 Proteins, Tail, Transcription Factors
Show Abstract · Added August 1, 2014
The adult mammalian heart possesses little regenerative potential following injury. Fibrosis due to activation of cardiac fibroblasts impedes cardiac regeneration and contributes to loss of contractile function, pathological remodelling and susceptibility to arrhythmias. Cardiac fibroblasts account for a majority of cells in the heart and represent a potential cellular source for restoration of cardiac function following injury through phenotypic reprogramming to a myocardial cell fate. Here we show that four transcription factors, GATA4, HAND2, MEF2C and TBX5, can cooperatively reprogram adult mouse tail-tip and cardiac fibroblasts into beating cardiac-like myocytes in vitro. Forced expression of these factors in dividing non-cardiomyocytes in mice reprograms these cells into functional cardiac-like myocytes, improves cardiac function and reduces adverse ventricular remodelling following myocardial infarction. Our results suggest a strategy for cardiac repair through reprogramming fibroblasts resident in the heart with cardiogenic transcription factors or other molecules.
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17 MeSH Terms
A lentiviral functional proteomics approach identifies chromatin remodeling complexes important for the induction of pluripotency.
Mak AB, Ni Z, Hewel JA, Chen GI, Zhong G, Karamboulas K, Blakely K, Smiley S, Marcon E, Roudeva D, Li J, Olsen JB, Wan C, Punna T, Isserlin R, Chetyrkin S, Gingras AC, Emili A, Greenblatt J, Moffat J
(2010) Mol Cell Proteomics 9: 811-23
MeSH Terms: Amino Acid Sequence, Animals, Cell Line, Cellular Reprogramming, Chromatography, Affinity, Chromosomal Proteins, Non-Histone, Humans, Kruppel-Like Transcription Factors, Lentivirus, Mice, Molecular Sequence Data, Multiprotein Complexes, Pluripotent Stem Cells, Protein Binding, Proteomics, Transcription Factors, Transcription, Genetic
Show Abstract · Added February 25, 2014
Protein complexes and protein-protein interactions are essential for almost all cellular processes. Here, we establish a mammalian affinity purification and lentiviral expression (MAPLE) system for characterizing the subunit compositions of protein complexes. The system is flexible (i.e. multiple N- and C-terminal tags and multiple promoters), is compatible with Gateway cloning, and incorporates a reference peptide. Its major advantage is that it permits efficient and stable delivery of affinity-tagged open reading frames into most mammalian cell types. We benchmarked MAPLE with a number of human protein complexes involved in transcription, including the RNA polymerase II-associated factor, negative elongation factor, positive transcription elongation factor b, SWI/SNF, and mixed lineage leukemia complexes. In addition, MAPLE was used to identify an interaction between the reprogramming factor Klf4 and the Swi/Snf chromatin remodeling complex in mouse embryonic stem cells. We show that the SWI/SNF catalytic subunit Smarca2/Brm is up-regulated during the process of induced pluripotency and demonstrate a role for the catalytic subunits of the SWI/SNF complex during somatic cell reprogramming. Our data suggest that the transcription factor Klf4 facilitates chromatin remodeling during reprogramming.
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17 MeSH Terms