F- acts as a pro-differentiation element for SMC38, yet within the

F- acts as a pro-differentiation issue for SMC38, yet in the setting of vascular injury the net result of TGF- antagonism is lowered neointima formation31, 33. Our final results suggest that TGF- signaling in maturing monocyte/macrophages results in an activated cell that subsequently secretes things capable of further activating SMC upon vascular injury.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSupplementary MaterialRefer to Net version on PubMed Central for supplementary material.AcknowledgmentsNone.Arterioscler Thromb Vasc Biol. Author manuscript; obtainable in PMC 2015 April 01.Ostriker et al. Sources of FundingPageThis operate was supported by grants from the NIH to Drs. Nemenoff (2P01 HL014985) and Weiser-Evans (1R01 HL88643 and 2P01 HL014985) plus a fellowship grant in the American Heart Association (12PRE11800015; AO).NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptAbbreviationsSMC M M0 sM tM CM SRM vascular smooth muscle cell macrophage macrophages matured in the absence of SMC conditioned medium macrophage matured within the presence of SMC conditioned medium macrophage matured within the presence of recombinant TGF- conditioned medium culture medium containing 0.1 FBS
HHS Public AccessAuthor manuscriptNat Cell Biol. Author manuscript; offered in PMC 2014 January 01.Published in final edited type as: Nat Cell Biol. 2013 July ; 15(7): 87282. doi:10.1038/ncb2768.Author Manuscript Author Manuscript Author Manuscript Author ManuscriptProteomic and genomic approaches reveal essential functions of H3K9 methylation and Heterochromatin Protein-1 in reprogramming to pluripotencyRupa Sridharan1,2, Michelle Gonzales-Cope3, , Constantinos Chronis1, , Giancarlo Bonora1, Robin McKee1, Chengyang Huang1, Sanjeet Patel1, David Lopez1, Nilamadhab Mishra4, Matteo Pellegrini1, Michael Carey1, Benjamin A. Garcia3,#, and Kathrin Plath1,#1Universityof California Los Angeles, David Geffen School of Medicine, Division of Biological Chemistry, Jonsson Comprehensive Cancer Center, Molecular Biology Institute, Bioinformatics Interdepartmental Degree System, Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research3EpigeneticsProgram, Department of Biochemistry and Biophysics, Perelman School of Medicine, University of Pennsylvania, 1009C Stellar-Chance Laboratories, 422 Curie Boulevard, Philadelphia, PA, 19104, USA4Sectionon Rheumatology, Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, North CarolinaAbstractReprogramming of somatic cells into iPSCs includes a dramatic reorganization of chromatin. To recognize posttranslational histone modifications that alter in global abundance in the course of this course of action, we have applied a quantitative mass-spectrometry-based method. We found that iPSCs, compared to both the starting fibroblasts in addition to a late reprogramming intermediate (pre-iPSCs), are enriched for histone modifications related with active chromatin, and depleted for marks of transcriptional elongation along with a subset of repressive modifications including H3K9me2/me3.Ethacrynic acid Dissecting the contribution of H3K9methylation to reprogramming, we show that the H3K9methyltransferases Ehmt1, Ehmt2, and Setdb1 regulate international H3K9me2/me3 levels and that their depletion increases iPSC formation from both fibroblasts and pre-iPSCs.Acalabrutinib Similarly, inhibition of heterochromatin-protein-1 (Cbx3), a protein recognized to recognize H3K9methylation, enhances reprogramming.PMID:28630660 Genome-wide l.