ArticleThe Journal of biological chemistry2010
The Necdin-Wnt pathway causes epigenetic peroxisome proliferator-activated receptor gamma repression in hepatic stellate cells.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 55 citations in OpenAlex.
- Prader-Willi syndrome protein necdin regulates the nucleocytoplasmic distribution and dopaminergic neuron development.Scientific reports · 2024Article
- Review
- Necdin: A purposive integrator of molecular interaction networks for mammalian neuron vitality.Genes to cells : devoted to molecular & cellular mechanisms · 2021Review
- Necdin regulates BMAL1 stability and circadian clock through SGT1-HSP90 chaperone machinery.Nucleic acids research · 2020Article
- Metabolic Coordination of Pericyte Phenotypes: Therapeutic Implications.Frontiers in cell and developmental biology · 2020Review
- Dickkopf-related protein 1 is a progestomedin acting on the bovine embryo during the morula-to-blastocyst transition to program trophoblast elongation.Scientific reports · 2019Article
- Elimination of Wnt Secretion From Stellate Cells Is Dispensable for Zonation and Development of Liver Fibrosis Following Hepatobiliary Injury.Gene expression · 2019Article
- Wnt-β-catenin signalling in liver development, health and disease.Nature reviews. Gastroenterology & hepatology · 2019Review
- AEBP1 expression increases with severity of fibrosis in NASH and is regulated by glucose, palmitate, and miR-372-3p.PloS one · 2019Article
- Aortic carboxypeptidase-like protein, a WNT ligand, exacerbates nonalcoholic steatohepatitis.The Journal of clinical investigation · 2018Article
- Naringin in Ganshuang Granule suppresses activation of hepatic stellate cells for anti-fibrosis effect by inhibition of mammalian target of rapamycin.Journal of cellular and molecular medicine · 2017Article
- Wnt Pathway Stabilizes MeCP2 Protein to Repress PPAR-γ in Activation of Hepatic Stellate Cells.PloS one · 2016Article
- Morphogen-related therapeutic targets for liver fibrosis.Clinics and research in hepatology and gastroenterology · 2015Review
- Metabolic reprogramming and cell fate regulation in alcoholic liver disease.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2015Review
- β-Catenin Signaling and Roles in Liver Homeostasis, Injury, and Tumorigenesis.Gastroenterology · 2015Review
- Perinatal nicotine exposure suppresses PPARγ epigenetically in lung alveolar interstitial fibroblasts.Molecular genetics and metabolism · 2015Article
- Epigenetic control of skin and hair regeneration after wounding.Experimental dermatology · 2015Review
- Differentiation of progenitors in the liver: a matter of local choice.The Journal of clinical investigation · 2013Review
- Peroxisome proliferator-activated receptor-γ as a therapeutic target for hepatic fibrosis: from bench to bedside.Cellular and molecular life sciences : CMLS · 2013Review
- Specific changes in the expression of imprinted genes in prostate cancer--implications for cancer progression and epigenetic regulation.Asian journal of andrology · 2012Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hepatic stellate cells (HSCs), vitamin A-storing liver pericytes, undergo myofibroblastic trans-differentiation or "activation" to participate in liver wound healing. This cellular process involves loss of regulation by adipogenic transcription factors such as peroxisome proliferator-activated receptor γ (PPARγ). Necdin, a melanoma antigen family protein, promotes neuronal and myogenic differentiation while inhibiting adipogenesis. The present study demonstrates that necdin is selectively expressed in HSCs among different liver cell types and induced during their activation in vitro and in vivo. Silencing of necdin with adenovirally expressed shRNA, reverses activated HSCs to quiescent cells in a manner dependent on PPARγ and suppressed canonical Wnt signaling. Promoter analysis, site-directed mutagenesis, and chromatin immunoprecipitation demonstrate that Wnt10b, a canonical Wnt induced in activated HSCs, is a direct target of necdin. Necdin silencing abrogates three epigenetic signatures implicated in repression of PPARγ: increased MeCP2 (methyl CpG binding protein 2) and HP-1α co-repressor recruitments to Pparγ promoter and enhanced H3K27 dimethylation at the exon 5 locus, again in a manner dependent on suppressed canonical Wnt. These epigenetic effects are reproduced by antagonism of canonical Wnt signaling with Dikkopf-1. Our results demonstrate a novel necdin-Wnt pathway, which serves to mediate antiadipogenic HSC trans-differentiation via epigenetic repression of PPARγ.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.