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Human BMSCs protein analysis that interact with TRAF4 during adipogenic differentiation

ABSTRACT: To explore the mechanism underlying the negative regulation of adipogenesis by TRAF4, we performed the LC-MS/MS experiments to identify the proteins that interact with TRAF4 during adipogenic differentiation.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Stem Cell, Cell Culture

SUBMITTER: Huiyong Shen

LAB HEAD: Huiyong Shen

PROVIDER: PXD017524 | Pride | 2020-05-27

REPOSITORIES: Pride

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TRAF4 acts as a fate checkpoint to regulate the adipogenic differentiation of MSCs by activating PKM2.

Cen Shuizhong S Li Jinteng J Cai Zhaopeng Z Pan Yiqian Y Sun Zehang Z Li Zhaofeng Z Ye Guiwen G Zheng Guan G Li Ming M Liu Wenjie W Yu Wenhui W Wang Shan S Xie Zhongyu Z Wang Peng P Shen Huiyong H

EBioMedicine 20200401

<h4>Background</h4>Mesenchymal stem cells (MSCs) selectively differentiate into adipocytes or osteoblasts, and several molecules control the fate determination of MSCs. Understanding these key checkpoints greatly contributes to the ability to induce specific MSC differentiation for clinical applications. In this study, we aimed to explore whether TNF receptor-associated factor 4 (TRAF4) affects MSC adipogenic differentiation, which we previously reported that could positively regulated the osteo ...[more]

PMID: 32268273

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AFF4 regulates cellular adipogenic differentiation via targeting autophagy

Project description:AFF4 was discovered as a scaffold protein of Super Elongation Complex (SEC) and exhibites an essential function on osteogenesis, tumorigenesis and odontogenesis. However, the adipogenic biological functions of AFF4 need further explorations. Here, we demonstrate that knockdown of AFF4 inhibits adipogenesis in both human mesenchymal stem cells (hMSCs) and lineage-committed 3T3-L1 preadipocytes. Conditional knocking down of Aff4 in transgenic mouse presents a thin body phenotype and impeded adipogenesis. Mechanistically, we define autophagy signaling as a crucial downstream of AFF4 through the combination of RNA-seq and ChIP-seq analyses. Depletion of AFF4 mediates the transcription of crutial autophagy genes ATG5 and ATG16L1. Simultaneous overexpression of ATG5 and ATG16L1 rescues the lineage commitment of AFF4-deficient cells. Our data elucidate that AFF4 is indispensable for adipogenic differentiation and reveal a novel mechanism for adipogenesis at transcriptional level.

2023-02-28 | GSE197354 | GEO

Chidamide suppresses adipogenic differentiation of bone marrow derived mesenchymal stem cells

Project description:To explore the potential mechanism of chidamide in BM-MSC-mediated adipogenesis, we have employed mRNA microarray expression profiling platform to identify significant differential genes associated with adipogenic differentiation and chidamide management.

2022-04-13 | GSE199466 | GEO

Surface Topography Enhances Differentiation of Mesenchymal Stem Cells Towards Osteogenic and Adipogenic Lineages

Project description:Surface topography impacts on cell growth and differentiation, but it is not trivial to generate homogeneous surface structures and to define the specific morphological parameters of relevance. In this study, we have compared gene expression profiles of mesenchymal stem cells (MSCs) on nanostructured groove/ridge surfaces. Patterns were generated in polyimide using multi beam laser interference. These structures affected cell size and orientation of human MSCs. Furthermore, the nano-patterns with a periodicity of 650 nm increased differentiation towards osteogenic and adipogenic lineages. However, in absence of differentiation media the surface structures did neither induce differentiation, nor lineage-specific gene expression changes – as assessed by genome wide gene expression profiles with Affymetrix microarray technology. Our results demonstrate that grooves and ridges at a periodicity of 650 nm enhance the propensity of MSCs to differentiate towards adipogenic and/or osteogenic lineages – but they do not directly govern lineage-specific gene expression changes. 9 samples were hybridized to the GeneChip Human Gene 2.0 ST Array (Affymetrix). In comparison to the manuscript the donor IDs refer as follows: donor 1 = AT57; donor 2 = AT58; donor 3 = AT61.

2015-08-25 | E-GEOD-61113 | biostudies-arrayexpress

DNA demethylase ALKBH1 promotes adipogenic differentiation via regulation of HIF-1 signaling

Project description:DNA 6-adenine methylation (6mA), as a novel adenine modification existing in eukaryotes, shows essential functions in embryogenesis and mitochondrial transcriptions. ALKBH1 is a demethylase of 6mA and plays critical roles in osteogenesis, tumorigenesis, and adaptation to stress. However, the integrated biological functions of ALKBH1 still require further exploration. Here, we demonstrate that knockdown of ALKBH1 inhibits adipogenic differentiation in both human mesenchymal stem cells (hMSCs) and 3T3-L1 preadipocytes, while overexpression of ALKBH1 leads to increased adipogenesis. Using a combination of RNA-seq and N6-mA-DNA-IP-seq analyses, we identify hypoxia-inducible factor-1 (HIF-1) signaling as a crucial downstream target of ALKBH1 activity. Depletion of ALKBH1 leads to hypermethylation of both HIF-1α and its downstream target GYS1. Simultaneous overexpression of HIF-1α and GYS1 restores the adipogenic commitment of ALKBH1-deficient cells. Taken together, our data indicate that ALKBH1 is indispensable for adipogenic differentiation, revealing a novel epigenetic mechanism that regulates adipogenesis.

2021-12-12 | GSE177059 | GEO

Brown Adipogenic Reprogramming Induced by a Small Molecule

Project description:Transcriptome analysis of early adipogenesis induced by basal adipogenesis medium(AM) and AM+Bex for 2 days in C2C12 cells Global gene expression profiling has shown Bex induced adipogenic genes expression change We analyzed 4 samples from basal adipogenesis medium(AM) and AM+Bex(10uM) treated C2C12 cells using the Affymetrix Mouse Gene 1.0 ST platform. Array data was processed by Affymetrix Expression Console and Transcriptome Analysis Console (TAC) software.

2013-11-15 | E-GEOD-52364 | biostudies-arrayexpress

Brown Adipogenic Reprogramming Induced by a Small Molecule

2013-11-15 | GSE52364 | GEO

Surface topography enhances differentiation of mesenchymal stem cells towards osteogenic and adipogenic lineages

Project description:Surface topography impacts on cell growth and differentiation, but it is not trivial to generate defined surface structures and to assess the relevance of specific topographic parameters. In this study, we have systematically compared in vitro differentiation of mesenchymal stem cells (MSCs) on a variety of groove/ridge structures. Micro- and nano-patterns were generated in polyimide using reactive ion etching or multi beam laser interference, respectively. These structures affected cell spreading and orientation of human MSCs, which was also reflected in focal adhesions morphology and size. Time-lapse demonstrated directed migration parallel to the nano-patterns. Overall, surface patterns clearly enhanced differentiation of MSCs towards specific lineages: 15 um ridges increased adipogenic differentiation whereas 2 um ridges enhanced osteogenic differentiation. Notably, nano-patterns with a periodicity of 650 nm increased differentiation towards both osteogenic and adipogenic lineages. However, in absence of differentiation media surface structures did neither induce differentiation, nor lineage-specific gene expression changes. Furthermore, nanostructures did not affect the YAP/TAZ complex, which is activated by substrate stiffness. Our results provide further insight into how structuring of tailored biomaterials and implant interfaces - e.g. by multi beam laser interference in sub-micrometer scale - do not induce differentiation of MSCs per se, but support their directed differentiation.

2018-09-20 | E-MTAB-7177 | biostudies-arrayexpress

RNA-seq of ZFP30 knock-down and knock-out in mouse 3T3-L1 and IBA cells during adipogenic differentiation

Project description:We show that a hitherto poorly characterized KRAB domain-containing zinc-finger (ZF) transcription factor, ZFP30, positively regulates adipogenesis. We demonstrate ZFP30’s function in murine in vitro and in vivo models, as well as in human stromal vascular fraction cells. We reveal through mechanistic studies that ZFP30 directly targets and activates Pparg2 by binding a retrotransposon-derived enhancer, suggesting a process of adipogenic exaptation. We further show that ZFP30 recruits the co-regulator KRAB-associated protein 1 (KAP1), which, surprisingly, acts as a ZFP30 co-activator in this adipogenic context. We show that a hitherto poorly characterized KRAB domain-containing zinc-finger (ZF) transcription factor, ZFP30, positively regulates adipogenesis. We demonstrate ZFP30’s function in murine in vitro and in vivo models, as well as in human stromal vascular fraction cells. To globally characterize ZFP30’s target landscape, we performed transcriptomic analyses after Zfp30 reduction or absence, in 3T3-L1 and in IBA cells, respectively. As we already observed significant (p<0.01, t-test) reduction in adipogenic marker gene expression in Zfp30 KD samples after two days of adipogenic induction, we included day 0 and day 2 measurements in both 3T3-L1 and IBA cells, and two additional time-points (2 hours and day 4) in IBA cells.

2019-03-01 | E-MTAB-6995 | biostudies-arrayexpress

Expression profiling of mouse bone marrow skeletal progenitors with osteogenic and adipogenic potential and adipogenic progenitors treated with IFNγ.

Project description:Bone marrow stromal cells (BMSCs) were isolated from the femora and tibiae of irtTA-GBD*-TAg transgenic mice. Using cellular cloning we established skeletal progenitors with unipotent osteogenic and adipogenic properties. Previous RNA-seq analysis of more progenitor types revealed differential expression in members of the Interferon-gamma (IFNγ) signaling pathway. Treatment of adipogenic progenitors with IFNγ inhibited adipogenesis and promoted osteogenesis. RNA-seq analysis of osteogenic, adipogenic and IFNγ treated adipogenic clones revealed factors controlling the osteogenic versus adipogenic commitment of bone marrow skeletal progenitors.

2018-07-02 | GSE114475 | GEO

Development of a 3D fatty infiltration platform to model, at higher scale, the impact of LY2090314 compound on fibro/adipogenic progenitor adipogenic drift

Project description:In human dystrophies, the progressive muscle wasting is exacerbated by ectopic deposition of fat and fibrous tissue originating from fibro/adipogenic progenitors (FAPs). In degenerating muscles, the ability of these cells to adjuvate a successful healing is attenuated and FAPs aberrantly expand and differentiate into adipocytes and fibroblasts. Thus, arresting the fibroadipogenic fate of FAPs, without affecting their physiological role, represents a valuable therapeutic strategy for patients affected by muscle diseases. Here, using a panel of adipose progenitor cells including human-derived FAPs coupled with pharmacological perturbations and proteome profiling, we report that LY2090314 interferes with a genuine adipogenic program acting as WNT surrogate for the stabilization of a competent -catenin transcriptional complex. To predict the beneficial impact of LY2090314 in limiting ectopic deposition of fat in human muscles, we combined the Poly-Ethylene-Glycol-Fibrinogen biomimetic matrix with these progenitor cells to create a miniaturized 3D model of adipogenesis. Using this scalable system, we demonstrated that a two-digit nanomolar dose of this compound is effective to repress adipogenesis in a higher 3D scale, thus offering a concrete proof for the use of LY2090314 to limit FAP-derived fat infiltrates in dystrophic muscles.

2023-06-13 | PXD040479 | Pride

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