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Effect of glutamine treatment on human brain microvascular endothelial cells

ABSTRACT: We found glutamine levels were positively associated with a greater risk of stroke. After treatment with glutamine, HBMECs exhibited enhanced proliferation, migration, and EndMT, all reversed by ITGB4 knockdown. In ITGB4-transfected HBMECs, the MAPK-ERK-TGF-β/BMP pathway was activated, with Smad4 knockdown reversing the EndMT. Furthermore, atorvastatin suppressed the EndMT by inhibiting Smad1/5 phosphorylation and promoting Smad4 ubiquitination in ITGB4-transfected HBMECs. Finally, ITGB4 upregulation was confirmed in the superficial temporal arteries of patients with moyamoya.

ORGANISM(S): Homo sapiens

PROVIDER: GSE259423 | GEO | 2024/05/01

REPOSITORIES: GEO

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Operation of the atypical canonical BMP signaling pathway during human odontogenesis

Project description:BMP (bone morphogenetic protein) signaling plays essential roles in the regulation of early tooth development. It is well acknowledged that with binding of extracellular BMP ligands to the type I and type II transmembrane serine/threonine kinase receptor complexes when triggering of the BMP canonical signaling pathway, receptor activated Smad1/5/8 in cytoplasm bind to Smad4, the central mediator of the canonical BMP signaling pathway, to form transfer complexes for entering the nucleus and regulating target gene expression. However, our recent studies reveal the functional operation of a novel BMP mediated signaling pathway named as the atypical BMP canonical signaling pathway in mouse developing tooth, which is Smad1/5/8 dependent but Smad4 independent. In the current study, we investigated whether this atypical BMP canonical signaling is conserved in human odontogenesis. We showed that pSmad1/5/8 is required for expression of MSX1, a well-defined BMP signaling target gene, in human dental mesenchyme, but the typical BMP canonical signaling is indeed not operating in the early human developing tooth, as assessed by the absence of pSMAD1/5/8-SMAD4 complexes in the dental mesenchyme and expression of MSX1 and translocation of pSMAD1/5/8 induced by BMP4 protein is SMAD4-independent in dental mesenchymal cells. Moreover, RNA-Seq data sets comparing the transcriptome profiles of human dental mesenchymal cells with and without SMAD4 knockdown by siRNA displays unchanged expression profiles of pSMAD1/5/8 downstream target genes, further affirming the functional operation of the atypical canonical BMP signaling pathway in a manner of SMAD1/5/8-dependent but SMAD4-independent in the dental mesenchyme during early odontogenesis.

2021-09-30 | GSE179474 | GEO

TGF-beta signalling through SMAD1/5 is required for epithelial-to-mesenchymal transition

Project description:TGF-beta treatment leads to SMAD1/5 phosphorylation. However, the ability of SMAD1/5 to bind chromatin downstream of TGF-beta signalling is unknown. We performed ChIP-sequencing for pSMAD1/5 and SMAD3 to identify binding sites for pSMAD1/5 upon TGF-beta stimulation and identified preferential pSMAD1/5 binding at SMAD1/5:SMAD4 consensus sites.

2018-02-16 | GSE92443 | GEO

Genome-wide analysis of ERG- and FLI1-binding in HUVECs, and histone modifications in HUVECs treated with siControl or siERG+siFLI1

Project description:Endothelial-to-mesenchymal transition (EndMT) in which endothelial cells lose their characteristics and acquire mesenchymal property has recently been recognized as a driver of disease progression in wide range of pathologies. However, the regulatory mechanism of EndMT has not been fully understood. Here, we found that combined knockdown of two ETS family transcription factors, ERG and FLI1, induced EndMT. Hence, we analyzed functions of ERG and FLI1 using gene expression microarray and ChIP-seq to elucidate the regulatory mechanism of EndMT.

2018-11-23 | GSE109695 | GEO

Expression data in HUVECs treated with siERG, siFLI1, or both

2018-11-23 | GSE109662 | GEO

Effect of BMP4 and noggin on gene expression in murine R1 ES cells

2010-03-01 | GSE20527 | GEO

Gene expression profiling on innervated and denervated muscles of Smad4 KO and control mice.

Project description:To identify novel atrophy-related genes, which are controlled by BMP signaling, we performed gene expression profiling on innervated and 14 days denervated muscles of Smad4 knockout and control mice, focusing on genes that were differentially upregulated in denervated Smad4-/- muscles compared to controls. Among the different genes our attention was attracted by a gene that encodes for a novel f-box protein (Fbxo30) belonging to the SCF complex family of the ubiquitin ligases. Cell size is determined by the balance between protein synthesis and degradation. This equilibrium is affected by hormones, nutrients, energy levels, mechanical stress and cytokines. Mutations that inactivate Myostatin lead to important muscle growth in animals and humans. However, the signals and pathways responsible for this hypertrophy remain largely unknown. Here we find that BMP signaling, acting through Smad1/5/8, is the fundamental hypertrophic signal. Inhibition of BMP signaling causes muscle atrophy, abolishes the hypertrophic phenotype of Myostatin knockout and strongly exacerbates the effects of denervation and fasting. BMP-Smad1/5/8 negatively regulates a novel gene (Fbxo30) that encodes an ubiquitin ligase, that is required for muscle loss. Collectively, these data identify a critical role for the BMP pathway in adult muscle maintenance, growth and atrophy. Gene expression profiling on innervated and 14 days denervated muscles of Smad4 knockout and control mice. Three independent experiments were performed for each experimental condition using different animals for each experiment.

2013-09-17 | E-GEOD-49826 | biostudies-arrayexpress

Effect of BMP4 and noggin on gene expression in murine R1 ES cells

Project description:To confirm that the SMAD1/5- and SMAD4-associated genes are direct transcriptional regulators in mESCs in response to BMP, we treated undifferentiated R1 ES cells with BMP4 or with the BMP4 antagonist noggin, which can inhibit BMP signaling effectively for 4 h. Undifferentiated R1 ES cells were treated for 4 h with BMP4 or with the BMP4 antagonist noggin, which can inhibit BMP signaling effectively. Untreated R1 ES cells served as the control.

2010-03-07 | E-GEOD-20527 | biostudies-arrayexpress

Quantitative proteomics of the SMAD transcription factor family reveals IPO5 as a BMP Receptor-SMAD specific importin

Project description:Gene-specific transcription factors (GSTFs) control of gene transcription by DNA binding and specific protein complex recruitment, which regulates promoter accessibility for transcription initiation by RNA polymerase II. GSTFs that are frequently mutated in colon and rectal carcinomas are Suppressor of Mothers Against Decapentaplegic 2 (SMAD2) and SMAD4, which play an important role in the TGF-β signaling pathways controlling cell fate and proliferation (ref.). The SMAD protein family is a diverse and it can be divided into three subclasses: receptor activated SMADs, inhibitory SMADs and the common SMAD4 co-activator. To study protein interactors of the SMAD protein family we generated a quantitative proteomics pipeline that allows for inducible expression of GFP-tagged SMAD proteins followed by affinity purification and MS analysis. The nuclear importin IPO5 was identified as a novel interacting protein of SMAD1. Overexpression of IPO5 shows forced BMP R-SMAD nuclear localization confirming a functional relationship between BMP but not TGF-β R-SMADs and IPO5. Finally we provide evidence that the length of the lysine stretch in the NLS is involved in importin selection.

2016-10-10 | PXD004529 | Pride

Zka virus (ZIKV) persistently infects primary human brain microvascular endothelial cells

Project description:ZIKV alters transcriptional responses of infected cells to avoid immune detection. We have compared the transcriptional responses of ZIKV-infected hBMECs and mock-infected hBMECs. Examination of transcriptional responses of ZIKV-infected hBMECs versus mock-infected hBMECs

2017-07-15 | GSE98889 | GEO

A global view on the role of SMAD4 gene in porcine follicular granulosa cells by RNA-Seq

Project description:Sma- and Mad-related protein 4 (SMAD4) is closely associated with the development of ovarian follicular. However, current knowledge of the genome-wide view on the role of SMAD4 gene in mammalian follicular granulosa cells (GCs) is still largely unknown. In the present study, RNA-Seq was performed to investigate the effects of SMAD4 knockdown by RNA interference (SMAD4-siRNA) in porcine follicular GCs. A total of 1025 differentially expressed genes (DEGs), including 530 upregulated genes and 495 downregulated genes, were identified in SMAD4-siRNA treated GCs compared with that treated with NC-siRNA. Furthermore, functional enrichment analysis indicated that upregulated DEGs in SMAD4-siRNA treated cells were mainly enriched in cell-cycle related processes, interferon signaling pathway, and immune system process, while downregulated DEGs were mainly involved in extracellular matrix organization/disassembly, pathogenesis, and cell adhesion. In particular, cell cycle and TGF-Î² signaling pathway were discovered as the canonical pathways changed under the SMAD4 silencing. Taken together, our data reveals SMAD4 knockdown alters the expression of numerous genes involved in key biological processes of the development of follicular GCs and provides a novel global clue of the role of SMAD4 gene in porcine follicular GCs. mRNA profiles of NC-siRNA treated and SMAD4-siRNA treated porcine GCs were generated by RNA sequencing using Ion Torren Proton

2016-07-25 | E-GEOD-76833 | biostudies-arrayexpress

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