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The analysis of the role of ALK-1/SMAD/ATOH8 axis in endothelial cells

ABSTRACT: The analysis of the role of ALK-1/SMAD/ATOH8 axis in endothelial cells

PROVIDER: PRJNA413483 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6144350.fastq.gz	Fastqsanger.gz
	SRR6144351.fastq.gz	Fastqsanger.gz
	SRR6144352.fastq.gz	Fastqsanger.gz
	SRR6144349.fastq.gz	Fastqsanger.gz
	SRR8521237.fastq.gz	Fastqsanger.gz

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SMAD1/5 binding pattern in human pulmonary arterial endothelial cells [ChIP-seq]

Project description:We showed that the BMPRII/ALK-1/SMAD/ATOH8 axis protects against the development of pulmonary arterial hypertension (PAH). We have performed ChIP-seq analyses to reveal the function of both SMAD and ATOH8.

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bHLH transcription factor ATOH8 depletion effect on endothelial cells: loss-of-function model [LOF]

Project description:Analysis of human umbilical vein endothelial cells (HUVECs) depleted for the transcription factor ATOH8.

2019-10-17 | GSE104684 | GEO

bHLH transcription factor ATOH8 overexpression effect on endothelial cells: gain-of-function model [GOF]

Project description:Analysis of human umbilical vein endothelial cells (HUVECs) adenovirally expressing the transcription factor ATOH8.

2019-10-17 | GSE104683 | GEO

The analysis of the role of ALK-1/SMAD/ATOH8 axis in endothelial cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-10-17 | GSE104685 | GEO

Loss of Atoh8 impairs macroautophagy

Project description:The basic helix-loop-helix (bHLH) transcription factor ‘Atoh8’ is involved in the regulaton of several developmental processes and pathologies. It regulates organogenesis, reprogramming, stem cell fate determination, and cancer development. However, the mech anisms underlying these observations remain unclear. Unlike many tissue-specific bHLH factors, Atoh8 is ubiquitously expressed during development as well as in adult tissue. In this study, we explored whether Atoh8 modulates basic cellular functions, which may reveal a common mechanism that could explain the diverse observations reported in the literature. In the present study, our findings indicate that the loss of Atoh8 impairs autophagy. We observed differential expression of LC3B-II, TFEB, and accumulation of p62 in the absence or downregulation of Atoh8 in multiple cell lines. Moreover, mass spectrometric analysis of protein lysates from the tibialis anterior (TA) muscle in both wildtype and Atoh8 knockout mice revealed a significant downregulation of proteins associated with the initiation of autophagy (DEPTOR, PRAS40), autophagosome maturation (PDCD6IP, CHMP5), and autolysosomal degradation (NPC2, CTSB, CTSL). Additionally, the analysis indicated altered metabolism in the absence of Atoh8. Moreover, we determined that persistently elevated levels of reactive oxygen species (ROS) may be the primary factor contributing to the impairment of autophagy in the absence or downregulation of Atoh8.Overall, this study underscores that Atoh8 is a crucial regulator of autophagy, and its reduction or absence disrupts the autophagic process.

2026-01-05 | PXD070896 | Pride

The ALK-1/SMAD/ATOH8 axis attenuates hypoxic responses and protects against the development of pulmonary arterial hypertension.

Project description:Dysregulated bone morphogenetic protein (BMP) signaling in endothelial cells (ECs) is implicated in vascular diseases such as pulmonary arterial hypertension (PAH). Here, we showed that the transcription factor ATOH8 was a direct target of SMAD1/5 and was induced in a manner dependent on BMP but independent of Notch, another critical signaling pathway in ECs. In zebrafish and mice, inactivation of Atoh8 did not cause an arteriovenous malformation-like phenotype, which may arise because of dysregulated Notch signaling. In contrast, Atoh8-deficient mice exhibited a phenotype mimicking PAH, which included increased pulmonary arterial pressure and right ventricular hypertrophy. Moreover, ATOH8 expression was decreased in PAH patient lungs. We showed that in cells, ATOH8 interacted with hypoxia-inducible factor 2α (HIF-2α) and decreased its abundance, leading to reduced induction of HIF-2α target genes in response to hypoxia. Together, these findings suggest that the BMP receptor type II/ALK-1/SMAD/ATOH8 axis may attenuate hypoxic responses in ECs in the pulmonary circulation and may help prevent the development of PAH.

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Liver expression of Bmp6, Smad7, Id1 and Atoh8 is regulated by iron stores

Project description:Background & Aims: Although hepcidin expression was shown to be induced by the BMP signaling pathway, it is not yet known how iron regulates hepcidin and which of the BMP molecules is the endogenous regulator of iron homeostasis in vivo. We therefore assessed liver transcription profiles of mice fed an iron-deficient or an iron-enriched diet and looked for genes that were regulated similarly to hepcidin in that context. Methods: Genome-wide liver expression profiles of mice of the B6 and D2 genetic backgrounds subjected to iron-deficient, -balanced, or -enriched diets were obtained using Agilent Whole Genome microarrays. Real-time quantitative-PCR and western-blots were used to confirm microarray results and compare gene expression variations induced by secondary iron deficiency or iron overload with those consecutive to Smad4 or Hamp1-deficiency. Results: Among 1419 transcripts significantly modulated by the dietary iron content, four were regulated similarly to the hepcidin genes Hamp1 and Hamp2. They are coding for Bmp6, the regulator of Bmp/Smad signal transduction Smad7, the negative regulator of basic helix-loop-helix (bHLH) proteins Id1, and a protein with a bHLH domain, Atoh8. The iron overload developed by Smad4 and Hamp1-deficient mice also increased Bmp6 transcription. Body iron stores influence Smad1/5/8 phosphorylation and, as shown by analysis of mice with liver-specific disruption of Smad4, the binding partner for the receptor-activated Smads is necessary for activation of Smad7, Id1, and Atoh8 transcription by iron. Conclusions: Liver expression of Bmp6, Smad7, Id1, and Atoh8 is regulated by body iron stores and may participate in hepcidin regulation through the Bmp/Smad pathway. Keywords: response to dietary iron content

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The m6A-mediated TGF-β-SMAD signaling axis regulates ccRCC progression [LACE-seq]

Project description:TGF-β-SMAD signaling pathway plays an important role in progression of various tumors. However, posttranscriptional regulation such as N6-methyladenosine (m6A) of TGF-β-SMAD signaling axis remains incompletely understood. Here, we reveal that Insulin like growth factor 2 mRNA binding protein 2 (IGF2BP2) is low expression as well as associated with poor prognosis in clear cell renal cell carcinoma (ccRCC) patients and inhibits proliferation as well as promotes metastasis of ccRCC cells. To explore the underlying mechanism of IGF2BP2 in ccRCC, RNA-seq, RIP-seq and LACE-seq were performed to investigate the downstream targets of IGF2BP2.

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The m6A-mediated TGF-β-SMAD signaling axis regulates ccRCC progression [RNA-seq]

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