Similar Datasets
Project description:We subjected human podocytes with and without alpha-Galactosidase knockdown to proteomic analysis.
2018-10-17 | PXD007080 | Pride
Project description:Atoh8 is a transcription factor of the basic-helix-loop-helix (bHLH) family that is expressed in multiple tissues during embryonic development but whose specific functions remain unknown. The gene encoding Atoh8 is induced by various lineage- determining bHLH transcription factors in cell culture, suggesting a possible common role of this gene in multiple bHLH-driven differentiation programs. In the pancreas, the pro-endocrine bHLH factors Neurogenin3 (Neurog3) and NeuroD1 activate Atoh8 expression. Moreover, Atoh8 is expressed in the embryonic pancreas confirming its participation in the pancreatic transcriptional cascade. This work aims at gaining insight into the molecular function of Atoh8 during the endocrine differentiation program initiated by Neurog3 in the pancreas. To this aim, we have generated a recombinant adenovirus encoding an Atoh8-specific shRNA (Ad-shAtoh8) and used it to down-regulate expression of the Atoh8 gene in Neurog3-expressing pancreatic ductal cells (mPAC), a cellular model of endocrine cell differentiation. Thus, we have compared global changes in gene expression profiles between cells treated with Ad-Neurog3+shControl and cells treated with Ad-Neurog3+shAtoh8 using Affymetrix microarrays. Our results show that Atoh8 silencing significantly affects the expression of 293 genes in Neurog3-expressing mPAC cells. Gene Ontology analysis has revealed cell cycle as the biological function most significantly represented among the modified genes. These results uncover a potential function of Math6 as a regulator of cell cycle progression and provide novel insights into the link between Neurog3 and the regulation of the cell cycle. mPAC cells (mouse pancreatic duct cells) overexpressing Neurogenin3 were divided in 2 groups according to the shRNA encoded by the recombinant adenoviruses used: 1) Scramble shRNA (control for the infection effect), 2) Atonal Homolog 8-specific shRNA. Experiment was performed three independent times (3 independent biological replicates).
2014-10-10 | E-GEOD-43536 | biostudies-arrayexpress
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
Project description:We report trancriptional changes between wildtype mouse immortalized podocytes and compared to podocytes with shRNA-knockdown of Pdss2.
2021-02-01 | GSE164272 | GEO
Project description:Purpose: Next-generation sequencing (NGS) was used to identify cellular pathways and genes through systems-based analysis. The goals of this study are to identify NGS-derived transcriptome profiling (RNA-seq) in control and Myo1c knockdown human podocytes upon TGFβ stimulation. These high-throughput data were further validated through qRT–PCR methods to confirm the cellular pathways and genes affected due to genetic knockdown of Myo1c and TGF-β stimulation. Methods: Human control and Myo1c knockdown podocytes were differentiated for 14 days by thermoswitching from 33⁰C to 37⁰C and removal of growth factors, insulin-transferrin-selenium from the medium. These podocytes were incubated overnight in RPMI medium with 0.1% FBS and stimulated with 5ng/ml of TGF-β in the same medium for a period of 48 hours. Control and TGF-β stimulated podocytes were processed for RNA isolation and submitted to Novogene for RNA-Seq. All the experiments were performed in triplicates. Conclusions: Our study is first to describe the detailed analysis of TGF-β stimulated Myo1c knockdown podocyte transcriptomes using the RNA-seq technology. A comparative analysis of the differential expression profile was obtained between control vs. Myo1c knockdown podocytes, and control vs. Myo1c knockdown podocytes that were stimulated with TGF-β. Complex genetic network and genes effected due to Myo1c knockdown and TGF-β stimulation will provide a platform to define biological pathways in podocytes where Myo1c participates.
2018-08-21 | GSE118816 | GEO
Project description:The growth hormone plays a significant role in normal renal function and overactive growth hormone signaling has been implicated in proteinuria in diabetes. Earlier studies from our group have shown that the glomerular podocytes, which play an essential role in renal filtration, express the growth hormone receptor, suggesting the direct action of growth hormone on these cells. Nevertheless, the precise mechanism and the downstream pathways that are induced by the excess growth hormone in these podocytes leading to diabetic nephropathy are not clearly established. To compressively understand the growth hormone’s effect on podocytes at transcript level we performed RNA-Sequencing. Conditionally immortalized human podocytes were employed in this study.
2020-08-28 | GSE140308 | GEO
Project description:Transcriptomic analysis of human podocytes
| PRJNA800332 | ENA
Project description:Atoh8 is a transcription factor of the basic-helix-loop-helix (bHLH) family that is expressed in multiple tissues during embryonic development but whose specific functions remain unknown. The gene encoding Atoh8 is induced by various lineage- determining bHLH transcription factors in cell culture, suggesting a possible common role of this gene in multiple bHLH-driven differentiation programs. In the pancreas, the pro-endocrine bHLH factors Neurogenin3 (Neurog3) and NeuroD1 activate Atoh8 expression. Moreover, Atoh8 is expressed in the embryonic pancreas confirming its participation in the pancreatic transcriptional cascade. This work aims at gaining insight into the molecular function of Atoh8 during the endocrine differentiation program initiated by Neurog3 in the pancreas. To this aim, we have generated a recombinant adenovirus encoding an Atoh8-specific shRNA (Ad-shAtoh8) and used it to down-regulate expression of the Atoh8 gene in Neurog3-expressing pancreatic ductal cells (mPAC), a cellular model of endocrine cell differentiation. Thus, we have compared global changes in gene expression profiles between cells treated with Ad-Neurog3+shControl and cells treated with Ad-Neurog3+shAtoh8 using Affymetrix microarrays. Our results show that Atoh8 silencing significantly affects the expression of 293 genes in Neurog3-expressing mPAC cells. Gene Ontology analysis has revealed cell cycle as the biological function most significantly represented among the modified genes. These results uncover a potential function of Math6 as a regulator of cell cycle progression and provide novel insights into the link between Neurog3 and the regulation of the cell cycle.
2019-01-05 | GSE43537 | GEO
Project description:Extravillous trophoblasts (EVTs) play a vital role in placental development by anchoring the placenta to the uterine wall, invading the maternal decidua, and remodeling maternal spiral arteries. ATOH8, a basic helix-loop-helix (bHLH) transcription factor, is central to regulating trophoblast dynamics at the maternal-fetal interface, where it orchestrates their invasive potential, proliferative capacity, and differentiation in mice. By coordinating these processes, ATOH8 ensures the formation of a functional placental structure critical for sustaining pregnancy. Although ATOH8 has been implicated in decidualization—a key preparatory event in human endometrial stromal fibroblasts essential for placental development, its precise mechanisms and contributions to human trophoblast function remain unresolved. To understand the role of ATOH8 in EVT differentiation, we performed RNA sequencing of ATOH8-depleted EVT and control EVT.
2025-12-04 | GSE293496 | GEO
Project description:Podocytes play an important filtration role in the kidney. We examined culture condition for efficient podocyte induction and established a method to selectively induce podocytes from human iPS cells. To understand how expression profiles of human iPS cell-derived podocytes were close to that in vivo, we isolated human adult podocytes for human adult kidney. Purified RNAs from human iPS cells, nephron progenitor cells, human immortalized podocyte cell line, human iPS cell-derived podocytes, and sorted human adult podocytes were analyzed by RNA-seq.
2019-01-15 | GSE116471 | GEO