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Effect of Molidustat treatment on hepatocellular carcinoma cells Huh7

ABSTRACT: Molidustat is an inhibitor of prolyl hydroxylase that activates the hypoxia response pathway. We analyzed the transcriptome of liver cells treated with this drug and the consequences on metabolic reprogramming.

ORGANISM(S): Homo sapiens

PROVIDER: GSE242340 | GEO | 2024/07/01

REPOSITORIES: GEO

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Bulk RNA sequecning of control and Dimethyloxalylglycine (DMOG) treated Human Primary Pulmonary artery endothelial cells (ATCC: PCS-100-022)

Project description:We assessed the role of prolyl hydroxylase inhibiton using DMOG on angiogenic competance and metabolic reprogramming of endothelial cells.

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Proteomic analysis of vascular tissue from critical limb ischemia mouse models treated with Etrinabdione

Project description:Vasculogenic therapies have been investigated for the treatment of peripheral artery disease (PAD) with very limited success in clinical trials. The isoform PP2A (protein phosphatase 2)/B55alpha inhibits the activity of the prolyl hydroxylase 2 (PHD2) and activates the hypoxia inducing factor-1alpha (HIF-1alpha), playing a key role in in vessel remodeling. Thus, PP2A/B55alpha activators may have the potential to induce angiogenesis and arteriogenesis. Herein we investigated the pharmacological attributes of VCE-004.8 (Etrinabdione) and its effectiveness in a murine model of critical limb ischemia.

2024-04-03 | PXD050360 | Pride

Transcriptome-wide expression changes over time in cultured primary human monocytes due to DMOG treatment

Project description:RNA sequencing of primary human monocytes cultured with and without hypoxia-mimetic agent DMOG (Dimethyloxalylglycine). Monocytes isolated from PBMCs of 7 healthy donors were cultured with and without DMOG for 24hrs and harvested at 0, 2, 10 or 24hrs for RNA sequencing. DMOG suppresses HIF Prolyl hydroxylase (HIF-PH) activity by acting as a small molecule competitive inhibitor. HIF-PH inhibition leads to increase in endogenous HIF protein levels and mimics aspects of hypoxia. This RNA-seq study allows analysis of transciptome-wide expression pattern changes over time due to DMOG treatment.

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Genome-wide chromatin accessibility changes over time in cultured primary human monocytes due to DMOG treatment

Project description:ATAC sequencing of primary human monocytes cultured with and without hypoxia-mimetic agent DMOG (Dimethyloxalylglycine). Monocytes isolated from PBMCs of 7 healthy donors were cultured with and without DMOG for 24hrs and harvested at 0, 2, 10 or 24hrs for RNA sequencing. DMOG suppresses HIF Prolyl hydroxylase (HIF-PH) activity by acting as a small molecule competitive inhibitor. HIF-PH inhibition leads to increase in endogenous HIF protein levels and mimics aspects of hypoxia. This ATAC-seq study allows analysis of genome-wide changes to chromatin accessibility due to DMOG treatment.

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Inhibition of prolyl hydroxylase promotes the reprogramming of Sox9+ renal progenitor cells and renal regeneration

Project description:Mammalian kidney has very limited ability to repair or regenerate after acute kidney injury (AKI). The maladaptive repair of AKI promotes the progression to chronic kidney disease (CKD). Therefore, it is extremely urgent to explore new strategies to promote the repair/regeneration of injured renal tubules after AKI. It has been shown that hypoxia induces heart regeneration in adult mice. However, it is unknown whether hypoxia can induce kidney regeneration after AKI. In this study, we used a prolyl hydroxylase domain inhibitor (PHDI), MK-8617, to mimic hypoxia condition and found that MK-8617 significantly ameliorates ischemia reperfusion injury (IRI) induced acute kidney injury. We then showed that MK-8617 dramatically facilitates renal regeneration via promoting the proliferation of injured renal proximal tubular cells (RPTCs) after IRI-induced AKI. We then performed bulk mRNA sequencing and discovered that multiple nephrogenesis- related genes were significantly upregulated with MK-8617 pretreatment. Furthermore, we showed that MK-8617 may alleviate proximal tubule injury via stabilizing HIF-1α protein specifically in renal proximal tubular cells. We also demonstrated that MK-8617 promotes the reprogramming of renal proximal tubular cells to Sox9+ renal progenitor cells, and the regeneration of renal proximal tubules. In summary, we discovered that inhibition of prolyl hydroxylase improves renal proximal tubule regeneration after IRI-induced AKI via promoting the reprogramming of renal proximal tubular cells to Sox9+ renal progenitor cells.

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Project description:Transcriptional effects of prolyl hydroxylase inhibition by hypoxia and molidustat

| PRJNA721596 | ENA

Mitochondria EglN1 drivers breast cancer progression by controlling metabolic adatation to hypoxic stress

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2023-08-29 | PXD041653 | Pride

MicroRNA profiling of human breast cancer cell line MCF7 under conditions of hypoxia

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Expression data from the hepatic stellate cell line LX-2 after treatment with DMOG and from the liver sinusoidal endothelial cell line TRP3 after incubation with conditioned medium of DMOG-treated LX-2

Project description:Expression data from the hepatic stellate cell line LX-2 after treatment with the prolylhydroxylase inhibitor dimethyloxalylglycine (DMOG) and from the liver sinusoidal endothelial cell line TRP3 after incubation with conditioned medium of DMOG-treated LX-2 Prolyl-hydroxylase inhibitors such as dimethyloxalylglycine (DMOG) stabilize HIF-1α, thereby chemically inducing hypoxia, which also accelerates liver volume increase when given with portal rerouting. We used microarrays to clarify the cellular crosstalk of the different cell types in accelerated liver regeneration by examining the role of hepatic stellate cells (HSC) and liver sinusoidal endothelial cells (LSEC).

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2017-08-23 | GSE95244 | GEO

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