Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GEO accession GSE261640 is currently private and is scheduled to be released on Apr 01, 2026.

ABSTRACT: GEO accession GSE261640 is currently private and is scheduled to be released on Apr 01, 2026.

PROVIDER: PRJNA1088152 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Hippo deficient cardiac fibroblasts differentiate into osteochondroprogenitors (ST)

Project description:We investigated how Hippo-deficient cardiac fibroblasts (CFs) alter their cell state and interact with immune cells during cardiac fibrosis. To study the role of the Hippo pathway in CFs, we conditionally knocked out Lats1/2 specifically in the CFs of mouse hearts (Lats1/2CKO). To test the role of Hippo-deficient CF-induced macrophages, we treated the control and Lats1/2CKO mice with or without CSF1R inhibitor to block macrophage expansion and performed ST.

2025-10-07 | GSE261640 | GEO

Hippo deficient cardiac fibroblasts differentiate into osteochondroprogenitors (snMultiomics)

Project description:Hippo deficient cardiac fibroblasts differentiate into osteochondroprogenitors (snMultiomics)

| PRJNA1088488 | ENA

Hippo deficient cardiac fibroblasts differentiate into osteochondroprogenitors (snRNA-Seq)

Project description:Hippo deficient cardiac fibroblasts differentiate into osteochondroprogenitors (snRNA-Seq)

| PRJNA1088151 | ENA

Hippo deficient cardiac fibroblasts differentiate into osteochondroprogenitors (snMultiomics)

Project description:We investigated how Hippo deficient CFs alter their cell state and interact with immune cells during cardiac fibrosis. To study the role of the Hippo pathway in CFs, we conditionally knocked out Lats1/2 specifically in the CFs of mouse hearts (Lats1/2-CF) and performed single-nucleus RNA sequencing (snRNA-seq) and single-nucleus multiomics to profile the cellular landscape of the right atria, with and without Csf1r inhibitor

2025-10-07 | GSE261719 | GEO

Hippo deficient cardiac fibroblasts differentiate into osteochondroprogenitors (snRNA-Seq)

Project description:We investigated how Hippo deficient CFs alter their cell state and interact with immune cells during cardiac fibrosis. To study the role of the Hippo pathway in CFs, we conditionally knocked out Lats1/2 specifically in the CFs of mouse hearts (Lats1/2-CF) and performed single-nucleus RNA sequencing (snRNA-seq) to profile the cellular landscape of the left and right atria.

2025-10-07 | GSE261641 | GEO

Hippo deficient cardiac fibroblasts promote atrial remodeling

Project description:Hippo deficient cardiac fibroblasts promote atrial remodeling

| PRJNA1088149 | ENA

The Hippo pathway regulates density-dependent proliferation of iPSC-derived cardiac myocytes

Project description:Inducing cardiac myocytes to proliferate is considered a potential therapy to target heart disease, however, modulating cardiac myocyte proliferation has proven to be a technical challenge. The Hippo pathway is a kinase signaling cascade that regulates cell proliferation during the growth of the heart. Inhibition of the Hippo pathway increases the activation of the transcription factors YAP/TAZ, which translocate to the nucleus and upregulate transcription of pro-proliferative genes. The Hippo pathway regulates the proliferation of cancer cells, pluripotent stem cells, and epithelial cells through a cell-cell contact-dependent manner, however, it is unclear if cell density-dependent cell proliferation is a consistent feature in cardiac myocytes. Here, we used cultured human iPSC-derived cardiac myocytes (hiCMs) as a model system to investigate this concept. hiCMs have a comparable transcriptome to the immature cardiac myocytes that proliferate during heart development in vivo. Our data indicate that a dense syncytium of hiCMs can regain cell cycle activity and YAP expression and activity when plated sparsely or when density is reduced through wounding. We found that combining two small molecules, XMU-MP-1 and S1P, increased YAP activity and further enhanced proliferation of low-density hiCMs. Importantly, these compounds had no effect on hiCMs within a dense syncytium. These data add to a growing body of literature that link Hippo pathway regulation with cardiac myocyte proliferation and demonstrate that regulation is restricted to cells with reduced contact inhibition.

2021-09-08 | GSE176142 | GEO

Hippo Deficiency Leads to Cardiac Dysfunction with Cardiomyocyte De-differentiation

Project description:The Hippo pathway regulates organ size by modulating cell proliferation and apoptosis. It is activated by myocardial stress and contributes to myocardial injury by promoting cardiomyocyte apoptosis. We investigated the role of the endogenous Hippo pathway in the stressed heart, using cardiac-specific WW45 knockout mice (WW45 cKO). Unexpectedly, chronic suppression of the Hippo pathway exacerbated the progression of heart failure induced by pressure overload (PO), despite reducing apoptosis and promoting cardiomyocyte proliferation. WW45 downregulation induced upregulation of YAP and TEF-1 target genes, including oncostatin M (OSM), and fetal-type genes involved in de-differentiation, as well as myofibrillar disorganization and dysfunction in cardiomyocytes. OSM upregulation further upregulated YAP/TEF-1, thereby potentiating de-differentiation. Suppression of any component of the amplification loop, namely YAP, TEF-1, or OSM, inhibited the effect of Hippo downregulation. Thus, cardiomyocytes under stress risk apoptotic death by activating the Hippo pathway in order to maintain differentiation and contraction against hemodynamic overload.

2019-03-01 | GSE92970 | GEO

ETS2 and Mesp1 trans-differentiate human dermal fibroblasts into cardiac progenitors

Project description:We explored the role of mammalian ETS1/2 and Mesp homologues of cardiogenic transcription factors of Ciona intestinalis, to convert primary human dermal fibroblasts into cardiac progenitors. ETS1/2 and Mesp homologues of cardiogenic transcription factors of Ciona intestinalis, to convert primary human dermal fibroblasts into cardiac progenitors. Here we show murine Ets2 has an obligatory role for directing cardiac progenitors during cardiopoesis in embryonic stem cells. ETS2 converted fibroblasts into KDR/Flk1+ replicative cells but, like the purported cardiac master regulatory gene Mesp1, could not by itself generate cardiac progenitors de novo from fibroblasts. Co-expression of both Ets2 and Mesp1, however, successfully reprogrammed differentiated fibroblasts into cardiac progenitors, as shown by the de novo appearance of core cardiac transcription factors, gap junction proteins, sarcomeric proteins, electrical activity and contractility. ETS2 and Mesp1 sit at the pinnacle of the cardiopoesis regulatory hierarchy and are well suited for treating human heart disease. Co-expression of both Ets2 and Mesp1, reprogrammed differentiated fibroblasts into cardiac progenitors All sample were done in triplicates, controls were NHDF and ETS2 only infected cells. NHDF were first infected with Doxycyline redulated (Doxy-) ETS2 lentivirus and supplemented with doxycycline for 1 week, sequentially cells were infected with Doxy-Mesp1 and treated for 1 more week. Cells were then aggegated to form EB and hangdrop for 1 week, at the end of that period cells were plated and samples were taken every 24 hrs

2012-06-30 | E-GEOD-29709 | biostudies-arrayexpress

Hippo deficient cardiac fibroblasts promote atrial remodeling

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

2025-10-07 | GSE261643 | GEO