TGFβ signaling in retinal tissue repair
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ABSTRACT:
PROVIDER: PRJNA546014 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:TGFβ signaling in retinal tissue repair [Mus Musculus]
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Project description:TGFβ signaling in retinal tissue repair [Danio Rerio]
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Project description:In mammals, retinal damage is followed by Müller glia cell activation and proliferation. While retinal gliosis persists in adult mammals after an insult or disease, some vertebrates, including zebrafish, have the capacity to regenerate. We believe we are the first group to show that gliosis is a fibrotic-like process in mammals’ eyes caused by differential activation of canonical and non-canonical TGFβ signaling pathways.
2019-11-03 | GSE132141 | GEO
Project description:In mammals, retinal damage is followed by Müller glia cell activation and proliferation. While retinal gliosis persists in adult mammals after an insult or disease, some vertebrates, including zebrafish, have the capacity to regenerate. We believe we are the first group to show that gliosis is a fibrotic-like process in mammals’ eyes caused by differential activation of canonical and non-canonical TGFβ signaling pathways.
2019-11-03 | GSE132140 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2019-11-03 | GSE132142 | GEO
Project description:Increasing evidence points to an active stromal involvement in cancer initiation and progression. Cytokines derived from tumor cells are believed to modulate stromal cells to produce growth and angiogenic factors which in turn provide the tumor with the necessary microenvironment for expansion and invasion. Transforming growth factor beta (TGFβ) has been implicated as a candidate cytokine to mediate this communication. However, how its signaling in stromal cells regulates tumorigenesis and tumor progression remains unresolved. We show that normal, pre-senescent fibroblasts or prostate stromal cells cotransplanted with prostate carcinoma cells subcutaneously into nude mice reduced tumor latency and accelerated tumor growth. When their TGFβ signaling was blocked, the fibroblasts and stromal cells still stimulated tumor initiation, but no longer supported tumor growth as control cells did. The loss of the tumor growth-promoting activity of the stromal cells with attenuated TGFβ signaling was not associated with altered cellular senescence or tumor angiogenicity. TGFβ and the medium conditioned by the prostate carcinoma cells stimulated myofibroblast differentiation of the intact stromal cells, but not the stromal cells with attenuated TGFβ signaling. Gene microarray and quantitative RTPCR analyses showed that TGFβ upregulated a host of genes in stromal cells that are involved in tissue remodeling and wound healing. Thus, our study provides evidence for TGFβ as a supporting agent in tumor progression through the induction of a perpetual wound healing process in the tumor microenvironment. Keywords: Human prostate stromal cells (PrSC)
2007-04-28 | GSE7389 | GEO
Project description:Transforming growth factor β (TGFβ) signaling is essential in cell growth and differentiation. Yet, the role of the individual TGFβ signaling components in human tissue homeostasis and transformation is still incompletely understood. Here we dissected the importance of the core components in the TGFβ signaling pathway by CRISPR/Cas9 genome editing of human keratinocytes. The edited keratinocytes were used for human organotypic skin cultures and global quantitative proteomics and phosphoproteomics by mass spectrometry. Characterization of cells and human organotypic skin tissues showed control of epithelial differentiation by Smad4-dependent TGF signaling through cell cycle regulation and ECM expression. In contrast, we found that the combined Smad4 dependent and independent pathways, governed by TGFβRII, controls epithelial homeostasis and prevents invasive growth by blocking epithelial inflammation and activation of p38 and ERK signaling. The study provides a framework for exploration of signaling pathways in human 3D tissue models and with global phosphoproteomics.
2023-02-09 | PXD024935 | Pride
Project description:Transforming growth factor β (TGFβ) signaling is a core pathway of fibrosis, but the molecular regulation of the activation of latent TGFβ remains incompletely understood. Here, we demonstrate a crucial role of WNT5A/JNK/ROCK signaling that rapidly coordinates the activation of latent TGFβ in fibrotic diseases. WNT5A was identified as predominant non-canonical WNT ligand in fibrotic diseases such as systemic sclerosis, sclerodermatous chronic graft-versus-host disease and idiopathic pulmonary fibrosis, stimulating fibroblast-to-myofibroblast transition and tissue fibrosis by activation of latent TGFβ. The activation of latent TGFβ requires rapid JNK- and ROCK-dependent cytoskeletal rearrangements and integrin αV (ITGAV). Conditional Knockout of WNT5A or its downstream targets prevented activation of latent TGFβ, rebalanced TGFβ signaling and ameliorated experimental fibrosis. We thus uncovered a novel mechanism for the aberrant activation of latent TGFβ in fibrotic diseases and provided evidence for targeting WNT5A/JNK/ROCK signaling in fibrotic diseases as a new therapeutic approach.
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Project description:Human amniotic epithelial stem cell-derived retinal pigment epithelium cells repair retinal degeneration
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Project description:Heterogeneity of leukemia stem cells (LSCs) is involved in their collective chemoresistance. To eradicate LSCs, it is necessary to understand the mechanisms underlying their heterogeneity. Here, we aimed to identify signals responsible for variation in LSCs in human acute myeloid leukemia (AML). While healthy human hematopoietic stem/progenitor cells robustly expressed endothelial cell-selective adhesion molecule (ESAM), AML cells exhibited heterogeneous ESAM expression. Interestingly, ESAM- and ESAM+ AML cells were mutually interconvertible, and RNA sequencing revealed activation of TGFβ signaling in these cells. AML cells secreted TGFβ1, which autonomously activated TGFβ pathway and induced their phenotypic variation. Surprisingly, TGFβ signaling blockade inhibited the variation and proliferation of AML cells. Therefore, autonomous TGFβ signaling underlying LSC heterogeneity may be a promising therapeutic target.
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