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Collagen signaling and matrix stiffness regulate multipotencyin glandular epithelial stem cells in mice [bulk RNA-Seq]

ABSTRACT: Collagen signaling and matrix stiffness regulate multipotencyin glandular epithelial stem cells in mice [bulk RNA-Seq]

PROVIDER: PRJNA1017847 | ENA |

REPOSITORIES: ENA

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Collagen signaling and matrix stiffness regulate multipotencyin glandular epithelial stem cells in mice [bulk RNA-Seq]

Project description:Glandular epithelia, including mammary gland (MG) and prostate, are composed of luminal and basal cells. During embryonic development, glandular epithelia arise from multipotent stem cells (SCs) giving rise to basal and luminal cells. However, these multipotent SCs are replaced after birth by unipotent basal and unipotent luminal SCs. Different conditions, such as basal cell transplantation, luminal cell ablation, and oncogene expression, can reinduce multipotency in adult basal SC (BaSCs) of different glandular epithelia. The mechanisms regulating the reactivation of multipotency in BaSCs are incompletely understood. Here, we compared the transcriptional signature of BaSCs from MG and prostate in different conditions associated with multipotency in adult mice and uncovered that Collagen I expression was commonly upregulated across the different conditions associated with multipotency. Using MG and prostate organoids, we demonstrated that increasing collagen concentration or stiffness of the extracellular matrix (ECM) promote BaSC multipotency. Single cell RNA-seq of MG organoids in the presence of high concentration of Collagen I or in a stiffer ECM activate a hybrid bipotent state and uncovered a gene signature and signaling pathways associated with bipotent BaSCs. Finally, we demonstrated the importance of 1integrin/FAK/AP-1 axis in the regulation of BaSC multipotency in response to Col1 signaling and ECM stiffness. Altogether our study uncovers the key role of Collagen signaling and ECM stiffness in the regulation of multipotency in glandular epithelia.

2024-11-12 | GSE243336 | GEO

Collagen signaling and matrix stiffness regulate multipotency in glandular epithelial stem cells in mice [scRNA-Seq]

2024-11-12 | GSE243335 | GEO

Collagen signaling and matrix stiffness regulate multipotency in glandular epithelial stem cells in mice

Project description:Collagen signaling and matrix stiffness regulate multipotency in glandular epithelial stem cells in mice

| PRJNA1017844 | ENA

Collagen signaling and matrix stiffness regulate multipotencyin glandular epithelial stem cells in mice [microarray]

Project description:Collagen signaling and matrix stiffness regulate multipotencyin glandular epithelial stem cells in mice [microarray]

| PRJNA1017848 | ENA

Collagen signaling and matrix stiffness regulate multipotency in glandular epithelial stem cells in mice [scRNA-Seq]

Project description:Collagen signaling and matrix stiffness regulate multipotency in glandular epithelial stem cells in mice [scRNA-Seq]

| PRJNA1017846 | ENA

Extracellular matrix proteome remodeling with substrate stiffness

Project description:Extracellular matrix proteomic profiling Mass spectrometry characterization illustrated a reprogrammed proteome in response to matrix stiffness, including a core subset of 84 ECM-specific proteins, including various ECM regulators and tissue-associated ECM-related proteins. Further, we observe remodeling of ECM proteome with softer substrates associated with metabolic/mitochondrial network (178 proteins), while with 40 kPa substrate (92 proteins enriched) resulting in networks associated with enrichment of collagen biosynthesis, integrin cell surface interactions, and extracellular matrix organization networks.

| MSV000092971 | MassIVE

Collagen signaling and matrix stiffness regulate multipotency in glandular epithelial stem cells in mice

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

2024-11-12 | GSE243338 | GEO

Collagen signaling and matrix stiffness regulate multipotencyin glandular epithelial stem cells in mice [microarray]

Project description:To understand the molecular mechanisms regulating multipotency after transplantation of mammary gland basal cells

2024-11-12 | GSE243337 | GEO

Biphasic Regulation of Epigenetic State by Matrix Stiffness during Cell Reprogramming [RNA-seq]

Project description:In this study, we investigate how matrix stiffness regulates chromatin reorganization and cell reprogramming, and find that matrix stiffness acts as a biphasic regulator of epigenetic state and fibroblast-to-neuron conversion efficiency, maximized at an intermediate stiffness of 20 kPa. ATAC-sequencing analysis shows the same trend of chromatin accessibility to neuronal genes at these stiffness levels. Concurrently, we observe peak levels of histone acetylation and histone acetyltransferase (HAT) activity in the nucleus on matrices at 20 kPa, and inhibiting HAT activity abolishes matrix stiffness effects. G-actin and cofilin, the co-transporters shuttling HAT into the nucleus, rises with decreasing matrix stiffness; however, reduced importin-9 on soft matrices limits nuclear transport. These two factors result in a biphasic regulation of HAT transport into the nucleus, which is directly demonstrated on matrices with dynamically tunable stiffness. These findings unravel a mechanism of the mechano-epigenetic regulation that is valuable for cell engineering in disease modeling and regenerative medicine applications.

2023-12-19 | GSE250068 | GEO

Biphasic Regulation of Epigenetic State by Matrix Stiffness during Cell Reprogramming [ATAC-seq]

2023-12-19 | GSE250066 | GEO