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Chromatin accessibility of genomic regions in human mesenchymal stem cells cultured in sliding hydrogels (SGs) and chemical hydrogels (CGs) undergoing chondrogenesis.

ABSTRACT: Chromatin accessibility of genomic regions in human mesenchymal stem cells cultured in sliding hydrogels (SGs) and chemical hydrogels (CGs) undergoing chondrogenesis.

PROVIDER: PRJNA998740 | ENA |

REPOSITORIES: ENA

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Chromatin accessibility of genomic regions in human mesenchymal stem cells cultured in sliding hydrogels (SGs) and chemical hydrogels (CGs) undergoing chondrogenesis.

Project description:Cells can deform their local microenvironment by exerting forces through pushing and pulling. Such interactions result in behaviors such as cell spreading, cell migration, or cell volume expansion, which occur on timescales of hours to days. However, whether cells can deform local niches at shorter timescales and how such interactions impact long-term cell fates remain largely unknown. Here we report “cell dancing”- a previously unknown cell behavior characterized by seconds-to-minutes scale deformation of the pericellular niche and enhanced cytoskeletal and nuclear dynamics. Using hydrogels that allow cells to deform their local 3D niche and mesenchymal stem cell chondrogenesis as a model system, we identify early-stage cell dancing essential for enhancing stem cell differentiation in 3D. This is mediated through nuclear mechanotransduction pathways that repress global chromatin accessibility, which is necessary for cell dancing-enhanced differentiation. We further demonstrate that cell dancing induces nuclear deformations and phospholipase A2 (PLA2) signaling, and small molecules targeting this pathway can further boost stem cell chondrogenesis. Finally, we validate that cell dancing can enhance stem cell differentiation towards multiple lineages and occurs in other commonly used hydrogel systems. These results establish cell dancing as a novel cell behavior in 3D that may be broadly applied to promote desirable cell fates and tissue outcomes.

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Patel2023 - miRNA-199a/b-5p regionation of chondrogenesis - enchanced

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Sliding of Bacillus subtilis Natto

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Project description:Human salivary gland organoids have opened tremendous possibilities for regenerative medicine in patients undergoing radiotherapy for the treatment of head and neck cancer. However, their clinical translation is greatly limited by the current use of Matrigel for organoid derivation and expansion. Here, we envisage that the use of a fully, synthetic hydrogel based on the oligo(-ethylene glycol) functionalized polymer polyisocyanopeptides (PICs) can provide an environment suitable for the generation and expansion of salivary gland organoids (SGOs) after optimization of PIC polymer properties. We demonstrate that PIC hydrogels decorated with the cell-binding peptide RGD allow SGO formation from salivary gland (SG)-derived stem cells. This self-renewal potential is preserved for only 4 passages. It was found that SGOs differentiated prematurely in PIC hydrogels affecting their self-renewal capacity. Similarly, SGOs show decreased expression of immediate early genes (IEGs) after culture in PIC hydrogels. Activation of multiple signalling pathways involved in IEG expression by β-adrenergic agonist isoproterenol, led to increased stem cell self-renewal capacity as measured by organoid forming efficiency (OFE). These results indicate that PIC hydrogels are promising 3D matrices for SGOs, with the option to be used clinically, after further optimization of the hydrogel and culture conditions.

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The protein kinase MLTK Is a key regulator for chondrogenesis.

Project description:Sox9 acts together with Sox5 or Sox6 as a master regulator for chondrocyte differentiation; however, how these transcription factors functionally interact and collaborate to regulate chondrogenesis remains unclear. Here we show that the protein kinase MLTK plays an essential role in the onset of chondrogenesis through triggering the induction of Sox6 by Sox9. Knockdown of MLTK in Xenopus embryos results in drastic loss of craniofacial cartilages without defects in neural crest formation. We also find that Sox6 is specifically induced during craniofacial chondrogenesis and this induction is inhibited by MLTK knockdown. Remarkably, Sox6-knockdown embryos display essentially the same phenotype as the MLTK-knockdown embryos; the drastic loss of cartilages and the marked down-regulation of genes involved in chondrogenesis. Microarray analysis reveals a remarkable similarity between Sox6-depleted and MLTK-depleted embryos in their gene expression pattern. Moreover, we find that ectopic expression of MLTK can induce Sox6 expression in a Sox9-dependent manner. These results identify a novel, key regulator for chondrogenesis. We used microarrays to describe the genome-wide gene expression profiles of xMLTK-depleted and xSox6-depleted embryos.

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