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Inorganic Biomaterials Shape the Transcriptome Profile to Induce Endochondral Differentiation

ABSTRACT: Inorganic Biomaterials Shape the Transcriptome Profile to Induce Endochondral Differentiation

PROVIDER: PRJNA795175 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17468366_1.fastq.gz	Fastqsanger.gz
	SRR17468366_2.fastq.gz	Fastqsanger.gz
	SRR17468367_1.fastq.gz	Fastqsanger.gz
	SRR17468367_2.fastq.gz	Fastqsanger.gz
	SRR17468368_1.fastq.gz	Fastqsanger.gz

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Inorganic Biomaterials Shape the Transcriptome Profile to Induce Endochondral Differentiation

Project description:We investigate cellular responses to traditional bioactive mineral-based nanomaterials, such as hydroxyapatite (nHA), whitlockite (nWH), silicon-dioxide (nSiO2), and the emerging synthetic 2D nanosilicates (nSi), on human mesenchymal stem cells (hMSCs). Specifically, using next-generation transcriptome sequencing (RNA-seq), we uncover key signaling pathways and transcriptome dynamics due to exposure to these inorganic nanomaterials. Whole-transcriptome sequencing identified a stabilized skeletal progenitor state in stem cells treated with nanosilicates that suggests endochondral differentiation of hMSCs, resulting in increased deposition of matrix mineralization compared with control or other treatment groups.

2024-06-01 | GSE193173 | GEO

Discerning Biomaterials-driven Transcriptome Dynamics to Induce Mesenchymal Stem Cell Differentiation

Project description:Bioactive materials harness the body’s innate regenerative potential by directing endogenous progenitor cells to facilitate tissue repair. Dissolution products of inorganic biomaterials provide unique biomolecular signaling for tissue-specific differentiation. We demonstrate the role of the inorganic biomaterial synthetic two-dimensional (2D) nanosilicates, and its ionic dissolution products on human mesenchymal stem cell differentiation. We utilize whole transcriptome sequencing (RNA-seq), to characterize the contribution of nanosilicates and its ionic dissolution products on endochondral differentiation. Our study highlights the modulatory role of ions in stem cell transcriptome dynamics by regulating lineage-specific gene expression patterns.

2022-05-04 | GSE193172 | GEO

Inorganic Biomaterials Shape the Transcriptome Profile to Induce Endochondral Differentiation.

Project description:Minerals play a vital role, working synergistically with enzymes and other cofactors to regulate physiological functions including tissue healing and regeneration. The bioactive characteristics of mineral-based nanomaterials can be harnessed to facilitate in situ tissue regeneration by attracting endogenous progenitor and stem cells and subsequently directing tissue-specific differentiation. Here, cellular responses of human mesenchymal stem/stromal cells to traditional bioactive mineral-based nanomaterials, such as hydroxyapatite, whitlockite, silicon-dioxide, and the emerging synthetic 2D nanosilicates are investigated. Transcriptome sequencing is utilized to probe the cellular response and determine the significantly affected signaling pathways due to exposure to these inorganic nanomaterials. Transcriptome profiles of stem cells treated with nanosilicates reveals a stabilized skeletal progenitor state suggestive of endochondral differentiation. This observation is bolstered by enhanced deposition of matrix mineralization in nanosilicate treated stem cells compared to control or other treatments. Specifically, use of 2D nanosilicates directs osteogenic differentiation of stem cells via activation of bone morphogenetic proteins and hypoxia-inducible factor 1-alpha signaling pathway. This study provides insight into impact of nanomaterials on cellular gene expression profile and predicts downstream effects of nanomaterial induction of endochondral differentiation.

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Discerning Biomaterials-driven Transcriptome Dynamics to Induce Mesenchymal Stem Cell Differentiation

Project description:Discerning Biomaterials-driven Transcriptome Dynamics to Induce Mesenchymal Stem Cell Differentiation

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Phlpp1 alters the murine chondrocyte phospho-proteome during endochondral bone formation

Project description:Appendicular skeletal growth and bone mass acquisition are controlled by a variety of growth factors, hormones, and mechanical forces in a dynamic process called endochondral ossification. In long bones, chondrocytes in the growth plate proliferate and undergo hypertrophy to drive bone lengthening and mineralization. Pleckstrin homology (PH) domain and leucine rich repeat phosphatase 1 and 2 (Phlpp1 and Phlpp2) are serine/threonine protein phosphatases that regulate cell proliferation, survival, and maturation via Akt, PKC, Raf1, S6k, and other intracellular signaling cascades. Germline deletion of Phlpp1 suppresses bone lengthening in part through parathyroid hormone receptor-dependent signaling in growth plate chondrocytes. Here, we demonstrate that Phlpp2 does not regulate endochondral ossification, and we define the molecular differences between Phlpp1 and Phlpp2 in chondrocytes. Phlpp2-/- mice are phenotypically indistinguishable from their wildtype (WT) littermates, with similar bone length, bone mass, and growth plate dynamics. Deletion of Phlpp2 had moderate effects on the chondrocyte transcriptome and proteome compared to WT cells. By contrast, Phlpp1/2-/- (double knockout) mice resembled Phlpp1-/- mice phenotypically and chondrocyte phospho-proteomes of Phlpp1-/- and Phlpp1/2-/- chondrocytes were different than WT and Phlpp2-/- chondrocyte phospho-proteomes. Data integration via multiparametric analysis identified alterations in Pdpk1 and Pak1/2 signaling pathways in chondrocytes lacking Phlpp1. In conclusion, these data demonstrate that Phlpp1, but not Phlpp2, regulates endochondral ossification through multiple and complex signaling cascades.

2024-10-22 | PXD055563 | Pride

β-NGF promotes cartilage to bone conversion, accelerating endochondral fracture repair

Project description:During endochondral fracture repair, a myriad of biochemical and phenotypic changes occur at the chondro-osseuous junction that regulate cartilage to bone conversion. Osteogenic and angiogenic factors have long been studied for accelerating fracture repair. In our concise study, we focused on the neurotrophic factor nerve growth factor (NGF) and its receptor tropomyosin receptor kinase A (TRKA) as understudied therapeutic targets for accelerating endochondral fracture repair. We first characterized endogenous expression of NGF and TRKA during endochondral repair of tibial fractures. We then analyzed gene expression data from β-NGF stimulated hypertrophic cartilage and observed a promotion in endochondral ossification associated markers. Additional gene ontology analyses revealed promotion of genes associated with Wnt activation, PDGF binding, and integrin binding. Subsequent histological analyses of in vivo samples confirmed Wnt activation following local β-NGF injections via reporter mice. Finally, we tested the therapeutic efficacy of local β-NGF injections in mice, which resulted in a decrease of cartilage and increase of bone volume. Moreover, the newly formed bone contained higher trabecular number, connective density, and bone mineral density. Collectively, we demonstrate the ability for β-NGF to promote endochondral fracture repair in a murine model and uncover mechanisms that will serve to further understand the molecular switches that occur during endochondral ossification.

2020-12-22 | GSE150092 | GEO

Human Macrophage Secretions on Biomaterials

Project description:Proteome analysis of human macrophage secretions post-exposure to biomaterials

2019-12-03 | MSV000084653 | MassIVE

Mesenchymal cell-derived septoclasts resorb cartilage during endochondral ossification and fracture healing

Project description:Mesenchymal cell-derived septoclasts resorb cartilage during endochondral ossification and fracture healing

2021-12-11 | GSE154076 | GEO

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Project description:SHAPE:Isoseq

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Inorganic P solubilized bacteria

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