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Mechanobiological stimulation in organ-on-a-chip systems reduces hepatic drug metabolic capacity in favor of regenerative specialization

ABSTRACT: Mechanobiological stimulation in organ-on-a-chip systems reduces hepatic drug metabolic capacity in favor of regenerative specialization

PROVIDER: PRJNA901992 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22302548_1.fastq.gz	Fastqsanger.gz
	SRR22302548_2.fastq.gz	Fastqsanger.gz
	SRR22302549_1.fastq.gz	Fastqsanger.gz
	SRR22302549_2.fastq.gz	Fastqsanger.gz
	SRR22302550_1.fastq.gz	Fastqsanger.gz

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Mechanobiological stimulation in organ-on-a-chip systems reduces hepatic drug metabolic capacity in favor of regenerative specialization

Project description:To investigate the effect of culture microenvironment in microphysiological systems on hepatocellular tissue performance in vitro, we established hepatocyte culture systems with gradually increased complexity. Gene expression profiles of culture hepatocytes were evaluated from 8 groups based on oxygen supplementation, oxygen tension, paracrine signaling from endothelial cells, and hemodynamic shear stress.

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Subsoil specialization

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Early regenerative capacity in the porcine heart

Project description:Background: The adult mammalian heart has limited ability to repair itself following injury. Zebrafish, newts and neonatal mice can regenerate cardiac tissue, largely by cardiac myocyte (CM) proliferation. It is unknown if hearts of young large mammals can regenerate. Methods: We examined the regenerative capacity of the pig heart in neonatal animals (ages: 2, 3 or 14 days postnatal) after myocardial infarction (MI) or sham procedure. Myocardial scar and left ventricular function were determined by cardiac magnetic resonance (CMR) imaging and echocardiography. Bromodeoxyuridine pulse-chase labeling, histology, immunohistochemistry and Western blotting were performed to study cell proliferation, sarcomere dynamics and cytokinesis and to quantify myocardial fibrosis. RNA-sequencing was also performed. Results: After MI, there was early and sustained recovery of cardiac function and wall thickness in the absence of fibrosis in 2-day old pigs. In contrast, older animals developed full-thickness myocardial scarring, thinned walls and did not recover function. Genome wide analyses of the infarct zone revealed a strong transcriptional signature of fibrosis in 14-day old animals that was absent in 2-day old pigs, which instead had enrichment for cytokinesis genes. In regenerating hearts of the younger animals, up to 10% of CMs in the border zone of the MI showed evidence of DNA replication that was associated with markers of myocyte division and sarcomere disassembly. Conclusions: Hearts of large mammals have regenerative capacity, likely driven by cardiac myocyte division, but this potential is lost immediately after birth.

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Platelets favor the outgrowth of established metastases

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Cis-Regulatory Accessibility Directs Muller Glial Development and Regenerative Capacity

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Cancer reduces transcriptome specialization.

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Quantitative proteomics after spinal cord injury in a regenerative and a non-regenerative stage in Xenopus laevis

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2018-01-25 | PXD006993 | Pride

miR106b inhibition improves myogenic regenerative capacity of murine and human muscle stem cells and attenuates muscular dystrophy phenotype

Project description:Satellite cells (SCs), the skeletal muscle stem cells, display functional heterogeneity linked to their regenerative potential. Dramatic changes in their behaviour are also associated to muscle wasting diseases. Therefore, understanding the mechanisms controlling satellite cell heterogeneous behaviour during muscle regeneration and diseases has become increasingly important for regenerative medicine. Here, we show that miR-106bis expressed in Myf5- quiescent SCs and downregulated during SC activation and muscle regeneration. In vitro and in vivo studies to show that miR106b inhibition enhances the regenerative capability of murine and human SCs by increasing myogenic precursors. miR106b is increased in dystrophic mice and intramuscular injection of antimiR enhances muscle regeneration accompanied by significant functional recovery. miR-106b is also elevated in human dystrophic SCs and its inhibition improves intrinsic proliferative defects, increasing their myogenic differentiation potential. Therefore, this study identifies miR-106b as compelling candidate to consider for potential clinical studies.

2022-07-01 | GSE134111 | GEO

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