Epimorphic Regeneration in the Mammalian Tympanic Membrane
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA806879 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18017036.fastq.gz | Fastqsanger.gz | |||
| SRR18017037.fastq.gz | Fastqsanger.gz | |||
| SRR18017038.fastq.gz | Fastqsanger.gz | |||
| SRR18017039.fastq.gz | Fastqsanger.gz | |||
| SRR18017040.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: The goal of this study was to characterize the transcriptional response to injury of the murine tympanic membrane at multiple time points using single-cell RNA sequencing. Methods: mRNA profiles of Unwounded (Pars Tensa and Pars Flaccida) and Wounded (Day 1, Day 3, Day 7 and Day 14) murine tympanic membranes from WT FVB mice. The sequence reads that passed quality filters were analyzed at the transcript isoform level from fastq to matrix files using standard 10x genomics pipeline via CellRanger Results: Using the 10x Genomics Cell Ranger pipeline, we analyzed over 10,000 cells per timepoint from the UW and WO tympanic membranes, mapping the reads to the mouse genome (build mm10). The cells were then clustered primarily using the single-cell software package Seurat version 4. Conclusions: Our study represents the first detailed analysis of the regeneration timeline of the injured murine tympanic membrane, generated by RNA-seq technology. Our results show the emergence of novel populations on the tympanic membrane as it regenerates and characterizes the changes in all layers of the organ.
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Project description:The data set compares the microRNA expression of two types of keratinocytes from the tympanic membrane and epidermis of the body. Healthy human samples were harvested for the analysis. Cells were cultivated to evaluate the effect of keratinocytes only. Few Chip Ids (11) were considered differentially expressed between the cell types.
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Project description:Rationale: Neonatal mice have the capacity to regenerate their hearts in response to injury, but this potential is lost after the first week of life. The transcriptional changes that underpin mammalian cardiac regeneration have not been fully characterized at the molecular level. Objective: The objectives of our study were to determine if myocytes revert the transcriptional phenotype to a less differentiated state during regeneration and to systematically interrogate the transcriptional data to identify and validate potential regulators of this process. Methods and Results: We derived a core transcriptional signature of injury-induced cardiac myocyte regeneration in mouse by comparing global transcriptional programs in a dynamic model of in vitro and in vivo cardiac myocyte differentiation, in vitro cardiac myocyte explant model, as well as a neonatal heart resection model. The regenerating mouse heart revealed a transcriptional reversion of cardiac myocyte differentiation processes including reactivation of latent developmental programs similar to those observed during de-stabilization of a mature cardiac myocyte phenotype in the explant model. We identified potential upstream regulators of the core network, including interleukin 13 (IL13), which induced cardiac myocyte cell cycle entry and STAT6/STAT3 signaling in vitro. We demonstrate that STAT3/periostin and STAT6 signaling are critical mediators of IL13 signaling in cardiac myocytes. These downstream signaling molecules are also modulated in the regenerating mouse heart. Conclusions: Our work reveals new insights into the transcriptional regulation of mammalian cardiac regeneration and provides the founding circuitry for identifying potential regulators for stimulating heart regeneration. Comparison of transcriptional programs of primary myocardial tissues sampled from neonatal mice and murine hearts undergoing post-injury regeneration, along with in vitro ESC-differentiated cardiomyocytes
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Project description:Utilization of lipids as energy substrates after birth causes cardiomyocyte (CM) cell-cycle arrest and loss of regenerative capacity in mammalian hearts. Beyond energy provision, proper management of lipid composition is crucial for cellular and organismal health, but its role in heart regeneration remains unclear. Here, we demonstrate widespread sphingolipid metabolism remodeling in neonatal hearts after injury and find that SphK1 and SphK2, isoenzymes producing the same sphingolipid metabolite sphingosine-1-phosphate (S1P), differently regulate cardiac regeneration. SphK2 is downregulated during heart development and determines CM proliferation via nuclear S1P-dependent modulation of histone acetylation. Reactivation of SphK2 induces adult CM cell-cycle re-entry and cytokinesis, thereby enhancing regeneration. Conversely, SphK1 is upregulated during development and promotes fibrosis through an S1P autocrine mechanism in cardiac fibroblasts. By fine-tuning the activity of each SphK isoform, we develop a therapy that simultaneously promotes myocardial repair and restricts fibrotic scarring to regenerate the infarcted adult hearts.
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Project description:The inability of the adult mammalian heart to regenerate following injury represents a major barrier in cardiovascular medicine. In contrast, the neonatal mammalian heart retains a transient capacity for regeneration, which is lost shortly after birth. Defining the molecular mechanisms that govern regenerative capacity in the neonatal period remains a central goal in cardiac biology. Here, we construct a transcriptional atlas of multiple cardiac cell populations, which enables comparative analyses of the regenerative (neonatal) versus non-regenerative (adult) state for the first time. This work provides a comprehensive transcriptional resource of multiple cardiac cell populations during cardiac development, repair and regeneration. Our findings define a transcriptional program underpinning the neonatal regenerative state and identifies an epigenetic barrier to re-induction of the regenerative program in adult cardiomyocytes.
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