Functional Compensation Precedes Recovery of Tissue Mass Following Acute Liver Injury
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA563047 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10042881_1.fastq.gz | Fastqsanger.gz | |||
| SRR10042881_2.fastq.gz | Fastqsanger.gz | |||
| SRR10042882_1.fastq.gz | Fastqsanger.gz | |||
| SRR10042882_2.fastq.gz | Fastqsanger.gz | |||
| SRR10042883_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 38 |
Similar Datasets
Project description:We identify a new phase of functional compensation following acute liver injury that occurs prior to cellular proliferation. By coupling single-cell RNA-seq with in situ transcriptional analyses in two independent murine liver injury models, we discover adaptive reprogramming to ensure expression of both injury response and core liver function genes dependent on macrophage-derived WNT/b-catenin signaling. Interestingly, transcriptional compensation is most prominent in non-proliferating cells, clearly delineating two separate phases of liver recovery. Overall, our work describes a new mechanism by which the liver maintains essential physiological functions prior to cellular reconstitution and characterizes macrophage-derived WNT signals required for this compensation.
2020-09-14 | GSE136679 | GEO
Project description:The liver plays a central role in metabolism, protein synthesis and detoxification. It possesses unique regenerative capacity upon injury. While many factors regulating cellular proliferation during liver repair have been identified, the mechanisms by which the injured liver maintains vital functions prior to tissue recovery are unknown. Here, we identify a new phase of functional compensation following acute liver injury that occurs prior to cellular proliferation. By coupling single-cell RNA-seq with in situ transcriptional analyses in two independent murine liver injury models, we discover adaptive reprogramming to ensure expression of both injury response and core liver function genes dependent on macrophage-derived WNT/β-catenin signaling. Interestingly, transcriptional compensation is most prominent in non-proliferating cells, clearly delineating two temporally distinct phases of liver recovery. Overall, our work describes a mechanism by which the liver maintains essential physiological functions prior to cellular reconstitution and characterizes macrophage-derived WNT signals required for this compensation.
| S-EPMC7677389 | biostudies-literature
Project description:We report the usage of ChIP-mass spectrometry in identifying proteins and histone modifications involved in Drosophila dosage compensation. We identified a chromatin targeting factor, CG4747, that is involved in recognition of H3K36me3 and robust recruitment of the Drosophila MSL complex to its correct targets on the male X chromosome.
2012-11-06 | GSE42025 | GEO
Project description:We report the usage of ChIP-mass spectrometry in identifying proteins and histone modifications involved in Drosophila dosage compensation. We identified a chromatin targeting factor, CG4747, that is involved in recognition of H3K36me3 and robust recruitment of the Drosophila MSL complex to its correct targets on the male X chromosome. ChIP-seq with PAP antibody of Drosophila larvae expressing C-terminally TAP-tagged CG4747.
2012-11-06 | E-GEOD-42025 | biostudies-arrayexpress
Project description:Gene dosage imbalance of heteromorphic sex chromosomes (XY or ZW) exists between the sexes, and with the autosomes. Mammalian X chromosome inactivation was long thought to imply a critical need for dosage compensation in vertebrates. However, mRNA abundance measurements that demonstrated sex chromosome transcripts are neither balanced between the sexes or with autosomes in monotreme mammals or birds brought sex chromosome dosage compensation into question. This study examines transcriptomic and proteomic levels of dosage compensation in platypus and chicken compared to mouse, a model eutherian species. We analyzed mRNA and protein levels in heart and liver tissues of chicken, mouse and platypus.
2024-07-30 | PXD040182 | Pride
Project description:ObjectivesThe detailed course of mental disorders at the acute and subacute stages of mild traumatic brain injury (mTBI), especially with regard to recovery from sleep disturbances, has not been well characterised. The aim of this study was to determine the course of depression, anxiety and sleep disturbance, following an mTBI.SettingWe recruited patients with mTBI from three university hospitals in Taipei and healthy participants as control group for this study.Participants100 patients with mTBI (35 men) who were older than 20 years, with a Glasgow Coma Scale score of 13-15 and loss of consciousness for <30 min, completed the baseline and 6-week follow-up assessments. 137 controls (47 men) without TBI were recruited in the study. None of the participants had a history of cerebrovascular disease, mental retardation, previous TBI, epilepsy or severe systemic medical illness.Primary outcome measuresThe Beck Anxiety Inventory (BAI), the Beck Depression Inventory II (BDI), the Epworth Sleepiness Scale (ESS) and the Pittsburgh Sleep Quality Index (PSQI) were assessed for the patients with mTBI at baseline and 6 weeks after mTBI and for the controls.ResultsThe ESS scores were not significantly different between the mTBI at baseline or at 6 weeks after mTBI and controls. Although the BAI, BDI and PSQI scores of the mTBI group were significantly different than those of the control group at baseline, all had improved significantly 6 weeks later. However, only the PSQI score improved to a level that was not significantly different from that of the control group.ConclusionsDaytime sleepiness is not affected by mTBI. However, mTBI causes depression and anxiety and diminished sleep quality. Although all these conditions improve significantly within 6 weeks post-mTBI, only sleep quality improves to a pre-mTBI level. Thus, recovery from mTBI-induced sleep disturbance occurs more rapidly than that of mTBI-induced depression and anxiety.
| S-EPMC3902386 | biostudies-literature
Project description:Traumatic brain injury (TBI) is one of the leading causes of death worldwide. Due to complex etiology, there are currently no effective treatments for TBI, and trauma survivors suffer from a variety of long-lasting health consequences. One of the pathological manifestations of TBI is neuroinflammation, which is thought to delay tissue repair and patient recovery. With nutritional support recently emerging as a vital step in improving TBI patients’ outcomes, we sought to evaluate the potential therapeutic benefits of nutritional supplements derived from bovine glandular tissues, which can deliver a variety of nutrients and bioactive molecules. We show that bovine thymus-derived extracts contain antigens found in neural tissues and are relevant to neuroinflammation, and supplementation of rats with thymus extracts induces production of IgG antibodies against neuronal and glial antigens. In a rat model of controlled cortical impact (CCI) we determined that animals supplemented with a nuclear extract of bovine thymus (TNF) display greatly improved performance on beam balance and spatial memory tests following CCI. Using RNA-Seq, we identified an array of signaling pathways that are modulated by TNF supplementation in rat hippocampus, including those involved in the process of autophagy. Finally, we demonstrate that TNF supplement-induced increase in blood levels of IgG autoantibodies against nervous system antigens correlates with better animal performance on behavioral tests. Together, our data show, for the first time, that a nutritional supplement containing nuclear fraction of bovine thymus is potent at enhancing the functional recovery from TBI in a rat model, modulates signaling pathways implicated in TBI pathology and recovery at gene and protein levels, and may be beneficial for reducing neuroinflammation and improving tissue repair.
2023-11-06 | GSE240927 | GEO
Project description:BackgroundAcute injury to skeletal muscle damages myofibers and fragment capillaries, impairing contractile function and local perfusion. Myofibers and microvessels regenerate from satellite cells and from surviving microvessel fragments, respectively, to restore intact muscle. Established models of injury have used myotoxins and physical trauma to demonstrate the concurrence of myogenesis and angiogenesis during regeneration. In these models, efferocytosis removes cellular debris while basal laminae persist to provide guidance during myofiber and microvessel regeneration. It is unknown whether the spatiotemporal coupling between myofiber and microvascular regeneration persists when muscle tissue is completely removed and local guidance cues are lost.MethodsTo test whether complete removal of skeletal muscle tissue affects the spatiotemporal relationship between myogenesis and angiogenesis during regeneration, subthreshold volumetric muscle loss was created with a biopsy punch (diameter, 2 mm) through the center of the gluteus maximus (GM) in adult mice. Regeneration into the void was evaluated through 21 days post-injury (dpi). Microvascular perfusion was evaluated in vivo by injecting fluorescent dextran into the circulation during intravital imaging. Confocal imaging and histological analyses of whole-mount GM preparations and tissue cross-sections assessed the growth of microvessels and myofibers into the wound.ResultsA provisional matrix filled with PDGFRα+ and CD45+ cells spanned the wound within 1 dpi. Regenerating microvessels advanced from the edges of the wound into the matrix by 7 dpi. Nascent microvascular networks formed by 10 dpi with blood-perfused networks spanning the wound by 14 dpi. In striking contrast, the wound remained devoid of myofibers at 7 and 10 dpi. Myogenesis into the wound was apparent by 14 dpi and traversed the wound by 21 dpi. Regenerated myofibers and microvessels were disorganized compared to the uninjured muscle.ConclusionsFollowing punch biopsy of adult skeletal muscle, regenerating microvessels span the wound and become perfused with blood prior to myofiber regeneration. The loss of residual guidance cues with complete tissue removal disrupts the spatiotemporal correspondence between microvascular and myofiber regeneration. We conclude that angiogenesis precedes myogenesis during regeneration following subthreshold volumetric muscle loss.
| S-EPMC9926536 | biostudies-literature
Project description:Long-term survival and integration of neural progenitor cells (NPCs) transplanted following spinal cord injury (SCI) have been observed. However, questions concerning the differentiation choice of NPCs, their mechanism of action and their contribution to functional recovery remains unanswered. Therefore, we investigated global transcriptomal changes in transplanted NPCs transplanted into SCI. We found that NPCs transplanted into SCI up-regulate genes related to nerve cell function and signaling and differentiation, and down-regulate genes related to cytokine signaling and apoptosis.
2019-04-24 | GSE125134 | GEO