Ontology highlight
ABSTRACT:
PROVIDER: PRJNA714691 | ENA |
REPOSITORIES: ENA
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Project description:the myoblast differentiation difference in normal and DM1 murine cell models
| PRJNA728453 | ENA
Project description:To study the gene expression profile difference in the myoblast differentiation of normal and DM1 groups, we performed RNA-seq on the total RNA samples collected from the in vitro myoblast differentiation day 4 of normal and DM1 C2C12 cell models. Normal and DM1 cell models were bulit by stably transfecting C2C12 cells with GFP-CUG5 and GFP-CUG200 plasmids. Each group contained three biological replicates. The expression matrix was obtained by Hisat2 followed by Stringtie.
2021-09-08 | GSE174119 | GEO
Project description:To study the gene expression profile difference caused by miR-322/-503 overexpression in the myoblast differentiation of DM1 group, we performed RNA-seq on the total RNA samples collected from the in vitro myoblast differentiation day 4 of control and miR-322/-503 overexpressing DM1 C2C12 cell models. The DM1 cell model was bulit by stably transfecting C2C12 cells with GFP-CUG200 plasmid. Each group contained three biological replicates. The expression matrix was obtained by Hisat2 followed by Stringtie.
2022-03-21 | GSE189897 | GEO
Project description:The effect of miR-322/-503 on myoblast differentiation in DM1 murine cell model
| PRJNA784964 | ENA
Project description:Background: Central nervous system (CNS) metastases represent a major problem in the treatment of HER2-positive breast cancer due to the disappointing efficacy of HER2-targeted therapies in the brain microenvironment. The antibody-drug conjugate ado-trastuzumab emtansine (T-DM1) has shown efficacy in trastuzumab-resistant systemic breast cancer. Here, we tested the hypothesis that T-DM1 could overcome trastuzumab resistance in preclinical models of brain metastases. Methods: We treated mice bearing BT474 or MDA-MB-361 tumors in the CNS (N=9-11 per group), or cancer cells grown in organotypic brain slice cultures with trastuzumab or T-DM1 at equivalent or equipotent doses. Using intravital imaging, molecular techniques and histological analysis we determined tumor growth, mouse survival, cancer cell apoptosis and proliferation, tumor drug distribution, and HER2 signaling. All statistical tests were two-sided. Results: T-DM1 significantly delayed the growth of HER2-positive breast cancer brain metastases compared to trastuzumab. These findings were consistent between HER2-driven and PI3K-driven tumors. The activity of T-DM1 resulted in a striking survival benefit (median survival for BT474 tumors: 28d for trastuzumab vs 112d for T-DM1, HR=6.2, 95% CI=6.1 to 85.84; P<.001). No difference in drug distribution and HER2-signaling was revealed between the two groups. However, T-DM1 led to a significant increase in tumor cell apoptosis (One-way ANOVA for ApopTag, p<.001), which was associated with mitotic catastrophe. Conclusions: T-DM1 can overcome resistance to trastuzumab therapy in HER2-driven and PI3K-driven breast cancer brain lesions due to the cytotoxicity of the DM1 component. Clinical investigation of T-DM1 for patients with CNS metastases from HER2-positive breast cancer is warranted. Comparison of trastuzumab (n=4) and TDM-1 (n=4) treated BT-474 human breast carcinoma cells growing in murine brain
2015-11-09 | E-GEOD-69042 | biostudies-arrayexpress
Project description:We screened for long intergenic non-coding RNAs (lincRNAs) that are highly and specifically expressed in the murine myoblast cell line C2C12 during the differentiation process.
2018-04-06 | GSE105118 | GEO
Project description:Myotonic Dystrophy (DM1), a common neuromuscular disease, has been shown to have detrimental effects on the livers of patients. To study whether DM1 is directly altering liver function or whether these effects are secondary to DM1 induced functional changes in other tissues, we sequenced the transcriptomes of hepatocytes from liver-specific and whole-body murine models of DM1. We found substantial transcriptomic alteration in the liver-specific model, along with distinguishable physiological changes in the livers of both the liver-specific and whole-body models. This data serves as a survey of transcriptomic alterations in occurring in the livers of DM1 patients.
2024-09-26 | GSE252827 | GEO
Project description:Epigenetic defects caused by hereditary or de novo mutations are implicated in various human diseases. It remains uncertain whether correcting the underlying mutation can reverse these defects in patient cells. Focusing on myotonic dystrophy type 1 (DM1), we discovered a fundamental difference between undifferentiated and differentiated cells. While in mutant human embryonic stem cells (hESCs), DNA methylation and H3K9me3 enrichments are completely abolished by repeat excision (2000CTG), in patients' myoblasts (CTG2600 expansion) repeat deletion fails to do so. This distinction stems from cell differentiation, and can be set back by reprogramming gene-edited myoblasts. We demonstrate that abnormal methylation in DM1 is distinctively maintained in the undifferentiated state by the activity of the de novo DNMTs (DNMT3b and/or DNMT3a). Overall, these findings highlight a crucial difference in heterochromatin maintenance between undifferentiated (sequence-dependent) and differentiated (sequence-independent) cells, underscoring the role of differentiation as a locking mechanism for repressive epigenetic modifications at the DM1 locus.
2024-02-06 | GSE128901 | GEO
Project description:Cells dynamically change their internal organization via continuous cell state transitions to mediate a plethora of physiological processes. Understanding such continuous processes is severely limited due to a lack of tools to measure the holistic physiological state of single cells undergoing a transition. We combined live-cell imaging and machine learning to quantitatively monitor skeletal muscle precursor cell (myoblast) differentiation during multinucleated muscle fiber formation. Our machine learning model predicted the continuous differentiation state of single primary murine myoblasts over time and revealed that inhibiting ERK1/2 leads to a gradual transition from an undifferentiated to a terminally differentiated state 7.5-14.5 hours post inhibition. Myoblast fusion occurred ~3 hours after predicted terminal differentiation. Moreover, we showed that our model could predict that cells have reached terminal differentiation under conditions where fusion was stalled, demonstrating potential applications in screening. This method can be adapted to other biological processes to reveal connections between the dynamic single-cell state and virtually any other functional readout.
2024-05-23 | PXD047198 | Pride
Project description:Myotonic dystrophy type 1 (DM1) is a progressive life-limiting neuromuscular disorder with no available cure. In the current study, we examined the extent to which 12-weeks of cycle ergometry can recuperate clinical and physiological metrics in DM1 patients. Furthermore, we studied the underlying mechanisms through which exercise elicits benefits in skeletal muscle. DM1 was associated with impaired muscle function, fitness, lung capacity, and mitochondrial function. Exercise training induced several clinical, physical, and metabolic advantages in DM1 patients. We highlight that exercise-induced molecular and cellular alterations in patients do not conform with previously published data in murine models and propose an alternative mechanism. Lastly, we briefly outline the involvement of small nucleolar RNAs as a novel component within the DM1 pathophysiology. Taken together, our data supports the efficacy of aerobic training to mitigate the relentless progression of DM1 in individuals affected.
2022-04-01 | GSE184951 | GEO