Post-prandial cardiac hypertrophy is sustained by mechanics, epigenetic, and metabolic reprogramming in pythons [ATAC-Seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1142401 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30049444_1.fastq.gz | Fastqsanger.gz | |||
| SRR30049444_2.fastq.gz | Fastqsanger.gz | |||
| SRR30049445_1.fastq.gz | Fastqsanger.gz | |||
| SRR30049445_2.fastq.gz | Fastqsanger.gz | |||
| SRR30049446_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Post-prandial cardiac hypertrophy is sustained by mechanics, epigenetic, and metabolic reprogramming in pythons [RNA-Seq]
| PRJNA1142400 | ENA
Project description:As ambush-hunting predators that consume large prey after long intervals of fasting, Burmese pythons evolved with unique adaptations for regulating organ structure and function. Among these is cardiac hypertrophy that develops within three days following a meal (1, 2), which we previously showed was initiated by circulating growth factors (3). Post-prandial cardiac hypertrophy in pythons also rapidly regresses with subsequent fasting (2); however, the molecular mechanisms that regulate the dynamic cardiac remodeling in pythons during digestion are largely unknown. In this study, we employed a multi-omics approach coupled with targeted molecular analyses to examine remodeling of the python ventricular transcriptome and proteome throughout digestion. We found that forkhead box protein O1 (FoxO1) signaling was suppressed prior to hypertrophy development and then activated with regression, which coincided with decreased and then increased expression, respectively, of FoxO1 transcriptional targets involved in protein degradation. To define the molecular mechanistic role of FoxO1 in hypertrophy regression, we used cultured mammalian cardiomyocytes treated with post-fed python plasma. Hypertrophy regression both in pythons and in vitro coincided with activation of FoxO1-dependent autophagy; however, introduction of a FoxO1-specific inhibitor prevented both regression of cell size and autophagy activation. Finally, to determine if FoxO1 activation could induce regression, we generated an adenovirus expressing a constitutively active FoxO1. FoxO1 activation was sufficient to prevent and reverse post-fed plasma-induced hypertrophy, which was partially prevented by autophagy inhibition. Our results indicate that modulation of FoxO1 activity contributes to the dynamic ventricular remodeling in post-prandial Burmese pythons.
2024-07-16 | GSE271793 | GEO
Project description:As ambush-hunting predators that consume large prey after long intervals of fasting, Burmese pythons evolved with unique adaptations for regulating organ structure and function. Among these is cardiac hypertrophy that develops within three days following a meal (1, 2), which we previously showed was initiated by circulating growth factors (3). Post-prandial cardiac hypertrophy in pythons also rapidly regresses with subsequent fasting (2); however, the molecular mechanisms that regulate the dynamic cardiac remodeling in pythons during digestion are largely unknown. In this study, we employed a multi-omics approach coupled with targeted molecular analyses to examine remodeling of the python ventricular transcriptome and proteome throughout digestion. We found that forkhead box protein O1 (FoxO1) signaling was suppressed prior to hypertrophy development and then activated with regression, which coincided with decreased and then increased expression, respectively, of FoxO1 transcriptional targets involved in protein degradation. To define the molecular mechanistic role of FoxO1 in hypertrophy regression, we used cultured mammalian cardiomyocytes treated with post-fed python plasma. Hypertrophy regression both in pythons and in vitro coincided with activation of FoxO1-dependent autophagy; however, introduction of a FoxO1-specific inhibitor prevented both regression of cell size and autophagy activation. Finally, to determine if FoxO1 activation could induce regression, we generated an adenovirus expressing a constitutively active FoxO1. FoxO1 activation was sufficient to prevent and reverse post-fed plasma-induced hypertrophy, which was partially prevented by autophagy inhibition. Our results indicate that modulation of FoxO1 activity contributes to the dynamic ventricular remodeling in post-prandial Burmese pythons.
2024-09-12 | PXD054079 | Pride
Project description:Constricting pythons, known for their ability to consume infrequent, massive meals, exhibit rapid and reversible cardiac hypertrophy following feeding. Our primary goal was to investigate how python hearts achieve this adaptive response after feeding. Isolated myofibrils increased force after feeding without changes in sarcomere ultrastructure and without increasing energy cost. Ca2+ transients were prolonged after feeding with no changes in myofibril Ca2+ sensitivity. Feeding reduced titin-based tension, resulting in decreased cardiac tissue stiffness. Feeding also reduced the activity of sirtuins, a metabolically-linked class of histone deacetylases, and increased chromatin accessibility. A transcription factor enrichment analysis on transposase-accessible chromatin with sequencing (ATAC-Seq) revealed the prominent role of transcription factors YY1 and NRF1 in post-feeding cardiac adaptation. Gene expression was also changed in favor of translation and metabolism. Finally, metabolomics analysis and ATP production assay demonstrated that cardiac adaptation after feeding not only increased energy demand but also energy production. These findings have broader implications for our understanding of cardiac adaptation across species and hold promise for the development of innovative approaches to address cardiovascular diseases.
2024-08-04 | GSE273554 | GEO
Project description:Constricting pythons, known for their ability to consume infrequent, massive meals, exhibit rapid and reversible cardiac hypertrophy following feeding. Our primary goal was to investigate how python hearts achieve this adaptive response after feeding. Isolated myofibrils increased force after feeding without changes in sarcomere ultrastructure and without increasing energy cost. Ca2+ transients were prolonged after feeding with no changes in myofibril Ca2+ sensitivity. Feeding reduced titin-based tension, resulting in decreased cardiac tissue stiffness. Feeding also reduced the activity of sirtuins, a metabolically-linked class of histone deacetylases, and increased chromatin accessibility. A transcription factor enrichment analysis on transposase-accessible chromatin with sequencing (ATAC-Seq) revealed the prominent role of transcription factors YY1 and NRF1 in post-feeding cardiac adaptation. Gene expression was also changed in favor of translation and metabolism. Finally, metabolomics analysis and ATP production assay demonstrated that cardiac adaptation after feeding not only increased energy demand but also energy production. These findings have broader implications for our understanding of cardiac adaptation across species and hold promise for the development of innovative approaches to address cardiovascular diseases.
2024-08-04 | GSE273555 | GEO
Project description:Regression of Post-Prandial Cardiac Hypertrophy in Burmese Pythons is Mediated by FoxO1
| PRJNA1133630 | ENA
Project description:Hippo effectors YAP/TAZ act as on-off mechanosensing switches by sensing modifications in extracellular matrix (ECM) composition and mechanics. The regulation of their activity has been described so far through a hierarchical model in which elements of Hippo pathway are under the control of Focal Adhesions (FAs). Here we unveiled the molecular mechanism by which cell spreading and RhoA GTPase control FA formation through YAP to stabilize the anchorage of actin cytoskeleton to cell membrane. This mechanism required YAP co-transcriptional function and involved the activation of genes encoding for integrins and FA docking proteins. Tuning YAP transcriptional activity led to the modification of cell mechanics, force development, adhesion strength, determined cell shaping, migration and differentiation. These results provide new insights into the mechanism of YAP mechanosensing activity and qualify Hippo effector as the key determinant of cell mechanics in response to ECM cues.
2017-05-17 | E-MTAB-5217 | biostudies-arrayexpress
Project description:Constricting pythons, known for their ability to consume infrequent, massive meals, exhibit rapid and reversible cardiac hypertrophy following feeding. Our primary goal was to investigate how python hearts achieve this adaptive response after feeding. Isolated myofibrils increased force after feeding without changes in sarcomere ultrastructure and without increasing energy cost. Ca2+ transients were prolonged after feeding with no changes in myofibril Ca2+ sensitivity. Feeding reduced titin-based tension, resulting in decreased cardiac tissue stiffness. Feeding also reduced the activity of sirtuins, a metabolically linked class of histone deacetylases, and increased chromatin accessibility. Transcription factor enrichment analysis on transposase-accessible chromatin with sequencing revealed the prominent role of transcription factors Yin Yang1 and NRF1 in postfeeding cardiac adaptation. Gene expression also changed with the enrichment of translation and metabolism. Finally, metabolomics analysis and adenosine triphosphate production demonstrated that cardiac adaptation after feeding not only increased energy demand but also energy production. These findings have broad implications for our understanding of cardiac adaptation across species and hold promise for the development of innovative approaches to address cardiovascular diseases.
| S-EPMC11388396 | biostudies-literature
Project description:Changes of inspiration: expiration ration from 1:2 to 1:1 could improve the arterial oxygenation and respiratory mechanics
| 2148174 | ecrin-mdr-crc