RNA-Seq Analyses of TGAC8 and WT mouse Left Ventricles
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE205234 | GEO | 2022/12/23
REPOSITORIES: GEO
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Project description:Four LV samples from WT and TGAC8 mouse hearts were analyzed. A subset of 8 muscle samples each corresponding to 4 controls and 4 TGAC8 LVs and one averaged reference sample were labeled with 10-plex tandem mass spectrometry tags (TMT) using standard TMT labeling protocol (Thermo Fisher).
TGAC8 labeling: TMT-126; TMT-127N; TMT-127C; TMT-130N
WT labeling: TMT-128N; TMT-128C; TMT-129N TMT-129C
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Project description:This dataset is a time series (1 hour [h], 4 hours, 24 hours, 48 hours, 1 week [w], and 8 weeks) intended to compare normal functioning left ventricles [lv + lv2] with infarcted [ilv] and non-infarcted left ventricles [nilv]. ilv samples are taken from the region between the LAD artery and the apex on a mouse with myocardial infarction. Lv2 samples are from the same region in a sham operated mouse. Nilv samples are taken from the region above the infartion and the left ventricle [lv] samples mimic that region in a sham mouse. The lv and lv2 samples can be compared as both are from normal functioning hearts. For more information visit http://cardiogenomics.med.harvard.edu/groups/proj1/pages/mi_home.html
2007-12-19 | E-GEOD-775 | biostudies-arrayexpress
Project description:Aims. We sought to analyze the physiological differences of human C-MSC between the left ventricle (LV) versus the right ventricle (RV) . Methods and results. Autoptic cardiac specimens from LV and RV were obtained from healthy donors. Part was used for tissue sections; part was processed to obtain C-MSC. Isogenic LV and RV C-MSC were compared as for surface markers expression, cell proliferation/death ratio, differentiation capabilities and transcriptomics. Our results indicated a greater presence of C-MSC in RV vs. LV total tissue. Moreover, more cells can be obtained from RV than from LV after isolation procedures. LV and RV C-MSC are characterized by the expression of the same surface markers. Functional studies revealed RV-LV C-MSC comparable groth curves but higher apoptosis rate within the LV cells. Moreover, higher propensity of the RV to to collagen deposition was obseved. Transcriptome analysis confirmed differences in the expression of genes related to apoptosis regulation and extracellular matrix organization. Alongside, we unveiled further pathways specifically associated to LV or RV C-MSC. Conclusions. These results contribute to understand the role of RV and LV C-MSC in physiological condition. Moreover, the obtained information can unravel their differential contribution to RV or LV- specific pathologic scenarios. RNA-Seq allowed identifying novel differentially expressed genes in RV vs. LV cells, which might uncover unappreciated mechanisms underlying ventricle-specific C-MSC regulation.
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Project description:RNA-Seq Analyses of TGAC8 and WT mouse Left Ventricles
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Project description:Cardiac fibrosis is a key aspect of heart failure, leading to reduced ventricular compliance and impaired electrical conduction in the myocardium. Various pathophysiologic conditions can lead to fibrosis in the left ventricle (LV) and/or right ventricle (RV). Despite growing evidence to support the transcriptomic heterogeneity of cardiac fibroblasts (CFs) in healthy and diseased states, there have been no direct comparisons of CFs in the LV and RV. Given the distinct natures of the ventricles, we hypothesized that LV and RV-derived CFs would display baseline transcriptomic differences that influence their proliferation and differentiation following injury. Bulk RNA sequencing of CFs isolated from healthy left and right cardiac ventricles indicated that left ventricle-derived CFs may be further along the myofibroblast transdifferentiation trajectory than cells isolated from the right ventricle. Single-cell RNA-sequencing (scRNA-seq) analysis of the two populations confirmed that Postn+ CFs are more enriched in the LV, whereas Igfbp3+ CFs were enriched in the RV at baseline. Notably, following pressure overload injury, the LV developed a larger subpopulation of pro-fibrotic Thbs4+/Cthrc1+ injury-induced CFs, while the RV showed unique expansion of two less-well characterized subpopulations of CFs (Igfbp3+ and Inmt+). These findings demonstrate that LV and RV-derived CFs display baseline subpopulation differences that may dictate their diverging responses to pressure overload injury. Further study of these subpopulations will elucidate their role in the development of fibrosis and inform whether LV and RV fibrosis require distinct treatments.
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Project description:Wild type, female, C57BL/6 mice were subjected to sham (n=6) surgery, or TAC + MI to cause progressive LV remodeling (n=12). At 2wks post-TAC, one group of mice underwent de-banding (HF-DB, n=6), whereas in a second group of mice the band remained intact (HF; n = 6). LV remodeling was evaluated by 2D echocardiography at 14 days post-TAC+MI , and 4 wks post-debanding. At 6 wks the hearts were excised and analyzed for changes in gene expression using transcriptional profiling. e-banding in the HF-DB mice resulted in normalization of LV volumes and LV mass, and normalization of cardiac myocyte hypertrophy at 6wks, without significant changes in myofibrillar collagen in the HF and HF-DB mice. Both LV ejection fraction (LVEF) and LV radial strain improved numerically following de-banding; however, both measurements remained significantly depressed in the HF-DB mice compared to sham, and were not significantly different from HF mice at 6wks. Reverse LV remodeling in the HF-DB mouse hearts was accompanied by a partial (80%) normalization of the genes that became dysregulated during LV remodeling, whereas 20% of genes remained persistently dysregulated following reverse LV remodeling.
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Project description:Cardiac fibrosis is a key aspect of heart failure, leading to reduced ventricular compliance and impaired electrical conduction in the myocardium. Various pathophysiologic conditions can lead to fibrosis in the left ventricle (LV) and/or right ventricle (RV). Despite growing evidence to support the transcriptomic heterogeneity of cardiac fibroblasts (CFs) in healthy and diseased states, there have been no direct comparisons of CFs in the LV and RV. Given the distinct natures of the ventricles, we hypothesized that LV and RV-derived CFs would display baseline transcriptomic differences that influence their proliferation and differentiation following injury. Bulk RNA sequencing of CFs isolated from healthy left and right cardiac ventricles indicated that left ventricle-derived CFs may be further along the myofibroblast transdifferentiation trajectory than cells isolated from the right ventricle. Single-cell RNA-sequencing (scRNA-seq) analysis of the two populations confirmed that Postn+ CFs are more enriched in the LV, whereas Igfbp3+ CFs were enriched in the RV at baseline. Notably, following pressure overload injury, the LV developed a larger subpopulation of pro-fibrotic Thbs4+/Cthrc1+ injury-induced CFs, while the RV showed unique expansion of two less-well characterized subpopulations of CFs (Igfbp3+ and Inmt+). These findings demonstrate that LV and RV-derived CFs display baseline subpopulation differences that may dictate their diverging responses to pressure overload injury. Further study of these subpopulations will elucidate their role in the development of fibrosis and inform whether LV and RV fibrosis require distinct treatments.
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Project description:LCMS Thermo Xcalibur .raw files from tryptic digests of 1-2 mg pieces of mouse heart ventricle. Mice were fed 99% D3-leucine Mouse Express from Cambridge Isotopes for an 8-week period. 3 mice were euthanized on days 0 (control), 5, 10, 18, 28, and 42, and 4 mice were euthanized on day 56.
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