Expression data from wild-type and cardiac specific miR-125b-1 knockout neonatal hearts
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PROVIDER: PRJNA662606 | ENA |
REPOSITORIES: ENA
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Project description:MicroRNA-125b is abundant in hearts while its function is not well understood. We used microarray to investigate the global changes of transcriptome for functional evaluation.
2020-09-10 | GSE157746 | GEO
Project description:In mammals, the neonatal heart regenerates within a short time after birth, but adults lack this ability. We have shown that metabolic reprogramming is critical for cardiomyocyte proliferation in the neonatal heart. Herein, we revealed that cardiac metabolic reprogramming could be regulated by altering global protein lactylation. 4D label-free proteomics and Kla omics were performed in postnatal Day 1 (P1), 5 (P5), and 7 (P7) mouse hearts, 2297 Kla sites from 980 proteins were identified, and 1262 Kla sites from 409 proteins were quantified. Functional clustering analysis of proteins with altered Kla sites revealed that the proteins were mainly involved in metabolic processes. The Kla levels in several fatty acid oxidation-related proteins showed high expression at P5, while glycolysis and cell cycle-related proteins were sustainedly decreased from P1-P7. Furthermore, we verified the Kla levels of several differentially modified proteins, including ACAT1, ACADL, PKM and NPM1, by coimmunoprecipitation and Western blotting. Overall, we reported the first comprehensive Kla map in the neonatal mouse heart, which will aid in understanding the regulatory network of metabolic reprogramming and cardiac regeneration.
2024-07-02 | PXD039257 | Pride
Project description:The heart of a newborn mouse has an exceptional capacity to regenerate from myocardial injury but lose it after a week of life, which has been utilized as a valuable model to explore the cues for heart regeneration. More and more researches indicated that glycoprotein played an important role in cardiac regeneration. Elucidating the glycosylation processes associated with heart regeneration will be beneficial for the molecular mechanism studies of heart regeneration as well as discovery of potential therapeutic strategies for human cardiac diseases. In this work, an integrated glycoproteomic and proteomic analysis were performed to investigate the differences in glycoprotein abundances and site-specific glycosylation occupancy between neonatal day 1 (P1) and day 7 (P7) of mouse hearts. The intact glycoepeptides were enriched and identified in both P1 and P7 hearts. To screen for differentially regulated glycoproteins, we compared the expression levels of intact glycopeptides between P1 and P7 hearts using label free quantification. Eventually, the glycosylation occupancy of site-specific N-glycans were obtained by comparing the alterations of intact glycopeptides with their corresponding protein expression levels obtained from global proteomic analysis. These altered glycosylation patterns among proteins between P1 and P7 mouse hearts have a significant potential to aid our understanding of the regenerative capacity loss in neonatal mouse hearts during the first week, thus leading to novel therapeutic approaches to recover the capacity.
2020-05-26 | PXD017139 | Pride
Project description:Myofibroblasts (MFs) are crucial components of the fibrotic remodeling after myocardial infarction (MI). We have previously demonstrated the centrality of AMPKα1 in post-MI remodeling. Here, we investigate the effects of MF-specific deletion of AMPKα1 on left ventricular (LV) adaptation following MI, and the underlying molecular mechanisms. Importantly, MF-restricted AMPKα1 conditional knockout (cKO) hearts exhibit exacerbated post-MI adverse LV remodeling and are characterized by exaggerated fibrotic response, compared to wild-type (WT) hearts. Myofibroblast proliferation significantly increases in cKO infarcted hearts, coincident with a significant reduction of Connexin 43 (Cx43) expression in MFs. Mechanistically, lack of AMPKα1 in MFs enhances miR-125b expression, which, in turn, downregulates Cx43. Collectively, our data demonstrate a cardinal role for MF-AMPKα1 in cardiac remodeling, as its lineage-specific inactivation accentuates fibrosis and LV dilatation following MI. The deleterious effects of MF-specific AMPKα1 deletion are mediated via Cx43, and its post-transcriptional regulation by miR-125b.
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Project description:MiR-125b possible targets were identified after transfecting a miRNA-mimic (miR-125b) and a scramble miRNA (Negative control) in MCF7 cell line and analyzing gene expression modifications.
2013-12-02 | E-MTAB-1604 | biostudies-arrayexpress
Project description:Since the proliferative capacity of cardiomyocytes is extremely limited in the adult mammalian hearts, the irreversible loss of cardiomyocytes following cardiac injury markedly reduces cardiac function, leading to cardiac remodeling and heart failure. However, the early neonatal mice have a strong ability in cardiomyocyte proliferation and cardiac regeneration after heart damage such as apical resection. Besides of cardiomyocytes, non-myocytes in heart tissue also play important roles in the regeneration process. Previous studies showed that cardiac macrophages, regulatory T cells and CD4+ T cells are all involved in regulating the myocardial regeneration process. However, the roles of other cardiac immune cells in cardiac regeneration remains to be elucidated. B cells is a prominent immune cell in injured heart; here we discovered the indispensable function of cardiac B cells in improving cardiomyocyte proliferation and heart regeneration in neonatal mice.
2023-06-02 | GSE205115 | GEO
Project description:The adult mammalian heart is incapable of regeneration following injury. In contrast, the neonatal mouse heart can efficiently regenerate during the first week of life. The molecular mechanisms that mediate the regenerative response and its blockade in later life are not understood. Here, by single-nucleus RNA sequencing, we map the dynamic transcriptional landscape of five distinct cardiomyocyte populations in healthy, injured and regenerating mouse hearts. We identify immature cardiomyocytes that enter the cell-cycle following injury and disappear as the heart loses the ability to regenerate. These proliferative neonatal cardiomyocytes display a unique transcriptional program dependent on NFYa and NFE2L1 transcription factors, which exert proliferative and protective functions, respectively. Cardiac overexpression of these two factors conferred protection against ischemic injury in mature mouse hearts that were otherwise non-regenerative. These findings advance our understanding of the cellular basis of neonatal heart regeneration and reveal a transcriptional landscape for heart repair following injury.
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Project description:Hearts Lacking Caveolin-1 Develop Hypertrophy with Normal Cardiac Substrate Metabolism Keywords: gene knockout
2009-03-04 | GSE10849 | GEO
Project description:The goal of this study is to define miR-125b-2 target genes in the hematopoietic system by genetic alteration of miR-125b expression levels. Here we report the identification of miR-125b-2 targets in the hematopoietic system by repressing miR125b in megakaryoblastic leukemia (AMKL) cell lines and overexpressing miR-125b-2 in hematopoietic stem and progenitor cells (CD34+-HSPCs)
2009-12-29 | GSE19680 | GEO
Project description:The neonatal mammalian heart is able to regenerate after injury by inducing cardiomyocyte proliferation. However, this regenerative capacity is virtually lost in the adult mammalian heart. Extracellular vesicles (EVs) have been shown to play an important cardioprotective role in heart repair. Here, we performed proteomic analysis of EVs from neonatal mouse heart tissues (Neo-EVs), EVs regenerated from neonatal heart tissues after apicoectomy (AR-Neo-EVs), and EVs from adult mouse hearts (Adu-EVs), to compare the differential changes in proteins among them.
2024-12-23 | PXD057343 | Pride