Project description:Evaluation of the differences between control and Myc-overexpressing hearts at the protein level and at different developmental stages.
Project description:To investigate the transcriptome changes in embryonic and postnatal mouse hearts, we performed gene expression profiling analysis using data obtained from RNA-seq of C57BL/6J mouse hearts at embryonic day 18.5 (E18.5d), postnatal 1st day (P1d) and postnatal 7th day (P7d).
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.
Project description:Our understanding of heart failure (HF) has been provided by indirect surrogates, such as post-mortem histology, cardiovascular imaging, and molecular characterisation in vivo and in vitro, rather than directly in pre-mortem human cardiac tissue. Using our heart bank of pre-mortem hearts procured according to the most stringent protocols, we examined ischemic (ICM) and dilated cardiomyopathy (DCM) -- the most common causes of HF and leading causes of cardiac transplantation1. We performed unbiased, comprehensive, paired proteomic and metabolomic analysis of 51 left ventricular (LV) samples from 44 cryopreserved pre-mortem human ICM and DCM hearts, including age-matched, healthy, histopathologically-normal donor controls of both genders for comparison. Data integration via pathway and correlation network analysis revealed overlapping and divergent disease pathways in ICM and DCM, and, strikingly, precise sex-specific differences within each disease that unveil the interaction of gender with HF. Identified core functional nodes in each disease may serve as novel therapeutic targets, and we provide all proteomic and metabolomic results via an interactive online repository (https://mengboli.shinyapps.io/heartomics/) as a publicly available resource.
Project description:Our understanding of heart failure (HF) has been provided by indirect surrogates, such as post-mortem histology, cardiovascular imaging, and molecular characterisation in vivo and in vitro, rather than directly in pre-mortem human cardiac tissue. Using our heart bank of pre-mortem hearts procured according to the most stringent protocols, we examined ischemic (ICM) and dilated cardiomyopathy (DCM) -- the most common causes of HF and leading causes of cardiac transplantation1. We performed unbiased, comprehensive, paired proteomic and metabolomic analysis of 51 left ventricular (LV) samples from 44 cryopreserved pre-mortem human ICM and DCM hearts, including age-matched, healthy, histopathologically-normal donor controls of both genders for comparison. Data integration via pathway and correlation network analysis revealed overlapping and divergent disease pathways in ICM and DCM, and, strikingly, precise sex-specific differences within each disease that unveil the interaction of gender with HF. Identified core functional nodes in each disease may serve as novel therapeutic targets, and we provide all proteomic and metabolomic results via an interactive online repository (https://mengboli.shinyapps.io/heartomics/) as a publicly available resource.
Project description:We generated the cardiac-specific knockout of Trbp (Trbp-cKO) in mice. We profiled the transcriptome in both wild-type and Trbp-cKO hearts, and found numerous genes were deregulated by deletion of Trbp. We also profiled miRNA expression both wild-type and Trbp-cKO hearts, and found expression of a subset of miRNA species was altered in Trbp-cKO hearts. Examine expression of mRNAs and miRNAs in wild-type and Trbp-cKO hearts
Project description:We report global RNA expression profiles from whole zebrafish hearts 24 hours after ventricle amputation. Zebrafish were exposed to atropine or water following surgery. 15 zebrafish hearts were pooled per microarray chip. Amputated hearts of zebrafish exposed to atropine was compared to hearts of zebrafish exposed to water.
Project description:This experiment sought to understand the transcriptomic changes that occur in the larval zebrafish heart following injury. 600 hearts were laser injured at 3 days post fertilisation, extracted 48 hours later and pooled into three groups of 200. RNA was extracted from the whole heart(s) and sent for sequencing along with 3 groups of 200 uninjured hearts, extracted and processed identically. RNA sequencing, quality control and alignment was performed by the commercial company GENEWIZ.