Reelin and Thrombospondin1 regulate cardiomyocyte proliferation through Vldlr
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA734577 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14711244_1.fastq.gz | Fastqsanger.gz | |||
| SRR14711244_2.fastq.gz | Fastqsanger.gz | |||
| SRR14711245_1.fastq.gz | Fastqsanger.gz | |||
| SRR14711245_2.fastq.gz | Fastqsanger.gz | |||
| SRR14711246_1.fastq.gz | Fastqsanger.gz |
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Project description:We performed RNA-Seq analysis of neoatal rat ventricular cardiomyocytes (NRVCs)which were treated with Reelin,or knocking down Vldlr,Thbs1,or overexpressing Vldlr to investigate the moleclular mechanism of Thbs1/Reelin-Vldlr to regulate cardiomyocyte proliferation.In addition,the day 1mouse cardiomyocytes in Myh6-Cre;Vldlr f/f mice ,Myh6-Cre;Vldlr f/+ mice ,versus Vldlr f/f mice were also performed to explore the fucntion of Vldlr which regulating cardiomyocyte proliferation in vivo.
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Project description:The neonatal mammalian heart is capable of substantial regeneration following injury through cardiomyocyte proliferation. However, this regenerative capacity is lost by postnatal (P) day 7. How to stimulate the adult cardiomyocyte to re-enter the cell cycle is still unknown. Accumulating evidence suggests that cardiomyocyte proliferation depends on its metabolic state. Due to the tight connection between the tricarboxylic acid cycle (TCA) and cell proliferation, we analyzed the TCA metabolites between P0.5 and P7 mouse hearts and found that α-ketoglutarate (α-KG) ranked first among the decreased metabolites. The intraperitoneal injection of exogenous α-KG extended the window of cardiomyocyte proliferation during heart development and promoted heart regeneration after myocardial infarction (MI) by inducing adult cardiomyocyte proliferation. This was confirmed in Ogdh-siRNA-treated mice with increased α-KG levels. Mechanistically, α-KG activates Jmjd3, a histone lysine demethylase, that decreases H3K27me3 expression and deposition of H3K4me3 at the promoters of cell cycle and structural maturation genes in cardiomyocytes. Our present study shows that α-KG promotes cardiomyocyte proliferation by Jmjd3-dependent demethylation and inactivation of H3K27me3 andH3K4me3, which is a potential therapeutic approach for treating MI and heart failure.
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Project description:Background—YAP, the nuclear effector of Hippo signaling, regulates cellular growth and survival in multiple organs, including the heart, by interacting with TEAD sequence specific DNA-binding proteins. Recent studies showed that YAP stimulates cardiomyocyte proliferation and survival. However, the direct transcriptional targets through which YAP exerts its effects are poorly defined. Methods and Results—To identify genes directly regulated by YAP in cardiomyocytes, we combined differential gene expression analysis in YAP gain- and loss-of-function with genome-wide identification of YAP bound loci using chromatin immunoprecipitation and high throughput sequencing. This screen identified Pik3cb, encoding p110β, a catalytic subunit of phosphoinositol-3-kinase (PI3K), as a candidate YAP effector that promotes cardiomyocyte proliferation and survival. We validated YAP and TEAD occupancy of a conserved enhancer within the first intron of Pik3cb, and show that this enhancer drives YAP-dependent reporter gene expression. Yap gain- and loss-of-function studies indicated that YAP is necessary and sufficient to activate the PI3K-Akt pathway. Like Yap, Pik3cb gain-of-function stimulated cardiomyocyte proliferation, and Pik3cb knockdown dampened the YAP mitogenic activity. Reciprocally, Yap loss-of-function impaired heart function and reduced cardiomyocyte proliferation and survival, all of which were significantly rescued by AAV-mediated Pik3cb expression. Conclusion—Pik3cb is a crucial direct target of YAP, through which the YAP activates PI3K-AKT pathway and regulates cardiomyocyte proliferation and survival. Yap wild type ChIPseq and input
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Project description:Objective: Retinal angiomatous proliferation (RAP) represents a special form of neovascular age-related macular degeneration. Immune cells accumulate at RAP, but so far it is unclear whether these cells are resident retinal microglial cells (MG) or blood infiltrating monocytes (MO) and whether these cells can influence RAP formation. The aim of this study is to determine the relative contribution of MG and MO to RAP and to define the transcriptional profile of the dominant cell population. Methods: Vldlr -/- Knockout mice were crossed with MG-specific Cx3cr1CreER/+:Rosa26-Tomfl/+ re-porter mice (MG-Tom). The resulting Vldlr-/-:MG-Tom mice received tamoxifen injection at day 1 after birth (P1), leading to expression of Tomato fluorochrome (Tom) in myeloid cells. Myeloid cells were examined at P17, P31, and P42 by immunohistochemical Iba1 staining and retinal Tom expression. In addition, Tom-positive MG were isolated at P17 by fluorescence-activated cell sorting, and the transcriptional profile of MG was analyzed by RNA sequencing. MG Tom mice, also injected at P1 with tamoxifen, served as controls for RNA-Seq. Results: Our data show that at the beginning of RAP formation (P17), hardly any MO migrates from blood into tissues (0.2±0.5 MO/RAP, 2.0±0.8 MG/RAP). During the course of RAP formation, this changes only slightly (P31: 0.6±2.2 MO/RAP, 10.3±12.8 MG/RAP; P42: 0.6±2.4 MO/RAP, 14.3±9.4 MG/RAP). RNA sequencing of the isolated MG identified 140 differentially expressed genes (DEG), of which 67 were upregulated and 73 were downregulated upon RAP formation. Gene ontology enrichment analysis of the 140 DEGs revealed that they contribute primarily to immune-associated processes, such as leukocyte migration and chemotaxis, regulation of the immune system and immune response, and wound responses. Retinal MG thereby express the pro-angiogenic soluble factor Spp1 (log2FC 1.8) in addition to Ccl2 and Cxcl14 during RAP formation. Conclusion: Our data indicate that resident MG represent the dominant immune cell population during retinal angiomatous proliferation in the Vldlr knockout mouse. RNA sequencing of MG reveals upregulation of immune-associated processes and of pro-angiogenic factors, such as Spp1. Cell-specific modulation of MG may thus form the basis of a future therapeutic option for the treatment of RAP.
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