Stromal cells rapidly reorganize cell composition during would healing. Resident stromal cells secrete systemic ligands and mobilize immune cells from bone marrow. Subsequently resident cells and mobilized immune cells cooperate together for efficient wound healing.
Surgical Injury and Ischemia Prime the Adipose Stromal Vascular Fraction and Increase Angiogenic Capacity in a Mouse Limb Ischemia Model.
Age, Specimen part
View SamplesEstrogens are well known steroid hormones necessary to maintain bone health. In addition, mechanical loading, which estrogen signaling may intersect with the Wnt/-catenin pathway, is also essential for bone health. As osteocytes are known as the major mechanosensory cells embedded in mineralized bone matrix, osteocyte ER deletion mice (EROcy/Ocy) were generated by mating ER floxed mice with Dmp1-Cre mice to determine functions of ER in osteocytes. Trabecular bone mineral density of female, but not male EROcy/Ocy mice was significantly decreased. Bone formation parameters in EROcy/Ocy were significantly decreased while osteoclast parameters were unchanged. This suggests that ER in osteocytes exerts osteoprotective function by positively controlling bone formation. To identify potential targets of ER, gene array analysis of Dmp1-GFP osteocytes FACS sorted from EROcy/Ocy and control mice was performed. Expression of Mdk and Sostdc1, both known inhibitors of Wnt, were significantly increased without alteration of the mature osteocyte marker Sost or -catenin. Hindlimb unloading exacerbated the trabecular bone loss, but surprisingly cortical bone was resistant. These studies show that ER in osteocytes has osteoprotective effects in trabecular bone through regulating expression of Wnt antagonists, but conversely plays a negative role in cortical bone loss due to unloading.
Estrogen receptor α in osteocytes regulates trabecular bone formation in female mice.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Androgen-induced Long Noncoding RNA (lncRNA) SOCS2-AS1 Promotes Cell Growth and Inhibits Apoptosis in Prostate Cancer Cells.
Specimen part, Cell line
View SamplesProstate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. We identified a novel androgen-regulated long non-coding (lnc) RNA, SOCS2-AS1.
Androgen-induced Long Noncoding RNA (lncRNA) SOCS2-AS1 Promotes Cell Growth and Inhibits Apoptosis in Prostate Cancer Cells.
Specimen part, Cell line
View SamplesWith the exception of imprinted genes and certain repeats, DNA methylation is globally erased during pre-implantation development. Recent studies have suggested that Tet3-mediated oxidation of 5-methylcytosine (5mC) and DNA replication-dependent dilution both contribute to global paternal DNA demethylation, but demethylation of the maternal genome occurs via replication. Here we present genome-scale DNA methylation maps for both the paternal and maternal genomes of Tet3-depleted and/or DNA replication-inhibited zygotes. In both genomes, we found that inhibition of DNA replication blocks DNA demethylation independently from Tet3 function, and that Tet3 facilitates DNA demethylation by coupling with DNA replication. For both, our data indicate that replication-dependent dilution is the major contributor to demethylation, but Tet3 plays an important role, particularly at certain loci. Our study therefore both defines the respective functions of Tet3 and DNA replication in paternal DNA demethylation and reveals an unexpected contribution of Tet3 to demethylation of the maternal genome. Overall design: In this data set, we include RNA-Seq data of mouse 2-cell embryos and blastocysts derived from both wildtype and Tet3-null oocytes
Tet3 and DNA replication mediate demethylation of both the maternal and paternal genomes in mouse zygotes.
No sample metadata fields
View SamplesmRNA sequencing analysis of FACS-purified leptotene/zygotene (L/Z) spermatocytes Overall design: Compare transcriptomes of WT, Pld6 KO, and Dnmt3l KO germ cells in the F1 hybrid background of B6 and MSM to study these mutations affecting gene expression due to nearby retrotransposons.
Switching of dominant retrotransposon silencing strategies from posttranscriptional to transcriptional mechanisms during male germ-cell development in mice.
Cell line, Subject
View Samples3 subtypes of cortical projection neurons were purified by fluorescence-activated cell sorting at 4 different stages of development from mouse cortex. A detailed description of the data set is described in Arlotta, P et al (2005).
Neuronal subtype-specific genes that control corticospinal motor neuron development in vivo.
Specimen part
View SamplesMammalian oocytes can reprogram somatic cells into totipotent state, which allows animal cloning through somatic cell nuclear transfer (SCNT). However, the great majority of SCNT embryos fail to develop to term due to poorly defined reprogramming defects. Here we demonstrate that histone H3 lysine 9 trimethylation (H3K9me3) in donor nuclei is a major epigenetic barrier that prevents efficient nuclear reprogramming in mouse oocytes. Comparative transcriptome analysis of early embryos revealed reprogramming resistant regions (RRRs) where transcriptional activation at 2-cell embryos is inhibited by SCNT compared to in vitro fertilization (IVF). RRRs significantly overlap with H3K9me3 enrichment in donor somatic cells. Importantly, removal of the H3K9me3 by ectopic expression of an H3K9me3 demethylase Kdm4d in recipient oocytes not only reactivates most RRRs, but also greatly improves development of SCNT embryos. Furthermore, the use of Suv39h1/2-depleted somatic nuclei as donors also greatly improves the development of SCNT embryos. Our study thus reveals H3K9me3 as an epigenetic barrier in SCNT-mediated reprogramming and provides a feasible method for improving mammalian cloning efficiency. Overall design: Here we perform RNA-seq based transcriptome profiling in Donor (cumulus cells), in vitro fertilized (IVF) embryos at 1- and 2-cell stages, somatic cell nuclear transfer (SCNT) embryos at 1- and 2-cell stages, Kdm4d over-expressed 2-cell SCNT embryos, and catalytic domain mutated Kdm4d over-expressed 2-cell SCNT embryos with duplicates.Â
Embryonic development following somatic cell nuclear transfer impeded by persisting histone methylation.
No sample metadata fields
View SamplesGerminal center (GC) B cells cycle between two states, the light zone (LZ) and the dark zone (DZ), and in the latter they proliferate and hypermutate their immunoglobulin genes. How this functional transition takes place is still controversial. In this study, we demonstrate that ablation of Foxo1 after GC development led to the loss of the DZ GC B cells and disruption of the GC architecture. Mechanistically, even upon provision of adequate T cell help, Foxo1-deficient GC B cells showed less proliferative expansion than controls. Moreover, we found that the transcription factor BATF was transiently induced in LZ GC B cells in a Foxo1-dependent manner and that deletion of BATF similarly led to GC disruption. Thus, our results are consistent with a model where the switch from the LZ to the DZ is triggered after receipt of T cell help, and suggest that Foxo1-mediated BATF up-regulation is at least partly involved in this switch. Overall design: mRNA profiles of wild-type DZ, LZ, and Foxo1-deficient GC B cells were generated by deep sequencing in triplicate, using Illumina HiSeq 1500.
The transcription factor Foxo1 controls germinal center B cell proliferation in response to T cell help.
Specimen part, Subject
View SamplesWe found that CFIm68, a mRNA cleavage and polyadenylation factor implicated for alternative polyadenylation site choice, was co-purified with Thoc5, a component of human THO/TREX. Microarray analysis using human HeLa cells reveals knockdown of Thoc5 affects the expression of a subset of non-heat shock genes. Notably, depletion of Thoc5 attenuated the expression of the mRNAs polyadenylated at distal, but not proximal, polyadenylation sites, which phenocopied the depletion of CFIm68.
Human TREX component Thoc5 affects alternative polyadenylation site choice by recruiting mammalian cleavage factor I.
Cell line, Treatment
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