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MicroRNA miR-16 is anti-proliferative in enterocytes and exhibits diurnal rhythmicity in intestinal crypts

ABSTRACT: This is the first report to document circadian rhythmicity of specific microRNAs in rat jejunum. Our data provide a link between the anti-proliferative microRNA miR-16 and the intestinal proliferation rhythm and point to miR-16 as an important regulator of proliferation in jejunal crypts. This function may be essential to match proliferation and absorptive capacity with nutrient availability.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE20603 | GEO | 2010/08/13

SECONDARY ACCESSION(S): PRJNA124775

REPOSITORIES: GEO

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MicroRNA miR-16 is anti-proliferative in enterocytes and exhibits diurnal rhythmicity in intestinal crypts

Project description:This is the first report to document circadian rhythmicity of specific microRNAs in rat jejunum. Our data provide a link between the anti-proliferative microRNA miR-16 and the intestinal proliferation rhythm and point to miR-16 as an important regulator of proliferation in jejunal crypts. This function may be essential to match proliferation and absorptive capacity with nutrient availability. Time course data with 7 time points and 3 replicates per time point. Each 2-color array is hybridized against a reference from time point 0, and dye swaps are included.

2010-08-13 | E-GEOD-20603 | biostudies-arrayexpress

MicroRNA mir-16 is anti-proliferative in enterocytes and exhibits diurnal rhythmicity in intestinal crypts.

Project description:The intestine exhibits profound diurnal rhythms in function and morphology, in part due to changes in enterocyte proliferation. The regulatory mechanisms behind these rhythms remain largely unknown. We hypothesized that microRNAs are involved in mediating these rhythms, and studied the role of microRNAs specifically in modulating intestinal proliferation.Diurnal rhythmicity of microRNAs in rat jejunum was analyzed by microarrays and validated by qPCR. Temporal expression of diurnally rhythmic mir-16 was further quantified in intestinal crypts, villi, and smooth muscle using laser capture microdissection and qPCR. Morphological changes in rat jejunum were assessed by histology and proliferation by immunostaining for bromodeoxyuridine. In IEC-6 cells stably overexpressing mir-16, proliferation was assessed by cell counting and MTS assay, cell cycle progression and apoptosis by flow cytometry, and cell cycle gene expression by qPCR and immunoblotting.mir-16 peaked 6 hours after light onset (HALO 6) with diurnal changes restricted to crypts. Crypt depth and villus height peaked at HALO 13-14 in antiphase to mir-16. Overexpression of mir-16 in IEC-6 cells suppressed specific G1/S regulators (cyclins D1-3, cyclin E1 and cyclin-dependent kinase 6) and produced G1 arrest. Protein expression of these genes exhibited diurnal rhythmicity in rat jejunum, peaking between HALO 11 and 17 in antiphase to mir-16.This is the first report of circadian rhythmicity of specific microRNAs in rat jejunum. Our data provide a link between anti-proliferative mir-16 and the intestinal proliferation rhythm and point to mir-16 as an important regulator of proliferation in jejunal crypts. This function may be essential to match proliferation and absorptive capacity with nutrient availability.

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Bidirectional histone monoaminylation dynamics regulate neural rhythmicity

Project description:H3 monoaminylation dynamics are bidirectionally controlled by TG2 and facilitate neural rhythmicity.

2024-10-10 | GSE270432 | GEO

Bidirectional histone monoaminylation dynamics regulate neural rhythmicity

Project description:H3 monoaminylation dynamics are bidirectionally controlled by TG2 and facilitate neural rhythmicity.

2024-10-10 | GSE270429 | GEO

T cell activation decreases microRNA-15a/16 levels as a mechanism to promote MEK1-ERK1/2-Elk1 signaling for optimal proliferative capacity

Project description:While microRNAs (miRs) have been extensively studied in the context of malignancy and tumor progression, their functions in regulating T cell activation are less clear. We found reduced levels of miR-15a/16 at 3-18 h post-T cell receptor (TCR) stimulation, suggesting a role in shaping T cell activation. An inducible miR15a/16 transgenic mouse model was developed to determine how elevating miR-15a/16 levels during early stages of activation would affect T cell proliferation and to identify TCR signaling pathways regulated by this miR pair. Doxycyclin (DOX) induced expression of miR-15a/16 from 0-18 h post-TCR stimulation decreased ex vivo proliferation as well as in vivo antigen-specific proliferation. Bioinformatic and proteomic approaches were combined to identify MEK1 as a target of miR-15a/16. MEK1 targeting by miR-15a/16 was confirmed using miR mimics that decreased MEK1 containing the 3’-UTR target nucleotide sequence (UGCUGCUA) but did not decrease MEK1 containing a mutated control sequence (AAAAAAAA). Phosphorylation of downstream signaling molecules ERK1/2 and Elk1 were decreased with DOX-induced miR-15a/16 expression. In addition to MEK1, ERK1 was subsequently found to be targeted by miR-15a/16, with DOX induced miR-15a/16 reducing total ERK1 levels in T cells. These findings show that TCR stimulation reduces miR-15a/16 levels at early stages of T cell activation to facilitate increased MEK1 and ERK1, and this promotes sustained MEK1-ERK1/2-Elk1 signaling required for optimal proliferation.

2022-04-04 | PXD030935 | Pride

Bidirectional histone monoaminylation dynamics regulate neural rhythmicity

Project description:Bidirectional histone monoaminylation dynamics regulate neural rhythmicity

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Mmp14 is essential for circadian clock rhythmicity in fibroblasts

Project description:Membrane type I-matrix metalloproteinase (MT1-MMP/Mmp14) is an unusual MMP because it is essential for survival in mice with multiple organ systems being affected for reasons that are unclear. Here, we show that the protein (MT1-MMP) and gene (Mmp14) are under strict circadian clock control and conditional knockout in fibroblasts leads to ~16% of the proteome losing or inverting circadian rhythmicity. The result is loss of the actin cytoskeleton and cell-matrix adhesions and major imbalance of the matrisome. Lack of collagen-I monomer turnover results in excess fibril formation in the absence of Mmp14. In the absence of Mmp14, paired-like homeodomain transcription factor 2 (Pitx2) is upregulated and remains in the nucleus where it drives Plod2 expression. The overall result is accumulation of collagen fibrils and elevated pyridinoline crosslinking that renders collagen fibrils insoluble. In conclusion, Mmp14 is a master regulator of circadian rhythms affecting the actin cytoskeleton and cell microenvironment.

2023-10-31 | PXD031692 | Pride

Differential gene expression in intestinal mouse crypts after loss of KLF5

Project description:To determine potential targets of KLF5 we performed RNA-sequencing on jejunal crypts isolated from Klf5-deficient and wildtype mice, using three biological replicates per genotype. We identified 1,480 genes that showed significant differential expression with at least a 2-fold difference between Klf5-deficient and wildtype (q-value â¤ 0.05) (Figure 5A; Supplementary Table 1). Klf5 expression was significantly downregulated 2.7-fold. Comparison of gene expression after loss of KLF5 in the intestine. Isolated jejunal crypts from 3 wildtype and 3 knockout animals were compared.

2016-04-01 | E-GEOD-79758 | biostudies-arrayexpress

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