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MiR-30e in Aortic Smooth Muscle Cells and Bone Marrow Mesenchymal Stem Cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE65435 | GEO | 2015/01/30

SECONDARY ACCESSION(S): PRJNA273988

REPOSITORIES: GEO

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miR-30e targets IGF2-regulated osteogenesis in bone marrow-derived mesenchymal stem cells, aortic smooth muscle cells, and ApoE-/- mice.

Project description:AimsActivation of an osteogenic transcriptional program contributes to the initiation of aortic calcification in atherosclerosis. The role of microRNAs in regulating aortic calcification is understudied. We tested the hypothesis that miR-30e regulates an osteogenic program in bone marrow-derived mesenchymal stem cells (MSCs), aortic smooth muscle cells (SMCs), and ApoE(-/-) mice.Methods and resultsIn aortas of wild-type mice, we found that miR-30e is highly expressed in medial SMCs. In aortas of old ApoE(-/-) mice, we found that miR-30e transcripts are down-regulated in an inverse relation to the osteogenic markers Runx2, Opn, and Igf2. In vitro, miR-30e over-expression reduced the proliferation of MSCs and SMCs while increasing adipogenic differentiation of MSCs and smooth muscle differentiation of SMCs. In MSCs and SMCs over-expressing miR-30e, microarrays and qPCR showed repression of an osteogenic gene panel including Igf2. Inhibiting miR-30e in MSCs increased Igf2 transcripts. In SMCs, IGF2 recombinant protein rescued miR-30e-repressed osteogenic differentiation. Luciferase and mutagenesis assays showed binding of miR-30e to a novel and essential site at the 3'UTR of Igf2. In ApoE(-/-) mice, injections of antimiR-30e oligos increased Igf2 expression in the aortas and livers and significantly enhanced OPN protein expression and calcium deposition in aortic valves.ConclusionmiR-30e represses the osteogenic program in MSCs and SMCs by targeting IGF2 and drives their differentiation into adipogenic or smooth muscle lineage, respectively. Our data suggest that down-regulation of miR-30e in aortas with age and atherosclerosis triggers vascular calcification. The miR-30e pathway plays an important regulatory role in vascular diseases.

| S-EPMC4375408 | biostudies-literature

MiR-30e in Aortic Smooth Muscle Cells and Bone Marrow Mesenchymal Stem Cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-01-30 | E-GEOD-65435 | biostudies-arrayexpress

MiR-30e in Aortic Smooth Muscle Cells and Bone Marrow Mesenchymal Stem Cells [Experiment 3]

2015-01-30 | GSE65434 | GEO

MiR-30e in Aortic Smooth Muscle Cells and Bone Marrow Mesenchymal Stem Cells [Experiment 2]

2015-01-30 | GSE65432 | GEO

MiR-30e in Aortic Smooth Muscle Cells and Bone Marrow Mesenchymal Stem Cells [Experiment 1]

2015-01-30 | GSE65431 | GEO

MiR-30e in Aortic Smooth Muscle Cells and Bone Marrow Mesenchymal Stem Cells [Experiment 3]

Project description:MiR-30e represses the osteogenic program in mesenchymal stem cells (MSCs) and smooth muscle cells (SMCs) by targeting IGF2, and drives their differentiation into adipogenic or smooth muscle lineage, respectively. In Experiment 1, SMCs were cultured from mouse aortas and transduced with miR-30e or control lentivirus. In Experiment 2, MSCs were extracted from mouse bone marrow and transduced with miR-30e or control lentivirus. In Experiment 3, the MSCs were transfected with a scrambled oligo or anti-miR-30e oligo. In all 3 experiments, N=3 per group. RNA was extracted from each experiment and run on Affymetrix arrays.

2015-01-30 | E-GEOD-65434 | biostudies-arrayexpress

MiR-30e in Aortic Smooth Muscle Cells and Bone Marrow Mesenchymal Stem Cells [Experiment 2]

2015-01-30 | E-GEOD-65432 | biostudies-arrayexpress

MiR-30e in Aortic Smooth Muscle Cells and Bone Marrow Mesenchymal Stem Cells [Experiment 1]

2015-01-30 | E-GEOD-65431 | biostudies-arrayexpress

All-trans retinoic acid promotes smooth muscle cell differentiation of rabbit bone marrow-derived mesenchymal stem cells.

Project description:Bone marrow-derived mesenchymal stem cells are multipotent stem cells, an attractive resource for regenerative medicine. Accumulating evidence suggests that all-trans retinoic acid plays a key role in the development and differentiation of smooth muscle cells. In the present study, we demonstrate, for the first time, that rabbit bone marrow-derived mesenchymal stem cells differentiate into smooth muscle cells upon the treatment with all-trans retinoic acid. All-trans retinoic acid increased the expression of myocardin, caldesmon, 22-kDa smooth muscle cell-specific protein (SM22alpha), and SM-myosin heavy chains in rabbit bone marrow-derived mesenchymal stem cells, as detected by reverse transcription polymerase chain reaction (PCR). Immunostaining of SM22alpha and SM-myosin heavy chains using monoclonal antibodies also indicated smooth muscle cell differentiation of rabbit bone marrow-derived mesenchymal stem cells following the treatment with all-trans retinoic acid. In addition, more than 47% of bone marrow-derived mesenchymal stem cells demonstrated the contractile phenotype of smooth muscle cells. Western blot results showed that SM-1 and SM-2 were highly expressed in the differentiated cells. These results suggest that all-trans retinoic acid may serve as a potent agent for functional smooth muscle cell differentiation in tissue engineering.

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Sodium butyrate promotes the differentiation of rat bone marrow mesenchymal stem cells to smooth muscle cells through histone acetylation.

Project description:Establishing an effective method to improve stem cell differentiation is crucial in stem cell transplantation. Here we aimed to explore whether and how sodium butyrate (NaB) induces rat bone marrow mesenchymal stem cells (MSCs) to differentiate into bladder smooth muscle cells (SMCs). We found that NaB significantly suppressed MSC proliferation and promoted MSCs differentiation into SMCs, as evidenced by the enhanced expression of SMC specific genes in the MSCs. Co-culturing the MSCs with SMCs in a transwell system promoted the differentiation of MSCs into SMCs. NaB again promoted MSC differentiation in this system. Furthermore, NaB enhanced the acetylation of SMC gene-associated H3K9 and H4, and decreased the expression of HDAC2 and down-regulated the recruitment of HDAC2 to the promoter regions of SMC specific genes. Finally, we found that NaB significantly promoted MSC depolarization and increased the intracellular calcium level of MSCs upon carbachol stimulation. These results demonstrated that NaB effectively promotes MSC differentiation into SMCs, possibly by the marked inhibition of HDAC2 expression and disassociation of HDAC2 recruitment to SMC specific genes in MSCs, which further induces high levels of H3K9ace and H4ace and the enhanced expression of target genes, and this strategy could potentially be applied in clinical tissue engineering and cell transplantation.

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