ArticleMolecular biology of the cell2014
Olfactomedin 2, a novel regulator for transforming growth factor-β-induced smooth muscle differentiation of human embryonic stem cell-derived mesenchymal cells.
Article in Molecular biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 40 citations in OpenAlex.
- Olfactomedin 2 Promotes Atherosclerosis by Eliciting Smooth Muscle Foam Cell Formation.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Olfactomedin-2 at the Crossroads of Smooth Muscle Cell Plasticity.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Large-scale molecular endotype discovery in synovial fluid reveals osteoarthritis as a single biological continuum.Nature communications · 2026Article
- Large-Scale Proteomics Reveals New Candidate Biomarkers for Late-Onset Preeclampsia.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Defective Olfactomedin-2 connects adipocyte dysfunction to obesity.Nature communications · 2025Article
- High-throughput transcriptome analysis reveals a developmental increase in Acvr1c which mediates epigenetic repression of the gene encoding the pubertal brake, Makorin ring finger protein 3.NAR molecular medicine · 2025Article
- Fine-Tuned Expression of Evolutionarily Conserved Signaling Molecules in theInternational journal of molecular sciences · 2024Article
- DOCK2 Promotes Atherosclerosis by Mediating the Endothelial Cell Inflammatory Response.The American journal of pathology · 2024Article
- OLFM2 promotes epithelial-mesenchymal transition, migration, and invasion in colorectal cancer through the TGF-β/Smad signaling pathway.BMC cancer · 2024Article
- Molecular mechanism of specific DNA sequence recognition by NRF1.Nucleic acids research · 2024Article
- DOCK2 Promotes Asthma Development by Eliciting Airway Epithelial-Mesenchymal Transition.American journal of respiratory cell and molecular biology · 2023Article
- SPARC Is Highly Expressed in Young Skin and Promotes Extracellular Matrix Integrity in Fibroblasts via the TGF-β Signaling Pathway.International journal of molecular sciences · 2023Article
- DOCK2 Deficiency Attenuates Abdominal Aortic Aneurysm Formation-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Article
- Assessment and Distribution of Runs of Homozygosity in Horse Breeds Representing Different Utility Types.Animals : an open access journal from MDPI · 2022Article
- Identification of a neural development gene expression signature in colon cancer stem cells reveals a role foriScience · 2022Article
- Article
- Multiple functions of reversine on the biological characteristics of sheep fibroblasts.Scientific reports · 2021Article
- Comprehensive Analysis of the Transcriptome-Wide m6A Methylome in Pterygium by MeRIP Sequencing.Frontiers in cell and developmental biology · 2021Article
- Integration of single-cell datasets reveals novel transcriptomic signatures of β-cells in human type 2 diabetes.NAR genomics and bioinformatics · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Transforming growth factor-β (TGF-β) plays an important role in smooth muscle (SM) differentiation, but the downstream target genes regulating the differentiation process remain largely unknown. In this study, we identified olfactomedin 2 (Olfm2) as a novel regulator mediating SM differentiation. Olfm2 was induced during TGF-β-induced SM differentiation of human embryonic stem cell-derived mesenchymal cells. Olfm2 knockdown suppressed TGF-β-induced expression of SM markers, including SM α-actin, SM22α, and SM myosin heavy chain, whereas Olfm2 overexpression promoted the SM marker expression. TGF-β induced Olfm2 nuclear accumulation, suggesting that Olfm2 may be involved in transcriptional activation of SM markers. Indeed, Olfm2 regulated SM marker expression and promoter activity in a serum response factor (SRF)/CArG box-dependent manner. Olfm2 physically interacted with SRF without affecting SRF-myocardin interaction. Olfm2-SRF interaction promoted the dissociation of SRF from HERP1, a transcriptional repressor. Olfm2 also inhibited HERP1 expression. Moreover, blockade of Olfm2 expression inhibited TGF-β-induced SRF binding to SM gene promoters in a chromatin setting, whereas overexpression of Olfm2 dose dependently enhanced SRF binding. These results demonstrate that Olfm2 mediates TGF-β-induced SM gene transcription by empowering SRF binding to CArG box in SM gene promoters.
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