Apolipoprotein E (ApoE), a Bmp‐2 (bone morphogenetic protein) upregulated gene in mesenchymal progenitors (C3H10T1/2), is highly expressed in murine embryonic development
Abstract
Apolipoprotein E (ApoE) was identified as upregulated by Bmp‐2 (bone morphogenetic protein‐2) in the murine mesenchymal progenitor cell line C3H10T1/2 by a subtractive cloning strategy. Expression of recombinant Bmps in mesenchymal C3H10T1/2 progenitors results in the differentiation into the osteogenic, the chondrogenic, and the adipogenic lineage. In addition, ApoE is also expressed in primary osteoblasts isolated from murine calvariae late in the in vitro osteoblast developmental sequence. To infer possible roles of ApoE in organogenesis and tissue differentiation, ApoE expression during mouse embryonic development was analyzed in murine midgestation and late embryonic development by in situ hybridization. ApoE is highly expressed at many sites of organ development (liver, brain, heart, eye, lung), probably in a subset of neural crest cells and ectodermal derivatives suggestive for important functions of ApoE during embryonic differentiation and organ development.
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BMP2 was originally shown to upregulate APOE in a murine-mesenchymal progenitor cell line, suggesting a possible role of APOE in organogenesis and tissue differentiation.
“BMP2 was originally shown to upregulate APOE in a murine-mesenchymal progenitor cell line, suggesting a possible role of APOE in organogenesis and tissue differentiation [42].”
From Genome-wide analysis identifies novel loci influencing plasma apolipoprotein E concentration and Alzheimer’s disease risk (2023) · cites this paper as [42]
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Aslam, M. M., Fan, K.-H., Lawrence, E., Bedison, M. A., Snitz, B. E., DeKosky, S. T., Lopez, O. L., Feingold, E., & Kamboh, M. I. (2023) · Molecular Psychiatry · doi:10.1038/s41380-023-02170-4 · Cited by 39 · see citing works
ApoE expression across the CNS: Who, What, Where, When, and How (much)?
Nolt, G. L., Lucido, C. C., Smith, L. M., & Johnson, L. A. (2026) · Molecular Neurodegeneration Advances · doi:10.1186/s44477-026-00028-x · Cited by 2 · see citing works
- Authors
- Bächner, D., Schröder, D., Betat, N., Ahrens, M., & Gross, G.
- Affiliations
- Helmholtz Centre for Infection Research (DE)
- Corresponding author
- Gross, Gerhard
- ORCID
- Gross, Gerhard
- Venue
- BioFactors
- Publisher
- Wiley
- Published
- 1999-01
- Volume
- 9
- Issue
- 1
- Pages
- 11-17
- ISSN
- 0951-6433 (ISSN-L)
- 1872-8081
- OpenAlex
- W2140836551
- Cited by
- 35
- References
- 0
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 2 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 5 · 2014: 1 · 2012: 4
- FWCI
- 0.23
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- BioFactors (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Keywords
- apolipoprotein E, BMP-2, mesenchymal progenitor cells, C3H10T1/2 cells, subtractive cloning, osteogenic differentiation, chondrogenic differentiation, adipogenesis, osteoblasts, embryonic development, organogenesis, neural crest cells, gene expression
- MeSH terms
- Animals, Apolipoproteins E, Cell Differentiation, Cell Line, Cells, Cultured, Cloning, Molecular, Embryo, Mammalian, Embryonic and Fetal Development, Mesoderm, Mice, Inbred Strains, Neural Crest, Osteoblasts, Recombinant Proteins, Stem Cells, Transfection, Up-Regulation, In Situ Hybridization, Gene Expression Regulation, Developmental, Cell Lineage, Bone Morphogenetic Proteins, Mice
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