Mouse mesoderm-specific transcript inhibits adipogenic differentiation and induces trans-differentiation into hepatocyte-like cells in 3T3-L1 preadiocytes

The mesoderm-specific transcript (Mest) is an imprinted gene that is transcribed from the paternal allele. It is a marker of adipose tissue expansion; however, it is uncertain whether Mest expression promotes or suppresses adipogenic differentiation. To elucidate the effects of Mest expression on ad...

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Bibliographic Details
Published in:BMC research notes 2022-05, Vol.15 (1), p.164-6, Article 164
Main Authors: Kadota, Yoshito, Kawakami, Takashige, Sato, Masao, Suzuki, Shinya
Format: Article
Language:English
Subjects:
3T3-L1 Cells
Adipocyte
Adipocytes
Adipogenesis - genetics
Adipose tissue
Animals
Antibodies
Body fat
Cell Differentiation
Cell Transdifferentiation - genetics
Dexamethasone
Gene expression
Gene silencing
Glycogen
Hepatocyte
Hepatocytes
Lipid accumulation
Lipids
Mesoderm
Mesoderm specific transcript
Mice
Preadipocytes
Proteins
Research Note
siRNA
Statistical analysis
Stem cells
Trans-differentiation
α-Fetoprotein
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Summary:The mesoderm-specific transcript (Mest) is an imprinted gene that is transcribed from the paternal allele. It is a marker of adipose tissue expansion; however, it is uncertain whether Mest expression promotes or suppresses adipogenic differentiation. To elucidate the effects of Mest expression on adipogenic differentiation, we transfected an expression vector or siRNA for mouse Mest into 3T3-L1 mouse preadipocyte cell line. In differentiated 3T3-L1 adipocytes, Mest overexpression decreased lipid accumulation. Conversely, gene silencing of Mest increased the accumulation of lipid droplets in adipocytes. These results demonstrate that Mest negatively regulates adipocyte differentiation. Further, Mest induced trans-differentiation of 3T3-L1 cells into hepatocytes, and its overexpression induced the expression of hepatocyte marker genes, including albumin and α-fetoprotein. In the presence of dexamethasone, the forced expression of the Mest caused morphological changes in 3T3-L1 cells. Cells were flat and polygonal shapes, with an increased accumulation of intracellular glycogen and other features that are typical of hepatocytes. Therefore, Mest inhibits adipogenic differentiation of 3T3-L1 preadipocytes by inducing hepatocyte trans-differentiation.
ISSN:1756-0500
1756-0500
DOI:10.1186/s13104-022-06051-x