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Differentiated adipocytes in a 3T3-L1 cell line stained with Oil Red O. 3T3-L1 is a sub clonal cell line derived from the original 3T3 Swiss albino cell line of 1962. The 3T3 original cell line was isolated from a mouse embryo and propagated for this specific line of 3T3 cells is used to study adipose tissue-related diseases and dysfunctions.
In vitro studies on differentiation have used the pre-committed preadipocyte lineage, such as 3T3-L1 and 3T3-F442A cell line, or preadipocytes isolated from the stromal-vascular fraction of white adipose tissue. In vitro differentiation is a highly ordered process. Firstly, proliferating preadipocytes arrest growth usually by contact inhibition.
The expression of the KLF15 gene is markedly up-regulated during the differentiation of 3T3-L1 preadipocytes into adipocytes. Ectopic expression of KLF15 in NIH 3T3 or C2C12 cells triggered both lipid accumulation and the expression of PPAR-γ in the presence of inducers of adipocyte differentiation.
Adiponectin was first characterised in 1995 in differentiating 3T3-L1 adipocytes (Scherer PE et al.). [33] In 1996 it was characterised in mice as the mRNA transcript most highly expressed in adipocytes. [7] In 2007, adiponectin was identified as a transcript highly expressed in preadipocytes [34] (precursors of fat cells) differentiating into ...
Chemerin has been implicated in autocrine / paracrine signaling for adipocyte differentiation and also stimulation of lipolysis. [11] [12] Studies with 3T3-L1 cells have shown chemerin expression is low in pre-differentiated adipocytes [11] but its expression and secretion increases both during and after differentiation in vitro.
Aloxe3 appears necessary and sufficient for the differentiation of mouse 3T3-L1 fibroblast cells into adipocytes (i.e. fat cells); the function of Aloxe3 in this differentiation appears to be to its metabolism 12R-HpETE into hepoxilins A3 or B3 which directly activate(s) Peroxisome proliferator-activated receptor gamma which in turn initiates ...
For example, Murine Embryonic Fibroblasts (MEFs) from mice lacking both C/EBPβ and C/EBPδ show impaired adipocyte differentiation in response to adipogenic stimuli. [5] In contrast, ectopic expression of C/EBPβ and δ in 3T3-L1 preadipocytes promotes adipogenesis, even in the absence of adipogenic stimuli.
FITM2 has been identified as being overexpressed throughout the time 3T3-L1 (from the adipocyte cell line) is being differentiated which shows resemblance to the peroxisome proliferator-activated receptor gamma at a specific period when lipid droplets have been identified to build-up which results in the adipocyte phenotype that is seen in the ...