Suppression of CD36 attenuates adipogenesis with a reduction of P2X7 expression in 3T3-L1 cells

Abstract

Adipogenesis is a process of differentiation from preadipocyte into adipocyte, and is regulated by several transcription factors, including the peroxisome proliferator-activated receptor gamma (PPARγ) and the CCAAT-enhancer-binding protein alpha (C/EBPα). CD36 is a membrane protein which contributes to the metabolic disorders such as obesity. Although the previous study demonstrated CD36 participated in the progression of adipogenesis, the mechanism is still unclear. We report here that knockdown of CD36 expression by CD36 small interfering RNA (siRNA) resulted in a reduction of adipocyte differentiation and adipogenic protein expression. In addition, purinergic receptor P2X, ligand-gated ion channel 7 (P2X7) was downregulated in CD36-knockdown 3T3-L1 cells, suggesting that the suppression of CD36 attenuates adipogenesis via the P2X7 pathway in 3T3-L1 cells.

Lineage Identity and Location within the Dermis Determine the Function of Papillary and Reticular Fibroblasts in Human Skin

“…Accordingly, proliferation rates of murine fibroblasts are not only determined by their age and fibroblast lineage identity but also by the dermal composition (Lichtenberger et al, 2016).Thus, functional heterogeneity of distinct fibroblast subsets is defined by both their identity and microenvironment. For example, CD36 expression is higher in the lower dermis where adipogenesis occurs, which is coherent with its reported function (Gao et al, 2017a(Gao et al, , 2017b. Dermal microvascular endothelial cells also display heterogeneous CD36 expression depending on their localization within the dermis (Petzelbauer et al, 1993).…”

“…FAP þ CD90 þ also expressed high levels of COL11A1 and FMO1 (Figure 2e, and see Supplementary Figure S1g). Both FAP e CD90 þ and FAP þ CD90 þ fibroblasts displayed high expression levels of CD36 and PPARg, both of which are involved in fatty acid metabolism and adipogenesis (Gao et al, 2017a(Gao et al, , 2017bSiersbaek et al, 2010). These findings indicate that while FAP þ CD90 e cells represent papillary fibroblasts, FAP e CD90 þ cells depict reticular fibroblasts.…”

“…In the search for cell surface markers that might discriminate between papillary and reticular fibroblasts in human skin, we stained skin sections from healthy donors with antibodies targeting previously published fibroblast cell surface markers like THY-1/CD90 (Kisselbach et al, 2009;Ko et al, 2001), FAP (Park et al, 1999;Rettig et al, 1993), DPPIV/CD26 (Atherton et al, 1992(Atherton et al, , 1994a(Atherton et al, , 1994bDriskell et al, 2013) or FAT/CD36 (Berger et al, 2015;Gao et al, 2017a). Co-stainings with antibodies targeting these ( Figure 1a) and other markers, including the pan-fibroblast marker vimentin, confirms previous descriptions that various fibroblast subsets exist.…”

Lipoatrophy and metabolic disturbance in mice with adipose-specific deletion of kindlin-2

“…Oil Red O staining. In brief, following fixation of the mature adipocytes in 10% (v/v) formaldehyde solution for 30 minutes, the cells were stained with 0.5% Oil Red O for 30 minutes at room temperature, rinsed in PBS, as previously described (49).…”

Involvement of calcium channels in the regulation of adipogenesis

“…In 3T3-L1 pre-adipocytes, the extracellular ATP has been demonstrated to regulate hormone-induced adipocyte differentiation, which is mediated by P2Y receptors without affects pre-adipocyte proliferation [111]. It has been recently reported that knockdown of CD36, a membrane protein that has been demonstrated to participate in the progression of adipogenesis, resulted in a reduction of adipocyte differentiation and downregulation of purinergic receptor P2X7 expression, suggesting that the suppression of adipogenesis mediated by CD36 is probably via P2X7 pathway in 3T3-L1 cells [112]. Although P2 receptors have been proved to play a role in adipogenesis, the underlying mechanisms are still needed for further investigation.…”