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. 2022 Dec;11(1):588-600.
doi: 10.1080/21623945.2022.2123097.

SPRY4 promotes adipogenic differentiation of human mesenchymal stem cells through the MEK-ERK1/2 signaling pathway

Na Li  1   2 , Yunfei Chen  1 , Haiyan Wang  1 , Jing Li  1 , Robert Chunhua Zhao  1   3
Affiliations

SPRY4 promotes adipogenic differentiation of human mesenchymal stem cells through the MEK-ERK1/2 signaling pathway

Na Li et al. Adipocyte. 2022 Dec.

Abstract

Obesity is a chronic metabolic disorder characterized by the accumulation of excess fat in the body. Preventing and controlling obesity by inhibiting the adipogenic differentiation of mesenchymal stem cells (MSCs) and thereby avoiding the increase of white adipose tissue is safe and effective. Recent studies have demonstrated that Sprouty proteins (SPRYs) are involved in cell differentiation and related diseases. However, the role and mechanism of SPRY4 in MSC adipogenic differentiation remain to be explored. Here, we found that SPRY4 positively correlates with the adipogenic differentiation of human adipose-derived MSCs (hAMSCs). Via gain- and loss-of-function experiments, we demonstrated that SPRY4 promotes hAMSC adipogenesis both in vitro and in vivo. Mechanistically, SPRY4 functioned by activating the MEK-ERK1/2 pathway. Our findings provide new insights into a critical role for SPRY4 as a regulator of adipogenic differentiation, which may illuminate the underlying mechanisms of obesity and suggest the potential of SPRY4 as a novel treatment option.

Keywords: ERK1/2; SPRY4; adipogenic differentiation; hAMSCs; obesity.

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Conflict of interest statement

No potential conflict of interest was reported by the author(s).

Figures

Figure 1.
Figure 1.
SPRY4 positively correlated with hAMSC adipogenic differentiation capacity.
Figure 2.
Figure 2.
Downregulation of SPRY4 impaired hAMSC adipogenic differentiation in vitro.
Figure 3.
Figure 3.
Ectopic expression of SPRY4 promoted hAMSC adipogenic differentiation in vitro.
Figure 4.
Figure 4.
SPRY4 accelerated hAMSC heterotopic lipid formation in vivo.
Figure 5.
Figure 5.
MEK–ERK1/2 pathway inhibition suppressed adipogenic differentiation.
Figure 6.
Figure 6.
SPRY4 functioned by activating the MEK–ERK1/2 pathway.
See this image and copyright information in PMC

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