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Serum amyloid A3 deficiency impairs in vitro and in vivo adipocyte differentiation.

ABSTRACT: Obesity, caused by an excess adipose tissue, is one of the biggest health-threats of the 21^st century. Adipose tissue expansion occurs through two processes: (i) hypertrophy, and (ii) hyperplasia, the formation of new adipocytes, also termed adipogenesis. Recently, serum amyloid A3 (Saa3) has been implicated in adipogenesis. Therefore, the aim of this study was to investigate the effect of Saa3 on adipogenesis using both an in vitro and in vivo murine model. Saa3 gene silenced pre-adipocytes ha a lower expression of pro-adipogenic markers and less lipid accumulation, indicating impaired adipogenesis. Furthermore, male NUDE mice, injected with Saa3 gene silenced pre-adipocytes developed smaller fat pads with smaller adipocytes and lower expression of pro-adipogenic markers than their control counterparts. This confirms that Saa3 gene silencing indeed impairs adipogenesis, both in vitro and in vivo. These results indicate a clear role for Saa3 in adipogenesis and open new perspectives in the battle against obesity.

SUBMITTER: Vercalsteren E

PROVIDER: S-EPMC8078753 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature

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Serum amyloid A3 deficiency impairs in vitro and in vivo adipocyte differentiation.

Vercalsteren Ellen E Vranckx Christine C Vermeire Ines I Gooijen Max M Lijnen Roger R Scroyen Ilse I

Adipocyte 20211201 1

Obesity, caused by an excess adipose tissue, is one of the biggest health-threats of the 21<sup>st</sup> century. Adipose tissue expansion occurs through two processes: (i) hypertrophy, and (ii) hyperplasia, the formation of new adipocytes, also termed adipogenesis. Recently, serum amyloid A3 (Saa3) has been implicated in adipogenesis. Therefore, the aim of this study was to investigate the effect of Saa3 on adipogenesis using both an in vitro and in vivo murine model. Saa3 gene silenced pre-adi ...[more]

PMID: 33896367

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Project description:Liver fibrosis is a severe global health problem. However, no effective antifibrotic drugs have been approved. Surf4 is primarily located in the endoplasmic reticulum (ER) and mediates the transport of secreted proteins from the ER to the Golgi apparatus. Knockout of hepatic Surf4 (Surf4 LKO) in mice impairs very-low-density lipoprotein secretion without causing overt liver damage. Here, we found that collagen levels are significantly reduced in the liver of Surf4 LKO mice compared with control Surf4 flox mice, as demonstrated by proteomics, Western blot, and quantitative reverse transcription polymerase chain reaction. Therefore, this study aims to investigate whether and how hepatic Surf4 affects liver fibrosis. We observed that CCl4-induced liver fibrosis is significantly lower in Surf4 LKO mice than in Surf4 flox mice. Mechanistically, hepatic Surf4 deficiency reduces serum amyloid A1 (SAA1) secretion and hepatic stellate cell (HSC) activation. Surf4 coimmunoprecipitates and colocalizes with SAA1. Lack of hepatic Surf4 significantly reduces SAA1 secretion from hepatocytes, and SAA1 activates cultured human HSCs (LX-2 cells). Conditioned medium (CM) from Surf4-deficient primary hepatocytes activates LX-2 cells to a much lesser extent than CM from Surf4 flox primary hepatocytes, and this reduced effect is restored by the addition of recombinant SAA1 to CM from Surf4-deficient hepatocytes. Knockdown of SAA1 in primary hepatocytes or TLR2 in LX-2 cells significantly reduces LX-2 activation induced by CM from Surf4 flox hepatocytes but not from Surf4 LKO hepatocytes. Furthermore, knockdown of SAA1 significantly ameliorates liver fibrosis in Surf4 flox mice but does not further reduce liver fibrosis in Surf4 LKO mice. We also observe substantial expression of Surf4 and SAA1 in human fibrotic livers. Therefore, hepatic Surf4 facilitates SAA1 secretion, activates HSCs, and aggravates liver fibrosis, suggesting that hepatic Surf4 and SAA1 may serve as treatment targets for liver fibrosis.

Dataset Information

Serum amyloid A3 deficiency impairs in vitro and in vivo adipocyte differentiation.

Publications

Serum amyloid A3 deficiency impairs in vitro and in vivo adipocyte differentiation.

Similar Datasets

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