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Serum Amyloid A3 Gene Expression in Adipocytes is an Indicator of the Interaction with Macrophages.


ABSTRACT: The infiltration of macrophages into adipose tissue and their interaction with adipocytes are essential for the chronic low-grade inflammation of obese adipose tissue. In this study, we identified the serum amyloid A3 (Saa3) gene as a key adipocyte-derived factor that is affected by interaction with macrophages. We showed that the Saa3 promoter in adipocytes actually responds to activated macrophages in a co-culture system. Decreasing C/EBP? abundance in 3T3-L1 adipocytes or point mutation of C/EBP? elements suppressed the increased promoter activity in response to activated macrophages, suggesting an essential role of C/EBP? in Saa3 promoter activation. Bioluminescence based on Saa3 promoter activity in Saa3-luc mice was promoted in obese adipose tissue, showing that Saa3 promoter activity is most likely related to macrophage infiltration. This study suggests that the level of expression of the Saa3 gene could be utilized for the number of infiltrated macrophages in obese adipose tissue.

SUBMITTER: Sanada Y 

PROVIDER: S-EPMC5144138 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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Serum Amyloid A3 Gene Expression in Adipocytes is an Indicator of the Interaction with Macrophages.

Sanada Yohei Y   Yamamoto Takafumi T   Satake Rika R   Yamashita Akiko A   Kanai Sumire S   Kato Norihisa N   van de Loo Fons Aj FA   Nishimura Fusanori F   Scherer Philipp E PE   Yanaka Noriyuki N  

Scientific reports 20161208


The infiltration of macrophages into adipose tissue and their interaction with adipocytes are essential for the chronic low-grade inflammation of obese adipose tissue. In this study, we identified the serum amyloid A3 (Saa3) gene as a key adipocyte-derived factor that is affected by interaction with macrophages. We showed that the Saa3 promoter in adipocytes actually responds to activated macrophages in a co-culture system. Decreasing C/EBPβ abundance in 3T3-L1 adipocytes or point mutation of C/  ...[more]

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