title: C-reactive protein inhibits high-molecular-weight adiponectin expression in 3T3-L1 adipocytes via PI3K/Akt pathway.
abstract: Adiponectin, an adipose-specific protein hormone, is secreted from white adipose tissue and involved in glucose and lipid metabolism. It is assembled into low-molecular-weight trimer (LMW), middle-molecular-weight hexameric (MMW) and high-molecular-weight (HMW), among which HMW exhibits higher activity. In this study, we proved that C-reactive protein (CRP), an inflammatory marker, inhibited adiponectin expression, especially HMW in time-and dose-dependent manners. Furthermore, CRP decreased the HMW/total adiponectin ration and reduced adiponectin assembly by increasing ERp44, and decreasing Ero1-α and DsbA-L. CRP activated pAkt, the downstream of PI3K. Inhibition of PI3K or pAkt abolished the effect of CRP. Our study suggested that CRP decreased adiponectin expression and multimerization, while CRP-induced decline in adiponectin might be mediated through the PI3K/Akt pathway.
authors.affiliation: Department of Endocrinology, The Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China.
authors.forename: Yuanxin
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Public Laboratory Platform, First Affiliated Hospital of Najing Medical University, Nanjing 210029, China.
authors.forename: Cuiping
authors.initials: C
authors.lastname: Liu
authors.affiliation: Public Laboratory Platform, First Affiliated Hospital of Najing Medical University, Nanjing 210029, China.
authors.forename: Chao
authors.initials: C
authors.lastname: Jiang
authors.affiliation: Department of Endocrinology, The Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China.
authors.forename: Su
authors.initials: S
authors.lastname: Wang
authors.affiliation: Department of Endocrinology, The Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China.
authors.forename: Qichao
authors.initials: Q
authors.lastname: Yang
authors.affiliation: Department of Endocrinology, The Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China.
authors.forename: Dan
authors.initials: D
authors.lastname: Jiang
authors.affiliation: Department of Endocrinology, The Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China. Electronic address: yuanguoyue@hotmail.com.
authors.forename: Guoyue
authors.initials: G
authors.lastname: Yuan
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism*; D052242:Adiponectin / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D002097:C-Reactive Protein / Q000378:metabolism* / Q000494:pharmacology; D015870:Gene Expression; D018836:Inflammation Mediators / Q000378:metabolism; D051379:Mice; D008970:Molecular Weight; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D055503:Protein Multimerization; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D052242:Adiponectin; C499919:Adipoq protein, mouse; D018836:Inflammation Mediators; D002097:C-Reactive Protein; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt