Endocan expression is increased in the placenta from obese women with gestational diabetes mellitus. (December 2016)

• Record Type: Journal Article
• Authors: Murthi, Padma; Sarkis, Ramona; Lim, Ratana; Nguyen-Ngo, Caitlyn; Pratt, Anita; Liong, Stella; Lappas, Martha
• Is Part Of: Placenta. Volume 48(2016:Dec.)
• Page Start: 38
• Page End: 48
• Publication Date: 2016-12
• Subjects: Endocan -- Placenta -- GDM -- Inflammation; Placenta -- Periodicals; Reproduction -- Periodicals; Placenta -- Periodicals; Placenta -- Périodiques; Reproduction -- Périodiques; 612.63
• DOI: 10.1016/j.placenta.2016.10.003
• Languages: English
• ISSNs: 0143-4004

Abstract

Abstract: Introduction: Endocan, a member of the proteoglycan family, is involved in a wide range of diseases including obesity and diabetes. The aim of this study was to determine the effect of (i) maternal obesity and gestational diabetes mellitus (GDM) on placental endocan expression; and (ii) endocan knockdown on markers of inflammation. Methods: Endocan mRNA and protein expression was determined in human placenta from (i) lean and obese and normal glucose tolerant (NGT) pregnant women (n = 10 patients per group); and (ii) women with GDM and BMI-matched NGT women (n = 40 patients per group). Primary villous trophoblast cells and HUVECs were used to assess the effect of endocan siRNA knockdown on pro-inflammatory cytokines. Results: There was no effect of maternal obesity on placental endocan expression. Further, endocan expression was not different between lean NGT and BMI-matched women with GDM. However, endocan mRNA and protein expression was significantly higher in placenta from obese women with GDM when compared to BMI-matched NGT women. Knockdown of endocan in villous trophoblast cells and HUVECs had no effect on infection- or inflammation-induced expression and secretion of IL-6, IL-8 and MCP-1. Discussion: Endocan expression is increased in the human placenta from obese women with GDM, and in response to pro-inflammatory stimuli. Loss-of-function studies in villous trophoblast cells and HUVECs revealed that endocan is not directly involved in the genesis or in the expression of pro-inflammatory cytokines induced by LPS or IL-1β. Further studies are required to elucidate the functional consequences of increased placental endocan expression in obese GDM pregnancies. Highlights: The proteoglycan endocan is increased in human placenta from obese women with gestational diabetes. LPS and IL-1β increase endocan expression in human primary trophoblast cells and HUVECs. Knockdown of endocan does not regulate pro-inflammatory cytokines from trophoblast cells. Knockdown of endocan does not regulate pro-inflammatory cytokines from HUVECs.