Padma Murthi1, Ramona Sarkis2, Ratana Lim3, Caitlyn Nguyen-Ngo3, Anita Pratt4, Stella Liong3, Martha Lappas5. 1. Department of Medicine, School of Clinical Sciences, Monash University, Victoria, Australia; Obstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and Gynaecology, University of Melbourne, Victoria, Australia. 2. Obstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and Gynaecology, University of Melbourne, Victoria, Australia. 3. Obstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and Gynaecology, University of Melbourne, Victoria, Australia; Mercy Perinatal Research Centre, Mercy Hospital for Women, Victoria, Australia. 4. Department of Maternal-Fetal Medicine Pregnancy Research Centre, Royal Women's Hospital and the Department of Obstetrics and Gynaecology, University of Melbourne, Parkville, Victoria, Australia. 5. Obstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and Gynaecology, University of Melbourne, Victoria, Australia; Mercy Perinatal Research Centre, Mercy Hospital for Women, Victoria, Australia. Electronic address: mlappas@unimelb.edu.au.
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.
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 obesewomen 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 obesewomen 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.
Authors: Suveena Ranzil; Stacey Ellery; David W Walker; Cathy Vaillancourt; Nadia Alfaidy; Alexander Bonnin; Anthony Borg; Euan M Wallace; Peter R Ebeling; Jan Jaap Erwich; Padma Murthi Journal: Placenta Date: 2019-05-23 Impact factor: 3.481
Authors: Aleksandra Klisić; Nebojša Kavarić; Vesna Spasojević-Kalimanovska; Jelena Kotur-Stevuljević; Ana Ninić Journal: J Med Biochem Date: 2021-01-26 Impact factor: 3.402
Authors: Lindsey A Sjaarda; Katherine A Ahrens; Daniel L Kuhr; Tiffany L Holland; Ukpebo R Omosigho; Brian T Steffen; Natalie L Weir; Hannah K Tollman; Robert M Silver; Michael Y Tsai; Enrique F Schisterman Journal: PLoS One Date: 2018-05-11 Impact factor: 3.240