title: Vitamin D rescues dysfunction of fetal endothelial colony forming cells from individuals with gestational diabetes.
abstract: BACKGROUND
  Gestational diabetes (GDM) is associated with long-term cardiovascular and metabolic diseases in offspring. However, the mechanisms are not well understood. We explored whether fetal exposure to a diabetic environment is associated with fetal endothelial progenitor cell dysfunction, and whether vitamin D can reverse the impairment.
  
  
  METHODS
  Nineteen women with uncomplicated pregnancies and 18 women with GDM were recruited before delivery. Time to first appearance of endothelial colony forming cell (ECFC) colonies and number of ECFC colonies formed from culture of cord peripheral blood mononuclear cells were determined. Angiogenesis-related functions of ECFCs in vitro were tested in the presence or absence of vitamin D.
  
  
  RESULTS
  Fetal ECFCs from GDM pregnancies formed fewer colonies in culture (P = 0.04) and displayed reduced proliferation (P = 0.02), migration (P = 0.04) and tubule formation (P = 0.03) compared to uncomplicated pregnancies. Fetal ECFCs exposed to hyperglycemia in vitro exhibited less migration (P < 0.05) and less tubule formation (P < 0.05) than normoglycemic control. Vitamin D significantly improved the dysfunction of fetal ECFCs from pregnancies complicated by GDM or after exposure of healthy ECFCs to hyperglycemia.
  
  
  CONCLUSIONS
  Fetal ECFCs from GDM pregnancies or ECFCs exposed to hyperglycemia in vitro exhibit reduced quantity and impaired angiogenesis-related functions. Vitamin D significantly rescues these functions. These findings may have implications for vascular function of infants exposed to a diabetic intrauterine environment.
authors: Department of Obstetrics and Gynecology, Hannover Medical School, Hannover, Germany; Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China. Electronic address: 514325204@qq.com.
authors: J
authors: J
authors: Gui
authors: Department of Obstetrics and Gynecology, Hannover Medical School, Hannover, Germany. Electronic address: Rohrbach.anne@mh-hannover.de.
authors: A
authors: A
authors: Rohrbach
authors: Department of Obstetrics and Gynecology, Hannover Medical School, Hannover, Germany. Electronic address: Borns.katja@mh-hannover.de.
authors: K
authors: K
authors: Borns
authors: Department of Obstetrics and Gynecology, Hannover Medical School, Hannover, Germany. Electronic address: hillemanns.peter@mh-hannover.de.
authors: P
authors: P
authors: Hillemanns
authors: Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China. Electronic address: fltj007@163.com.
authors: L
authors: L
authors: Feng
authors: Magee-Womens Research Institute and Department of Obstetrics, Gynecology & Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA, USA. Electronic address: chubel@mwri.magee.edu.
authors: C A
authors: CA
authors: Hubel
authors: Department of Obstetrics and Gynecology, Hannover Medical School, Hannover, Germany. Electronic address: vonversen-hoeynck.frauke@mh-hannover.de.
authors: F
authors: F
authors: von Versen-Höynck
mesh_terms: D000328:Adult; D002117:Calcitriol / Q000378:metabolism*; D002465:Cell Movement; D049109:Cell Proliferation; D002478:Cells, Cultured; D003114:Colony-Forming Units Assay; D016640:Diabetes, Gestational / Q000276:immunology / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000209:etiology* / Q000517:prevention & control; D019587:Dietary Supplements; D004730:Endothelium, Vascular / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005312:Fetal Blood; D053686:Fetal Stem Cells / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000209:etiology* / Q000517:prevention & control; D011247:Pregnancy; D034622:RNA Interference; D018167:Receptors, Calcitriol / Q000819:agonists / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D012189:Retrospective Studies; D056647:Systemic Vasculitis / Q000209:etiology* / Q000517:prevention & control; D014807:Vitamin D / Q000378:metabolism / Q000627:therapeutic use
chemical_list: D018167:Receptors, Calcitriol; C579457:VDR protein, human; D014807:Vitamin D; D002117:Calcitriol
keywords: Angiogenesis; Endothelial progenitor cells; Gestational diabetes mellitus; Migration