title: Circulating vascular progenitor cells and central arterial stiffness in polycystic ovary syndrome.
abstract: OBJECTIVE
  Subjects with Polycystic ovarian syndrome (PCOS) are at increased risk of Type 2 diabetes mellitus (T2DM). The mechanism of this enhanced risk is unclear. Circulating vascular progenitor cells (VPC) are immature bone marrow derived cells capable of differentiating into mature endothelial cells. VPC number/function and central arterial stiffness predict cardio-metabolic disease in at-risk populations.
  
  
  METHODS
  We studied VPC and arterial stiffness measures in non-obese PCOS subjects as compared to age and body mass index (BMI) matched healthy controls in a cross-sectional study.
  
  
  METHODS
  Fourteen subjects with PCOS and 12 controls of similar age, BMI (all <30 kg/m(2)) and metabolic profile were studied. VPC number and in vitro function were studied by flow cytometry and tube formation assays respectively. Augmentation index (AIx), a measure of central arterial stiffness, and central (aortic) blood pressures (BP) were measured by applanation tonometry.
  
  
  RESULTS
  Subjects with PCOS had a reduced number, mean±SEM, of circulating CD34(+)133(+) VPCs (317.5±51.0 vs. 558.3±101.2, p = 0.03) and impaired in vitro tube formation (completed tube area 1.0±0.06 vs. 1.2±0.05×10(6) µm(2) p = 0.02). PCOS subjects had significantly higher AIx (18.4±1.9% vs. 4.9±2.0%) and this difference remained significant even after adjustments for age, BMI and smoking (p = 0.003) in multivariate analyses. Central systolic and pulse pressure were higher in PCOS subjects but these differences were not statistically significant after adjustment for age. Brachial systolic and pulse pressures were similar. VPC number/function and arterial stiffness or BP measures were not correlated.
  
  
  CONCLUSIONS
  Non-obese PCOS is characterized by a reduced VPC number, impaired VPC function and increased central arterial stiffness. These changes in novel vascular risk markers may explain the enhanced risk of T2DM and CVD in PCOS.
authors.affiliation: Cardiovascular Division at Guy's and St Thomas and King's College Hospitals, King's College London, London, United Kingdom. cecile.dessapt@kcl.ac.uk
authors.forename: Cecile
authors.initials: C
authors.lastname: Dessapt-Baradez
authors.forename: Maria
authors.initials: M
authors.lastname: Reza
authors.forename: Ghayathri
authors.initials: G
authors.lastname: Sivakumar
authors.forename: Maria
authors.initials: M
authors.lastname: Hernandez-Fuentes
authors.forename: Kostas
authors.initials: K
authors.lastname: Markakis
authors.forename: Luigi
authors.initials: L
authors.lastname: Gnudi
authors.forename: Janaka
authors.initials: J
authors.lastname: Karalliedde
mesh_terms: D000071916:AC133 Antigen; D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D018952:Antigens, CD34 / Q000378:metabolism; D001158:Arteries / Q000503:physiopathology; D015992:Body Mass Index; D003430:Cross-Sectional Studies; D042783:Endothelial Cells / Q000166:cytology / Q000502:physiology*; D005260:Female; D006023:Glycoproteins / Q000378:metabolism; D006801:Humans; D010455:Peptides / Q000378:metabolism; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000503:physiopathology*; D013234:Stem Cells / Q000166:cytology / Q000502:physiology*; D055815:Young Adult
chemical_list: D000071916:AC133 Antigen; D015703:Antigens, CD; D018952:Antigens, CD34; D006023:Glycoproteins; D010455:Peptides