title: Proteomic profiles in hyperandrogenic syndromes.
abstract: BACKGROUND
  Polycystic ovary syndrome (PCOS) and congenital adrenal hyperplasia (CAH) represent the most common causes of hyperandrogenism. Although the etiopathogeneses of these syndromes are different, they share many clinical and biochemical signs, such as hirsutism, acne, and chronic anovulation. Experimental data have shown that peripheral T-lymphocytes function as molecular sensors, being able to record molecular signals either at staminal and mature cell levels, or hormones at systemic levels.
  
  
  METHODS
  Twenty PCOS women and 10 CAH with 21-hydroxylase deficiency, aged between 18-35 yr, were studied. T-cells purified from all patients and 20 healthy donors have been analyzed by 2-dimensional gel electrophoresis. Silver-stained proteomic map of each patient was compared with a control map obtained by pooling protein samples of the 20 healthy subjects.
  
  
  RESULTS
  Spots of interest were identified by peptide mass fingerprint. Computer analysis evidenced several peptidic spots significantly modulated in all patients examined. Some proteins were modulated in both syndromes, others only in PCOS or in CAH. These proteins are involved in many physiological processes as the functional state of immune system, the regulation of the cytoskeleton structure, the oxidative stress, the coagulation process, and the insulin resistance.
  
  
  CONCLUSIONS
  Identification of the physiological function of these proteins could help to understand ethiopathogenetic mechanisms of hyperandrogenic syndromes and its complications.
authors.affiliation: II Faculty of Medicine, Sapienza University of Rome, Rome, Italy. silvia.misiti@uniroma1.it
authors.forename: S
authors.initials: S
authors.lastname: Misiti
authors.forename: A
authors.initials: A
authors.lastname: Stigliano
authors.forename: M
authors.initials: M
authors.lastname: Borro
authors.forename: G
authors.initials: G
authors.lastname: Gentile
authors.forename: S
authors.initials: S
authors.lastname: Michienzi
authors.forename: L
authors.initials: L
authors.lastname: Cerquetti
authors.forename: B
authors.initials: B
authors.lastname: Bucci
authors.forename: N
authors.initials: N
authors.lastname: Argese
authors.forename: E
authors.initials: E
authors.lastname: Brunetti
authors.forename: M
authors.initials: M
authors.lastname: Simmaco
authors.forename: V
authors.initials: V
authors.lastname: Toscano
mesh_terms: D000293:Adolescent; D000312:Adrenal Hyperplasia, Congenital / Q000097:blood*; D000328:Adult; D000735:Androstenedione / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D015180:Electrophoresis, Gel, Two-Dimensional; D004958:Estradiol / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006908:Hydroxyprogesterones / Q000097:blood; D017588:Hyperandrogenism / Q000097:blood*; D007986:Luteinizing Hormone / Q000097:blood; D013058:Mass Spectrometry; D011085:Polycystic Ovary Syndrome / Q000097:blood*; D011388:Prolactin / Q000097:blood; D040901:Proteomics / Q000379:methods*; D012738:Sex Hormone-Binding Globulin / Q000378:metabolism; D013739:Testosterone / Q000097:blood; D055815:Young Adult
chemical_list: D006908:Hydroxyprogesterones; D012738:Sex Hormone-Binding Globulin; D013739:Testosterone; D000735:Androstenedione; D004958:Estradiol; D019314:Dehydroepiandrosterone Sulfate; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D006854:Hydrocortisone