title: Expression of adhesion, attachment and invasion markers in eutopic and ectopic endometrium: a link to the aetiology of endometriosis.
abstract: BACKGROUND
  Cell properties, such as attachment, adhesion and invasion, are important for the normal function of the endometrium. However, it is believed that the same properties may also be involved in the development of gynaecological diseases, such as endometriosis. Endometrial cells, shed by retrograde menstruation, may have an aberrant expression of molecules involved in these functions, leading to endometriosis. Therefore, the aim of this study was to investigate the expression of proteins involved in adhesion, attachment and invasion in eutopic and ectopic endometrium.
  
  
  METHODS
  Endometrial biopsy specimens were collected from healthy volunteers (controls: proliferative phase, n = 10; secretory phase, n = 15) and from endometriosis patients (proliferative phase: n = 9, secretory phase: n = 10). Biopsy specimens from endometriomas were also collected (proliferative phase: n = 9, secretory phase: n = 10). Expression of apolipoprotein E (ApoE), integrin β-2 (ITGB2), integrin β-7 (ITGB7), Laminin γ-1 (LAMC1), CD24 molecule (CD24) and junctional adhesion molecule-1 (JAM-1) was evaluated with real-time reverse transcriptase polymerase chain reaction and immunohistochemistry.
  
  
  RESULTS
  The endometrium from controls and women with endometriosis expressed ApoE, ITGB2, ITGB7, LAMC1, CD24 and JAM-1. Gene expression of ApoE and JAM-1 was decreased in both proliferative and secretory phase in the endometrium from women with endometriosis compared with control endometrium. Also, mRNA expression of LAMC1 was reduced in the endometrium from endometriosis patients compared with controls in the proliferative phase. An altered gene expression of CD24 was seen between the endometrium from endometriosis patients and endometriomas in the secretory phase. The ITGB2 protein expression was altered in epithelia cells between the endometrium from healthy volunteers and endometriosis patients in the secretory phase.
  
  
  CONCLUSIONS
  We have shown differential expression of adhesion, attachment and invasion proteins in proliferative and secretory endometrium from controls and endometriosis patients and in endometriomas. This study suggests that molecules with these properties may have a role in the anchoring of endometrial cells at ectopic sites, thus initiating the development of endometriosis.
authors: Division of Obstetrics and Gynecology, Department of Women's and Children's Health,  Karolinska Institutet/Karolinska University Hospital, SE-171 76 Stockholm,  Sweden.
authors: J
authors: J
authors: Sundqvist
authors: K L
authors: KL
authors: Andersson
authors: G
authors: G
authors: Scarselli
authors: K
authors: K
authors: Gemzell-Danielsson
authors: P G L
authors: PG
authors: Lalitkumar
mesh_terms: D000328:Adult; D001057:Apolipoproteins E / Q000096:biosynthesis; D001706:Biopsy; D018821:CD18 Antigens / Q000096:biosynthesis; D051927:CD24 Antigen / Q000096:biosynthesis; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D049109:Cell Proliferation; D004715:Endometriosis / Q000473:pathology*; D004717:Endometrium / Q000503:physiopathology*; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D039641:Integrin beta Chains / Q000096:biosynthesis; D007797:Laminin / Q000096:biosynthesis; D008597:Menstrual Cycle; D011956:Receptors, Cell Surface / Q000096:biosynthesis
chemical_list: D001057:Apolipoproteins E; D018821:CD18 Antigens; D051927:CD24 Antigen; D015815:Cell Adhesion Molecules; C407243:F11R protein, human; D039641:Integrin beta Chains; D007797:Laminin; D011956:Receptors, Cell Surface; C091368:integrin beta7; C089141:laminin gamma 1