PMID- 7962270
OWN - NLM
STAT- MEDLINE
DCOM- 19941129
LR  - 20071114
IS  - 0021-972X (Print)
IS  - 0021-972X (Linking)
VI  - 79
IP  - 4
DP  - 1994 Oct
TI  - Expression of adhesion molecules in human endometrial vasculature throughout the 
      menstrual cycle.
PG  - 1024-32
AB  - In the present study, we examined the pattern of expression of human leukocyte 
      antigen (HLA)-DR as well as several adhesion molecules implicated in leukocyte 
      trafficking, including ICAM-1, E-selectin, and VCAM-1 in human endometrium. All 
      of the vessels in endometrium exhibited HLA-DR and ICAM-1 throughout the 
      menstrual cycle. In the proliferative phase, endothelial cells in the 
      functionalis were weak to nonreactive for VCAM-1 and were E-selectin negative 
      (E-selectin-). Endothelial cells of the vessels in the basalis and within 
      myometrium were VCAM positive (VCAM-1+)/E-selectin-. In sharp contrast, in the 
      secretory phase, endothelial cells in the basalis were VCAM-1+/E-selectin+. 
      Surprisingly, endometrial glands, primarily those in the basalis, expressed 
      E-selectin and VCAM-1 during the entire menstrual cycle. Stromal cells were 
      ICAM-1+ and were focally HLA-DR+ around HLA-DR+ lymphoid cells during the entire 
      menstrual cycle and were E-selectin-/VCAM-1- during the proliferative phase. 
      Immunoreactivity for VCAM-1 and E-selectin, however, appeared in the stromal 
      cells in the upper functionalis in the secretory phase. Immunoreactivity for 
      VCAM-1 was the distinguishing feature that separated the lymphoid cells in the 
      aggregates from other nonaggregated lymphoid cells. Recruitment of leukocytes to 
      tissues is in part due to cytokine-regulated expression of specific molecules on 
      endothelial cells. Therefore, we tested the effects of cytokines on the 
      expression of these molecules in endothelial cells derived from microvasculature. 
      ICAM-1 and VCAM-1 were inducible in a dose-dependent fashion in the endothelial 
      cells by interleukin-1 alpha (IL-1 alpha), interferon-gamma (IFN gamma), and 
      tumor necrosis factor-alpha (TNF alpha). Expression of HLA-DR in endothelial 
      cells was inducible by IL-1 alpha and IFN gamma and not by TNF alpha. Expression 
      of E-selectin on endothelial cells was induced only by IL-1 alpha, not by IFN 
      gamma or TNF alpha. Cytokine treatment of endothelial cells significantly 
      enhanced the binding of leukocytes to endothelial cells. The data show a 
      heterogeneity in the vasculature of endometrium with respect to the expression of 
      various adhesion molecules. This heterogeneity is potentially related to the type 
      or amount of cytokine with which endothelial cells are activated. In addition, 
      unique cell- and site-specific expression of adhesion molecules in human 
      endometrium throughout the menstrual cycle may account for the distinct 
      distribution pattern of leukocytes in this tissue.
FAU - Tabibzadeh, S
AU  - Tabibzadeh S
AD  - Department of Pathology, University of South Florida Health Sciences Center, 
      Tampa 33612.
FAU - Kong, Q F
AU  - Kong QF
FAU - Babaknia, A
AU  - Babaknia A
LA  - eng
GR  - CA-46866/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Cytokines)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adult
MH  - Blood Vessels/metabolism
MH  - Cell Adhesion Molecules/*metabolism
MH  - Cells, Cultured
MH  - Cytokines/pharmacology
MH  - Endometrium/*blood supply/cytology/metabolism
MH  - Endothelium, Vascular/cytology/metabolism
MH  - Female
MH  - HLA-DR Antigens/metabolism
MH  - Humans
MH  - Leukocytes/drug effects/metabolism
MH  - Menstrual Cycle/*physiology
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1994/10/01 00:00
MHDA- 1994/10/01 00:01
CRDT- 1994/10/01 00:00
PHST- 1994/10/01 00:00 [pubmed]
PHST- 1994/10/01 00:01 [medline]
PHST- 1994/10/01 00:00 [entrez]
AID - 10.1210/jcem.79.4.7962270 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 1994 Oct;79(4):1024-32. doi: 10.1210/jcem.79.4.7962270.