Document Detail

Neutrophil depletion retards endometrial repair in a mouse model.
MedLine Citation:
PMID:  17186309     Owner:  NLM     Status:  MEDLINE    
The contribution of the high abundance of inflammatory cells present in the human endometrium prior to and during menstruation is unknown with respect to endometrial repair and/or menstruation. In this study, the presence and localisation of markers for key inflammatory cells have been examined in a mouse model of endometrial breakdown and repair and the functional contribution of neutrophils has been determined. In the model, decidualisation is artificially induced and progesterone support withdrawn; the endometrial tissue progressively breaks down by 24 h after progesterone withdrawal and, by 48 h, has usually undergone complete repair. Neutrophils have been identified in low abundance in decidual tissue, rise in number during breakdown and are most abundant during early repair. Macrophages are barely detectable during breakdown or repair in this model, whereas uterine natural killer cells are found only in intact decidua. The functional contribution of neutrophils to endometrial breakdown and repair has been assessed via neutrophil depletion by using the antibody RB6-8C5. This antibody significantly depletes neutrophils from the circulation and tissue, affects endometrial breakdown and markedly delays endometrial repair. This study has therefore demonstrated that neutrophils are the most abundant leucocyte in this model and that they play an important functional role in the processes of endometrial breakdown and repair.
Tu'uhevaha J Kaitu'u-Lino; Naomi B Morison; Lois A Salamonsen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-12-22
Journal Detail:
Title:  Cell and tissue research     Volume:  328     ISSN:  0302-766X     ISO Abbreviation:  Cell Tissue Res.     Publication Date:  2007 Apr 
Date Detail:
Created Date:  2007-04-13     Completed Date:  2007-10-01     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0417625     Medline TA:  Cell Tissue Res     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  197-206     Citation Subset:  IM    
Monash Medical Centre, Prince Henry's Institute of Medical Research, 246 Clayton Road, Clayton, Victoria 3168, Australia.
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MeSH Terms
Endometrium / cytology,  drug effects,  physiology*
Eosinophils / cytology,  drug effects
Killer Cells, Natural / cytology,  drug effects
Macrophages / cytology,  drug effects
Mice, Inbred C57BL
Models, Animal
Neutrophils / cytology*,  drug effects
Progesterone / pharmacology
Wound Healing / drug effects,  physiology*
Reg. No./Substance:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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