Document Detail

Endometriosis as a neurovascular condition: estrous variations in innervation, vascularization, and growth factor content of ectopic endometrial cysts in the rat.
MedLine Citation:
PMID:  17942489     Owner:  NLM     Status:  MEDLINE    
Endometriosis is a poorly understood, estradiol-dependent condition associated with severe pelvic pains and defined by vascularized endometrial growths outside the uterus. Endometriosis is produced in cycling rats by autotransplanting pieces of uterus onto abdominal arteries where they develop into cysts. The surgery induces vaginal and abdominal muscle hyperalgesia, whose severity is greatest in proestrus and nearly absent in estrus. The cysts contain growth factors and cytokines and develop their own sympathetic and sensory C- and Adelta-fiber innervation. Here, we used quantitative immunostaining and protein array analyses to test the hypothesis that the innervation and growth factor/cytokine content of the cysts, but not uterine horn, contribute to proestrous-to-estrous changes in hyperalgesic severity. If so, these characteristics in the cysts, but not the uterine horn, should change with estrous stage. In cysts, the density of sympathetic (but not sensory) neurites and amounts of NGF and VEGF proteins (but not cytokines IL-1, IL-6, IL-10, or TNF-alpha) were greater in proestrus than estrus. These changes were accompanied by vascular changes. Both sympathetic and sensory fibers in both stages colabeled with TrkA, indicating that changes in NGF could act on both afferent and efferent fibers. In contrast with the cysts, no changes occurred in the uterine horn between proestrus and estrus. Together, these results suggest that coordinated proestrous-to-estrous changes in innervation and vascularization of the cysts contribute to similar changes in hyperalgesic severity. The findings also encourage consideration of endometriosis as a neurovascular condition.
Guohua Zhang; Natalia Dmitrieva; Yan Liu; Kristina A McGinty; Karen J Berkley
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural     Date:  2007-10-17
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  294     ISSN:  0363-6119     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2008 Jan 
Date Detail:
Created Date:  2008-01-10     Completed Date:  2008-02-26     Revised Date:  2013-06-06    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R162-71     Citation Subset:  IM    
Program in Neuroscience, Florida State University, Tallahassee, FL 32306-1270, USA.
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MeSH Terms
Adrenergic Fibers / pathology
Cysts / blood supply*,  metabolism*,  pathology
Cytokines / metabolism
Disease Models, Animal
Endometriosis / complications,  metabolism*,  pathology
Endometrium / blood supply,  innervation*,  metabolism
Estrous Cycle / physiology*
Hyperalgesia / etiology,  metabolism
Nerve Growth Factor / metabolism*
Proestrus / physiology
Rats, Sprague-Dawley
Receptor, Nerve Growth Factor / metabolism
Receptor, trkA / metabolism
Signal Transduction / physiology
Vascular Endothelial Growth Factor A / metabolism
Grant Support
R01 NS011892-26/NS/NINDS NIH HHS; R01 NS011892-27/NS/NINDS NIH HHS; R01 NS011892-28/NS/NINDS NIH HHS; R01 NS11982/NS/NINDS NIH HHS
Reg. No./Substance:
0/Cytokines; 0/Receptor, Nerve Growth Factor; 0/Vascular Endothelial Growth Factor A; 9061-61-4/Nerve Growth Factor; EC, trkA

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

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