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Effect of stress on the expression of Nerve Growth Factor (NGF) and its receptor Trk‐A in an animal model of endometriosis
Author(s) -
Cruz Myrella L,
RodriguezRapale Victor A,
Altieri Joanne S,
Ramirez Antonio E,
Isidro Angel A,
Flores Idhaliz,
Appleyard Caroline B
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.849.2
The contribution of stress to the symptoms and progression of endometriosis, a chronic disease characterized by pain, peritoneal inflammation, adhesions and cysts, is unclear. There is evidence that new nerve growth around endometriotic lesions might help the abnormally located tissue to survive. Aim Examine the effect of stress on the expression of Nerve Growth Factor (NGF) and its receptor Trk‐A in an animal model of endometriosis. Methods Endometriosis was surgically induced in female Sprague‐Dawley rats by transplanting uterine horn tissue next to the intestinal mesentery (endo). One group of rats was also exposed to swim stress for 10 days (endo‐stress). Uterus and colon tissue were collected from all animals (endo, endo‐stress and an untreated normal group). For immunohistochemical analysis, tissues were incubated overnight with antibodies against NGF and Trk‐A, and scored blindly by 3 observers. Results In colon there was > 3‐fold increase of NGF and Trk‐A in muscle and mucosa in both the endo and endo‐stress groups vs normal (p<0.01 in muscle; n=6–8). A similar pattern was observed in uterus, with stress further increasing expression of both NGF and Trk‐A. This reached significance in the stroma (p<0.01). Conclusions NGF and its receptor appear to play an important role in the development of endometriosis, perhaps contributing to the impact of stress in this condition. 1F31GM082281 & R01HD05055.