Tissue specific localization of angiotensin-(1-7) and its receptor Mas in the uterus of ovariectomized rats.
The vasoactive peptide angiotensin (Ang)-(1-7) has vasodilator, antifibrotic and antihypertrophic properties, but little is known about its regulation in the uterus. The aim of this study was to evaluate Ang-(1-7) and its receptor Mas expression throughout rat uterine tissues, in ovariectomized animals treated with estrogen alone or combined with progestin. Adult Wistar rats (n = 19) were ovariectomized and randomly assigned into three different groups 1 week later. One group received a single dose of estradiol benzoate (1.5 mg/kg, i.m. injection, n = 6). Another group received estradiol associated with depot medroxyprogesterone acetate (3 mg/kg, i.m. injection, n = 6). Control group (n = 7) received oil injection. One week later, the rats were euthanized and their uteri were fixed and stained by immunohistochemistry, using a polyclonal antibody specific to Ang-(1-7) and its receptor Mas. Ang-(1-7) was detected in all uterine tissues, but it was weak or absent in the circular myometrium of treated animals. The intensity of the immunostaining decreased in the glandular epithelium of hormonally treated animals when compared to controls. In estrogen treated rats, Ang-(1-7) labeling was scattered and sometimes included the nuclei of glandular cells. We also detected Ang-(1-7) expression in longitudinal myometrium and uterine serosa. Mas receptor was present in all tissues with similar intensity among the tissue types in the control and estrogen plus progestin groups. In the estrogen group, Mas staining was stronger in the luminal and glandular epithelium when compared with stroma or circular myometrium. In conclusion, ovarian steroids are not required to allow endometrial expression of Ang-(1-7) and its receptor Mas in rats, as it remains abundant in ovariectomized animals. However, estrogen and progestin may modulate the distribution pattern of this peptide in the endometrium, especially in the glandular compartment.
Department of Obstetrics and Gynecology, Hospital das Clínicas, Federal University of Minas Gerais, Av. Alfredo Balena 110 - 9o andar, Belo Horizonte, MG 30130-100, Brazil.
João
J
Vaz-Silva
Rubens L
RL
Tavares
Márcia C
MC
Ferreira
Kinulpe
K
Honorato-Sampaio
Ines K D
IK
Cavallo
Robson A S
RA
Santos
Adelina M
AM
dos Reis
Fernando M
FM
Reis
D000803:Angiotensin I / Q000378:metabolism*; D000818:Animals; D004967:Estrogens / Q000008:administration & dosage / Q000378:metabolism; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D007150:Immunohistochemistry; D017258:Medroxyprogesterone Acetate / Q000008:administration & dosage; D009215:Myometrium / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D010052:Ovariectomy; D010446:Peptide Fragments / Q000378:metabolism*; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism*; D014599:Uterus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism
D004967:Estrogens; D010446:Peptide Fragments; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D043562:Receptors, G-Protein-Coupled; D000803:Angiotensin I; D017258:Medroxyprogesterone Acetate; C118790:angiotensin I (1-7)