Paper Information

Journal:   INTERNATIONAL JOURNAL OF MOLECULAR AND CELLULAR MEDICINE   SPRING 2016 , Volume 5 , Number 2; Page(s) 106 To 113.
 
Paper: 

EXPRESSION OF HCA2 RECEPTORS IN FEMORAL EPIPHYSIS AND METAPHYSIS OF RATS WITH DEXAMETHASONE-INDUCED OSTEOPOROSIS

 
 
Author(s):  SHOMALI TAHOORA*, KAMALPOUR MOHAMMAD, FAZELI MEHDI, RAFATI ALIREZA
 
* DIVISION OF PHARMACOLOGY AND TOXICOLOGY, DEPARTMENT OF BASIC SCIENCES, SCHOOL OF VETERINARY MEDICINE, SHIRAZ UNIVERSITY, SHIRAZ, IRAN
 
Abstract: 

The present study describes the changes in expression of hydroxy- carboxylic acid receptor 2 (HCA2 receptor) in femoral epiphysis and metaphysis of rats with glucocorticoid-induced osteoporosis (GIO).16 growing male Sprauge dawley rats were randomly divided into two equal groups consisting of normal control and rats that were rendered osteoporotic by receiving 0.1 mg/kg/day dexamethasone subcutaneously. After 4 weeks, all rats were sacrificed and immediately right and left femoral bones were removed for RT-qPCR and histological examination, respectively. Immunohistochemical parameters using a primary rabbit polyclonal GPR109A antibody in hematoxylin and eosin- counter stained slides were determined. HCA2 receptor expression was evaluated using RT- qPCR. Qualitative and histomorphometric evaluation of slides revealed the establishment of glucocorticoid- induced osteoporosis (GIO) in rats treated with dexamethasone. In immunohistochemical study, dexamethasone administration appreciably reduced receptor density in all evaluated cell types and in total slides as compared to control. mRNA level of HCA2 receptor gene was reduced in dexamethasone- treated group. GIO may be associated with down regulation of HCA2 receptors in proximal femoral bone of rats at mRNA as well as protein level in no- cell type-specific manner, although reduction in protein expression needs to be further confirmed by western blotting.

 
Keyword(s): GLUCOCORTICOID-INDUCED OSTEOPOROSIS, HYDROXYL-CARBOXYLIC ACID RECEPTOR 2, RT-QPCR, IMMUNOHISTOCHEMISTRY, RAT
 
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