Rat ADORA3 (Adenosine A3 Receptor) ELISA Kit

Background Adenosine receptors (ADORs) have been reported to play a role in experimental myopia. This study aimed to determine the distribution of ADORs in human retinal pigment epithelium (RPE) cells cultured in vitro. Methods Human RPE cells (cell line D407) were cultured in vitro. ADOR mRNA in APE was detected by reverse transcription polymerase chain reaction. ADOR protein expression in APE was confirmed by Western blotting analysis of cell lysates. Confocal fluorescence microscopy was used to study the subcellular distribution of ADORs. Results All four subtypes of ADORs mRNA and protein were expressed in human APE. This was confirmed by Western blotting analysis. The ADOR subtypes were differently distributed within the cells. ADORA1 was expressed in nucleus, perinucleus and cytoplasm of RPE. ADORA2A was concentrated mainly in one side of the perinucleus and cytoplasm of RPE. ADORA2B was strongly expressed in the nucleus, perinucleus and the cytoplasm, and ADORA3 was expressed weakly in the cytoplasm of APE. Conclusions ADORs are expressed in human RPE. The different distribution at the subcellular level suggests different functions of ADOR subtypes. Chin Med J 2011;124(8).1139-1144

Small mammals have the ability to enter torpor, a hypothermic, hypometabolic state, allowing impressive energy conservation. Administration of adenosine or adenosine 5'-monophosphate (AMP) can trigger a hypothermic, torpor-like state. We investigated the mechanisms for hypothermia using telemetric monitoring of body temperature in wild type and receptor knock out (Adoral(-/-), Adora3(-/-)) mice. Confirming prior data, stimulation of the A(3) adenosine receptor (AR) induced hypothermia via peripheral mast cell degranulation, histamine release, and activation of central histamine H-1 receptors. In contrast, A(1)AR agonists and AMP both acted centrally to cause hypothermia. Commonly used, selective A1AR agonists, including N-6-cyclopentyladenosine (CPA), N-6-cyclohexyladenosine (CHA), and MRS5474, caused hypothermia via both A(1)AR and A(3)AR when given intraperitoneally. Intracerebroventricular dosing, low peripheral doses of CI-ENBA [(+/-)-5'-chloro-5'-deoxy-N-6-endo-norbornyladenosine], or using Adora3(-/-) mice allowed selective stimulation of A(1)AR. AMP-stimulated hypothermia can occur independently of A(1)AR, A(3)AR, and mast cells. A(1)AR and A(3)AR agonists and AMP cause regulated hypothermia that was characterized by a drop in total energy expenditure, physical inactivity, and preference for cooler environmental temperatures, indicating a reduced body temperature set point. Neither A(1)AR nor A(3)AR was required for fasting-induced torpor. A(1)AR and A(3)AR agonists and AMP trigger regulated hypothermia via three distinct mechanisms. Published by Elsevier Ltd.