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		01/07/2009
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TSH induces co-localization of TSH receptor and Na/K-ATPase in human erythrocytes.

		

			

				Journal 
			

			

			
				
Cell biochemistry and function

				
Cell Biochem. Funct.

				

					Internet
					ISSN: 1099-0844
					Volume: 27
				

					
			

			

				Affiliations
			
			
				

										EU.IT.IT-52.Pisa
										Institute of Clinical Physiology CNR Pisa Italy. balzan@ifc.cnr.it
										

			

				authors
			
			
				

										N/A
										Balzan Silvana
										

				

										N/A
										Del Carratore Renata
										

				

										N/A
										Nicolini Giuseppina
										

				

										N/A
										Forini Francesca
										

				

										N/A
										Lubrano Valter
										

				

										N/A
										Simili Marcella
										

				

										N/A
										Benedetti Pier Alberto
										

				

										N/A
										Iervasi Giorgio
										

			

				Abstract
			
			
				

										Thyroid stimulating hormone (TSH) binds to a specific TSH receptor (TSHR) which activates adenylate cyclase and increases cAMP levels in thyroidal cells. Recent studies have reported the presence of TSH receptor in several extra-thyroidal cell types, including erythrocytes. We have previously suggested that TSH is able to influence the erythrocyte Na/K-ATPase ouabain binding properties through a receptor mediated mechanism. The direct interaction of TSH receptor with the Na/K-pump and a functional role of TSHR in erythrocytes was not demonstrated. The interaction of TSH receptor with Na/K-pump and a TSHR functional role are not yet demonstrated in erythrocytes. In this study, we examined the interaction between the two receptors after TSH treatment using immunofluorescence coupled to confocal microscopy and a co-immunoprecipitation technique. The cAMP dependent signalling after TSH treatment was measured to verify TSHR functionality. We found that TSH receptor and Na/K-ATPase are localized on the membranes of both erythrocytes and erythrocyte ghosts; TSH receptor responds to TSH treatment by increasing intracellular cAMP levels from two to tenfold. In ghost membranes TSH treatment enhances up to three fold co-localization of TSHR with Na/K-ATPase and co-immunoprecipitation confirms their direct physical interaction. In conclusion our results are compatible with the existence, in erythrocytes, of a functional TSHR that interacts with Na/K-ATPase after TSH treatment, thus suggesting a novel cell signalling pathway, potentially active in local circulatory control.
										
										

		

	

			


    	    

	
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