RGD Reference Report - beta1, beta2, and beta3 adrenoceptors and Na+/H+ exchanger regulatory factor 1 expression in human bronchi and their modifications in cystic fibrosis. - Rat Genome Database

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beta1, beta2, and beta3 adrenoceptors and Na+/H+ exchanger regulatory factor 1 expression in human bronchi and their modifications in cystic fibrosis.

Authors: Bossard, F  Silantieff, E  Lavazais-Blancou, E  Robay, A  Sagan, C  Rozec, B  Gauthier, C 
Citation: Bossard F, etal., Am J Respir Cell Mol Biol. 2011 Jan;44(1):91-8. Epub 2010 Mar 4.
RGD ID: 5129107
Pubmed: PMID:20203292   (View Abstract at PubMed)
DOI: DOI:10.1165/rcmb.2009-0372OC   (Journal Full-text)

To date, three beta-adrenoceptor (beta-AR) subtypes have been identified, but only beta(1)-ARs and beta(2)-ARs have been characterized in human lungs. Moreover, beta(2)-ARs physically interact with the cystic fibrosis transmembrane conductance regulator (CFTR) through the Na(+)/H(+) Exchanger Regulatory Factor 1 (NHERF1) protein. beta(3)-ARs, which stimulate CFTR activity in transfected cells, have not been identified in human lungs. This study aimed (1) to characterize the presence of beta-AR subtypes, especially beta(3)-AR, in human bronchi, and (2) to compare their expression as well as that of NHERF1 in non-cystic fibrosis (CF) versus advanced CF lung samples. In human non-CF bronchi, beta(1)-AR, beta(2)-AR, beta(3)-AR, and NHERF1 transcripts and proteins were expressed mainly in bronchial epithelial cells. Those results were strengthened by the native expression of beta(1)-AR, beta(2)-AR, and beta(3)-AR in a human epithelial cell line, 16HBE14o(-). All beta-AR subtypes stimulated CFTR activity. In CF bronchi, we demonstrated beta(1)-AR and beta(3)-AR overexpression, and NHERF1 and beta(2)-AR underexpression. The origin of this protein remodeling (involving the physical or functional absence of CFTR, infection, inflammation, or high adrenergic tone) deserves further investigation. These results evidence for the first time, to the best of our knowledge, the presence of beta(3)-ARs in human bronchi, and suggest their usefulness as a putative new pharmacologic target in lung diseases where fluid homeostasis is altered. Furthermore, NHERF1 may be a new therapeutic target in patients with CF, to facilitate the trafficking of mutated CFTR to plasma membrane.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
ADRB1Humancystic fibrosis  IEP  RGD 
ADRB2Humancystic fibrosis  IEP  RGD 
ADRB3Humancystic fibrosis  IEP protein:increased expression:bronchusRGD 
Adrb1Ratcystic fibrosis  ISOADRB1 (Homo sapiens) RGD 
Adrb1Mousecystic fibrosis  ISOADRB1 (Homo sapiens) RGD 
Adrb2Ratcystic fibrosis  ISOADRB2 (Homo sapiens) RGD 
Adrb2Mousecystic fibrosis  ISOADRB2 (Homo sapiens) RGD 
Adrb3Ratcystic fibrosis  ISOADRB3 (Homo sapiens)protein:increased expression:bronchusRGD 
Adrb3Mousecystic fibrosis  ISOADRB3 (Homo sapiens)protein:increased expression:bronchusRGD 

Objects Annotated

Genes (Rattus norvegicus)
Adrb1  (adrenoceptor beta 1)
Adrb2  (adrenoceptor beta 2)
Adrb3  (adrenoceptor beta 3)

Genes (Mus musculus)
Adrb1  (adrenergic receptor, beta 1)
Adrb2  (adrenergic receptor, beta 2)
Adrb3  (adrenergic receptor, beta 3)

Genes (Homo sapiens)
ADRB1  (adrenoceptor beta 1)
ADRB2  (adrenoceptor beta 2)
ADRB3  (adrenoceptor beta 3)


Additional Information