Bruna Eibel1, Melissa Kristochek1, Thiago R Peres1, Lucinara D Dias1, Daniela R Dartora1,2, Karina R Casali3, Renato A K Kalil1,4, Alexandre M Lehnen1,5, Maria Claudia Irigoyen1,6, Melissa M Markoski1,4. 1. Instituto de Cardiologia do Rio Grande do Sul/Fundação Universitária de Cardiologia (IC/FUC), Porto Alegre, Brazil. 2. Sainte-Justine University Hospital Research Center, University of Montreal, Montreal, Canada. 3. Universidade Federal de São Paulo (UNIFESP), São Paulo, Brazil. 4. Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Porto Alegre, Brazil. 5. Faculdade Sogipa de Educação Física (SOGIPA), Porto Alegre, Brazil. 6. Universidade de São Paulo (USP), Porto Alegre, Brazil.
Abstract
AIM: To examine the interference of β-blockers with the chemokine stromal cell-derived factor-1 (SDF-1) found in cell homing receptors, C-X-C chemokine receptor type 4 (CXCR-4) and CXCR-7, and regulatory proteins of homing pathways, we administered atenolol, carvedilol, metoprolol, and propranolol for 30 days using an orogastric tube to hypertensive rats. METHOD: We collected blood samples before and after treatment and quantified the levels of SDF-1 with enzyme-linked immunosorbent assay (ELISA). On day 30 of treatment, the spontaneously hypertensive rats (SHR) were euthanized, and heart, liver, lung, and kidney tissues were biopsied. Proteins were isolated for determining the expression of CXCR-4, CXCR-7, GRK-2 (G protein-coupled receptors kinase 2), β-arrestins (β1-AR and β2-AR), and nuclear factor kappa B (NFκB). RESULTS: We found that the study drugs modulated these proteins, and metoprolol and propranolol strongly affected the expression of β1-AR (P = .0102) and β2-AR (P = .0034). CONCLUSION: β-blockers modulated tissue expression of the proteins and their interactions following 30 days of treatment. It evidences that this class of drugs can interfere with proteins of cell homing pathways.
AIM: To examine the interference of β-blockers with the chemokine stromal cell-derived factor-1 (SDF-1) found in cell homing receptors, C-X-C chemokine receptor type 4 (CXCR-4) and CXCR-7, and regulatory proteins of homing pathways, we administered atenolol, carvedilol, metoprolol, and propranolol for 30 days using an orogastric tube to hypertensiverats. METHOD: We collected blood samples before and after treatment and quantified the levels of SDF-1 with enzyme-linked immunosorbent assay (ELISA). On day 30 of treatment, the spontaneously hypertensiverats (SHR) were euthanized, and heart, liver, lung, and kidney tissues were biopsied. Proteins were isolated for determining the expression of CXCR-4, CXCR-7, GRK-2 (G protein-coupled receptors kinase 2), β-arrestins (β1-AR and β2-AR), and nuclear factor kappa B (NFκB). RESULTS: We found that the study drugs modulated these proteins, and metoprolol and propranolol strongly affected the expression of β1-AR (P = .0102) and β2-AR (P = .0034). CONCLUSION: β-blockers modulated tissue expression of the proteins and their interactions following 30 days of treatment. It evidences that this class of drugs can interfere with proteins of cell homing pathways.