Utilize este identificador para referenciar este registo: http://hdl.handle.net/10400.22/1789
Título: Modulation of osteoclastogenesis by antihypertensive drugs
Autor: Oliveira, Teresa
Costa-Rodrigues, João
Ferraz, Ricardo
Prudêncio, Cristina
Fernandes, Maria Helena
Data: 2013
Editora: Bioscientifica
Relatório da Série N.º: Bone Abstracts; Vol. 1
Resumo: Despite its rigid structure, bone is a dynamic tissue that is in constant remodeling. This process requires the action of the bone-resorbing osteoclasts and the bone-synthesing osteoblasts. One of the adverse effects attributed to some antihypertensive agents is the ability to alter normal bone metabolism. However, their effective actions on human bone cells remain to be clarified. In this work, the effects of five calcium channel blockers, a class of antihypertensive drugs (AHDs), were investigated on osteoclastic differentiation. Osteoclastic cell cultures were established from precursor cells isolated from human peripheral blood, and were maintained in the absence (control) or in the presence of 10-8-10-4 M of different AHDs (amlodipine, felodipine, diltiazem, lercanidipine and nifedipine). Cell cultures were characterized throughout a 21 day period for tartrate-resistant acid phosphatase (TRAP) activity, number of TRAP+ multinucleated cells, presence of cells with actin rings and expressing vitronectin and calcitonin receptors, and apoptosis rate. Also, the involvement of several signaling pathways on the cellular response was addressed. It was observed that the tested AHDs had the ability to differentially affect osteoclastogenesis. At low doses, amlodipine and felodipine caused an increase on osteoclastic differentiation, while the other drugs inhibited it. At higher doses, all the molecules caused a decrease on the process. The tested AHDs also showed different effects on the analysed signaling pathways. In conclusion, AHDs appeared to have a direct effect on human osteoclast precursor cells, affecting their differentiation. Interestingly, some of them increased while others inhibited the process. Unraveling the mechanisms beneath these observations might help to explain the adverse effects on bone tissue described for this drug class.
URI: http://hdl.handle.net/10400.22/1789
ISSN: 2052-1219
Versão do Editor: http://www.bone-abstracts.org/ba/0001/ba0001pp221.htm
Aparece nas colecções:ESTSP - CQB - Posters apresentados em eventos científicos

Ficheiros deste registo:
Ficheiro Descrição TamanhoFormato 
POS_TeresaOliveira_2013.pdf9,72 kBAdobe PDFVer/Abrir


FacebookTwitterDeliciousLinkedInDiggGoogle BookmarksMySpace
Formato BibTex MendeleyEndnote Degois 

Todos os registos no repositório estão protegidos por leis de copyright, com todos os direitos reservados.