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BDNF-mediated migration of cardiac microvascular endothelial cells is impaired during ageing

This study indicates that brain-derived neurotrophic factor (BDNF) can promote young cardiac microvascular endothelial cells (CMECs) to migrate via the activation of the BDNF-TrkB-FL-PI3K/Akt pathway, which may benefit angiogenesis after myocardial infarction (MI). However, the ageing of CMECs led t...

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Detalles Bibliográficos
Autores principales: Cao, Liang, Zhang, Liang, Chen, Siyun, Yuan, Ziqiang, Liu, Shaokun, Shen, Xiaotao, Zheng, Xin, Qi, Xufeng, Lee, Kenneth KH, Chan, John Yeuk-Hon, Cai, Dongqing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BlackWell Publishing Ltd 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4393738/
https://www.ncbi.nlm.nih.gov/pubmed/22925160
http://dx.doi.org/10.1111/j.1582-4934.2012.01621.x
Descripción
Sumario:This study indicates that brain-derived neurotrophic factor (BDNF) can promote young cardiac microvascular endothelial cells (CMECs) to migrate via the activation of the BDNF-TrkB-FL-PI3K/Akt pathway, which may benefit angiogenesis after myocardial infarction (MI). However, the ageing of CMECs led to changes in the expression of receptor Trk isoforms in that among the three isoforms (TrkB-FL, TrkB-T1 and TrkB-T2), only one of its truncated isoforms, TrkB-T1, continued to be expressed, which leads to the dysfunction of its ligand, a decrease in the migration of CMECs and increased injury in ageing hearts. This shift in receptor isoforms in aged CMECs, together with changes in the ageing microenvironment, might predispose ageing hearts to decreased angiogenic potential and increased cardiac pathology.