Abstract
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.
Highlights
Coronary artery disease-induced myocardial infarction (MI) is one of the leading causes of morbidity and mortality in elderly individuals
The results suggested that brain-derived neurotrophic factor (BDNF) plays an important function in cardiac microvascular endothelial cells (CMECs), possibly using an autocrine/paracrine modality
The results of the transwell and real-time cell migration assays revealed that BDNF promoted CMEC migration in a dose-dependent manner, suggesting that BDNF acted as a chemotaxis factor for the CMECs to promote their migration
Summary
Coronary artery disease-induced myocardial infarction (MI) is one of the leading causes of morbidity and mortality in elderly individuals. Recent studies have shown that brain-derived neurotrophic factor (BDNF) and its receptor, TrkB, are expressed first during late gestation and persistently at high levels into adulthood in the endothelial cells lining the arteries and capillaries of the heart. BDNFÀ/À mice exhibit the impaired survival of TrkB-expressing endothelial cells in intramyocardial arteries and capillaries in the late gestational and early postnatal periods. BDNF overexpression in the mid-gestational mouse heart results in an increase in capillary density [4]. PCR showed that young and old CMECs both expressed BDNF. The expression level in old CMECs was higher than that in young. We examined the potential age-related decrease and impairment of BDNF, its receptor and the related angiogenic potential of CMECs and aged hearts
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