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Brain‐derived neurotrophic factor prevents the endothelial barrier dysfunction induced by interleukin ‐1β and tumor necrosis factor ‐α
Author(s) -
Matsuda S.,
Fujita T.,
Kajiya M.,
Kashiwai K.,
Takeda K.,
Shiba H.,
Kurihara H.
Publication year - 2015
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/jre.12226
Subject(s) - tumor necrosis factor alpha , regeneration (biology) , brain derived neurotrophic factor , neurotrophic factors , inflammation , endothelial dysfunction , neurotrophin , cytokine , vascular permeability , vascular endothelial growth factor , endothelial stem cell , microbiology and biotechnology , chemistry , immunology , biology , medicine , endocrinology , cancer research , in vitro , receptor , biochemistry , vegf receptors
Background and Objective Brain‐derived neurotrophic factor ( BDNF ) promotes the regeneration of periodontal tissue. Although a local inflammatory step is required to initiate the subsequent process of tissue regeneration, excessive inflammation may inhibit or delay tissue regeneration. Therefore, the regulation of inflammation is essential for periodontal tissue regeneration. In the present study, we examined the influence of BDNF on the human microvascular endothelial cell ( HMVEC ) barrier dysfunction induced by interleukin ( IL) ‐1β or tumor necrosis factor ( TNF) ‐α to determine the effects of BDNF on the regulation of local inflammation in periodontal tissue regeneration. Material and Methods Endothelial permeability was analyzed using a Dextran transport assay with transwell plates. The expression of vascular endothelial ( VE) ‐cadherin was assessed by immunoblotting and immunofluorescence microscopy. Results BDNF (25 ng/mL) inhibited increase induced in endothelial permeability by IL ‐1β and TNF ‐α. IL ‐1β and TNF ‐α decreased VE ‐cadherin protein levels, while BDNF recovered the reduction in HMVEC s. BDNF protected the increase induced in endothelial permeability by IL ‐1β and TNF ‐α through TrkB. The single addition of BDNF into the culture increased the expression of VE ‐cadherin in HMVEC s. Conclusion BDNF played an important role in inhibiting endothelial barrier dysfunction, which suggests that it may assist in enhancing periodontal tissue regeneration.