BDNF expression of macrophages and angiogenesis after myocardial infarction

Hong, Jihyung; Park, Hyoung-Min; Byun, Kyung Hee; Lee, Bong Hee; Kang, Woong Chol; Jeong, Goo‐Bo

doi:10.1016/j.ijcard.2014.08.019

Cited by 25 publications

(23 citation statements)

References 11 publications

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“…; Hong et al . ). In the whole LV, mBDNF protein was increased 1 and 6 h post MI in rats (Hang et al .…”

Section: Discussionmentioning

confidence: 97%

“…Immunohistochemical staining showed that BDNF protein increased early post MI in cardiomyocytes and was coexpressed with macrophages, which were infiltrated around endothelial cells in peri‐ and infarct areas (Hong et al . ). Halade et al .…”

Section: Discussionmentioning

confidence: 97%

“…In rats, brain‐derived neurotrophic factor (BDNF) protein is transiently increased in cardiomyocytes in infarct and peri‐infarct areas early post MI (Hong et al . ) and in the whole LV at 6 weeks post MI (Katare et al . ).…”

Section: Introductionmentioning

confidence: 99%

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Effects of exercise training on brain‐derived neurotrophic factor in skeletal muscle and heart of rats post myocardial infarction

Lee

Ahmad

Wang

et al. 2017

Experimental Physiology

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What is the central question of this study? Exercise training increases brain-derived neurotrophic factor (BDNF) in the hippocampus, which depends on a myokine, fibronectin type III domain-containing protein 5 (FNDC5). Whether exercise training after myocardial infarction induces parallel increases in FNDC5 and BDNF expression in skeletal muscle and the heart has not yet been studied. What is the main finding and its importance? Exercise training after myocardial infarction increases BDNF protein in skeletal muscle and the non-infarct area of the LV without changes in FNDC5 protein, suggesting that BDNF is not regulated by FNDC5 in skeletal muscle and heart. An increase in cardiac BDNF may contribute to the improvement of cardiac function by exercise training. Exercise training after myocardial infarction (MI) attenuates progressive left ventricular (LV) remodelling and dysfunction, but the peripheral stimuli induced by exercise that trigger these beneficial effects are still unclear. We investigated as possible mediators fibronectin type III domain-containing protein 5 (FNDC5) and brain-derived neurotrophic factor (BDNF) in the skeletal muscle and heart. Male Wistar rats underwent either sham surgery or ligation of the left descending coronary artery, and surviving MI rats were allocated to either a sedentary (Sed-MI) or an exercise group (ExT-MI). Exercise training was done for 4 weeks on a motor-driven treadmill. At the end, LV function was evaluated, and FNDC5 and BDNF mRNA and protein were assessed in soleus muscle, quadriceps and non-, peri- and infarct areas of the LV. At 5 weeks post MI, FNDC5 mRNA was decreased in soleus muscle and all areas of the LV, but FNDC5 protein was increased in the soleus muscle and the infarct area. Mature BDNF (mBDNF) protein was decreased in the infarct area without a change in mRNA. Exercise training attenuated the decrease in ejection fraction and the increase in LV end-diastolic pressure post MI. Exercise training had no effect on FNDC5 mRNA and protein, but increased mBDNF protein in soleus muscle, quadriceps and the non-infarct area of the LV. The mBDNF protein in the non-infarct area correlated positively with ejection fraction and inversely with LV end-diastolic pressure. In conclusion, mBDNF is induced by exercise training in skeletal muscle and the non-infarct area of the LV, which may contribute to improvement of muscle dysfunction and cardiac function post MI.

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“…; Hong et al . ). In the whole LV, mBDNF protein was increased 1 and 6 h post MI in rats (Hang et al .…”

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 97%

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Effects of exercise training on brain‐derived neurotrophic factor in skeletal muscle and heart of rats post myocardial infarction

Lee

Ahmad

Wang

et al. 2017

Experimental Physiology

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“…33,35 The intricate cross-talk between immune and nervous system is mediated by several molecules. Immune cells can produce neurotrophic factors, which are key mediators of new nerve outgrowth, and in particular, macrophages are proficient producers of neurotrophins, 36,37 including BDNF, 38,39 GDNF, 40 and NGF. [41][42][43] We have previously shown that NGF is a key element controlling nerve fiber sprouting in the colonic mucosa of patients with IBS.…”

Section: Discussionmentioning

confidence: 99%

Nerve fiber overgrowth in patients with symptomatic diverticular disease

Barbaro

Cremon

Fuschi

et al. 2019

Neurogastroenterology Motil

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Background Colonic diverticulosis is a common condition in industrialized countries. Up to 25% of patients with diverticula develop symptoms, a condition termed symptomatic uncomplicated diverticular disease (SUDD). The aim of the present study was to characterize neuroimmune interactions and nerve fiber plasticity in the colonic mucosa of patients with diverticula. Methods Controls, patients with diverticulosis and with SUDD were enrolled in the study. Mucosal biopsies were obtained close to diverticula (diverticular region) and in a normal mucosa (distant site), corresponding to sigmoid and descending colon in the controls. Quantitative immunohistochemistry was used to assess mast cells, T cells, macrophages, nerve fibers, and neuronal outgrowth (growth‐associated protein 43, GAP43+fibers). Key Results No difference emerged in mast cells and T cells among the three groups. Macrophages were increased in patients with SUDD and diverticulosis as compared to controls. Nerve fibers were enhanced in patients with SUDD and diverticulosis in comparison with controls in the diverticular region. GAP43+ fibers were increased only in patients with SUDD as compared to controls and to patients with diverticulosis in the diverticular region. In patients with SUDD, GAP43 density was increased in the diverticular region compared to distant site. Macrophages close to GAP43+ fibers were increased in the diverticular region of patients with SUDD. Significant correlations were found between GAP43+ fibers and immune cells. Conclusions and Inferences Patients with diverticula are characterized by increased macrophage counts, while nerve fiber sprouting is increased only in the diverticular region of patients with SUDD suggesting a role in symptom generation.

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“…Although it has been reported that high-fat diet feeding significantly increased Bdnf expression in adipose tissues, as described above, the results obtained by the adipocyte-specific Bdnf knockout strategy revealed that Bdnf is not expressed in adipocytes 23 . Considering the previous report showing that BDNF is expressed in M1 macrophages 27 , it is possible that a high-fat diet-induced pathological adipose tissue expansion creates hypoxia, which induces HIF1α levels and prevailing M1 macrophages, resulting in chronic inflammation and BDNF induction. In addition, because BDNF stimulates HIF1α expression 28, 29 , BDNF induction in pathological adipose tissue expansion might exacerbate chronic inflammation in the adipose tissues.…”

Section: Discussionmentioning

confidence: 99%

Visualizing changes in brain-derived neurotrophic factor (BDNF) expression using bioluminescence imaging in living mice

Izumi

Mori

Kiyama

et al. 2017

Sci Rep

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Brain-derived neurotrophic factor (BDNF) plays a fundamental role in expressing various neural functions including memory consolidation. Alterations of BDNF levels in the brain are associated with neurodegenerative and neuropsychiatric disorders. Therefore, it is important to understand how levels of BDNF are controlled. Recently we generated a novel transgenic mouse strain, termed the Bdnf-Luciferase transgenic (Bdnf-Luc Tg) mouse, to monitor changes in Bdnf expression. In the present study, we detected the bioluminescence signal from living Bdnf-Luc Tg mice after intraperitoneal administration of d-luciferin. Despite high levels of Bdnf expression in the brain, it was difficult to detect a signal from the brain region, probably because of its poorly penetrable (short-wavelength) bioluminescence. However, we could detect the changes in the bioluminescence signal in the brain region using a luciferin analogue generating a near-infrared wavelength of bioluminescence. We also found a strong correlation between increases in body weight and bioluminescence signal in the abdominal region of Tg mice fed a high-fat diet. These results show that changes in Bdnf expression can be visualized using living mice, and that the Tg mouse could be a powerful tool for clarification of the role of Bdnf expression in pathophysiological and physiological conditions.

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BDNF expression of macrophages and angiogenesis after myocardial infarction

Cited by 25 publications

References 11 publications

Effects of exercise training on brain‐derived neurotrophic factor in skeletal muscle and heart of rats post myocardial infarction

Effects of exercise training on brain‐derived neurotrophic factor in skeletal muscle and heart of rats post myocardial infarction

Nerve fiber overgrowth in patients with symptomatic diverticular disease

Visualizing changes in brain-derived neurotrophic factor (BDNF) expression using bioluminescence imaging in living mice

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