BDNF-mediated mitophagy alleviates high-glucose-induced brain microvascular endothelial cell injury

Jin, Hong; Zhu, Yi; Li, Yiping; Ding, Xiuyu; Ma, Wen-Qi; Han, Xi‐Qiong; Wang, Bilei

doi:10.1007/s10495-019-01535-x

Cited by 71 publications

(44 citation statements)

References 69 publications

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“…28 BDNF-induced mitophagy plays a protective role against endothelial cell damage in hyperglycemic conditions. 29 VEGF promotes signaling through an alternate VEGF receptor-2 in the setting of mitochondrial dysfunction and oxidative stress. 30 From this previous study, it is logical to conclude that the beneficial histological and functional results of PRP treatment are derived from the PRP-mediated delivery of IGF-1, BDNF, and VEGF.…”

Section: Discussionmentioning

confidence: 99%

Intracavernous Injection of Autologous Platelet-Rich Plasma Ameliorates Hyperlipidemia-Associated Erectile Dysfunction in a Rat Model

Huang

Chen

et al. 2021

Sexual Medicine

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Introduction Hyperlipidemia is associated with an increased risk of erectile dysfunction (ED) mediated by endothelial damage. Platelet-rich plasma (PRP) contains numerous angiogenic growth factors. Currently, evidence supporting the use of PRP for ED treatment is limited. Aim We investigated PRP in a rat model of hyperlipidemia-associated ED. Methods Thirty 2-month-old male Sprague–Dawley rats were randomly divided into 3 groups. 20 rats were fed a high-fat diet for 5 months and were randomly divided into 2 groups: (i) rats in the H group received supernatant injection into the corpus cavernosum weekly for 4 weeks; (ii) rats in the H + PRP group received PRP injection into the corpus cavernosum weekly for 4 weeks. 10 rats were fed a standard diet for 5 months and received supernatant injection into the corpus cavernosum weekly for 4 weeks (N group). 7 days after the 4th injection, all rats underwent erectile function testing and then euthanasia. Main outcome measures Erectile function was evaluated by measuring intracavernous pressure (ICP) and mean arterial pressure (MAP). Serum and penile tissue were collected for metabolic variable assessment and histochemical examination, respectively. Results Intracavernous pressure/MAP and area under the curve/MAP ratios were significantly higher in the N and H + PRP groups than in the H group. Insulin-like growth factor-1, brain-derived neurotrophic factor, and vascular endothelial growth factor levels were significantly higher in the H + PRP group than in the N and H groups. Corporal neuronal nitric oxide synthase, endothelial nitric oxide synthase, and endothelial cells were weakly expressed in the H group compared with the N and H + PRP groups. Intracorporal oxidative stress and apoptotic index were significantly higher in the H group than in the N and H + PRP groups. Conclusions This preclinical evidence suggests that clinical trials of PRP in men with ED should be considered. PRP may play a role in ED management. Huang YC, Wu CT, Chen MF, et al. Intracavernous Injection of Autologous Platelet-Rich Plasma Ameliorates Hyperlipidemia-Associated Erectile Dysfunction in a Rat Model. Sex Med 2021;9:100317.

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Section: Discussionmentioning

confidence: 99%

Intracavernous Injection of Autologous Platelet-Rich Plasma Ameliorates Hyperlipidemia-Associated Erectile Dysfunction in a Rat Model

Huang

Chen

et al. 2021

Sexual Medicine

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“…Finally, it is well known that NA strongly modulates growth factor (GF) synthesis and release by astrocytes (Follesa & Mocchetti, 1993;Furukawa et al, 1987;Juric et al, 2006;Kajitani et al, 2012;Krzan et al, 2001;Mocchetti et al, 1989). BDNF and FGF synthesized by astrocytes, aside from affecting neuron integrity, might interfere also on endothelial repair after different insults (Jin et al, 2019;Yang, Qiao, Meyer, & Friedl, 2009) and this might be one additional mechanism through which LC degeneration might interfere with BBB integrity. The release of FGF by astrocytes might also protect PC integrity and function under stressful conditions (such as hypoxia/ ischemia) through an overexpression of platelet-derived growth factor receptor-β (Arimura et al, 2012;Nakamura et al, 2016).…”

Section: Growth Factorsmentioning

confidence: 99%

Locus Coeruleus and neurovascular unit: From its role in physiology to its potential role in Alzheimer’s disease pathogenesis

Giorgi

Galgani²,

Puglisi-Allegra

et al. 2020

J of Neuroscience Research

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Locus coeruleus (LC) is the main noradrenergic (NA) nucleus of the central nervous system. LC degenerates early during Alzheimer's disease (AD) and NA loss might concur to AD pathogenesis. Aside from neurons, LC terminals provide dense innervation of brain intraparenchymal arterioles/capillaries, and NA modulates astrocyte functions. The term neurovascular unit (NVU) defines the strict anatomical/functional interaction occurring between neurons, glial cells, and brain vessels. NVU plays a fundamental role in coupling the energy demand of activated brain regions with regional cerebral blood flow, it includes the blood-brain barrier (BBB), plays an active role in neuroinflammation, and participates also to the glymphatic system. NVU alteration is involved in AD pathophysiology through several mechanisms, mainly related to a relative oligoemia in activated brain regions and impairment of structural and functional BBB integrity, which contributes also to the intracerebral accumulation of insoluble amyloid. We review the existing data on the morphological features of LC-NA innervation of the NVU, as well as its contribution to neurovascular coupling and BBB proper functioning. After introducing the main experimental data linking LC with AD, which have repeatedly shown a key role of neuroinflammation and increased amyloid plaque formation, we discuss the potential mechanisms by which the loss of NVU modulation by LC might contribute to AD pathogenesis. Surprisingly, thus far not so many studies have tested directly these mechanisms in models of AD in which LC has been lesioned experimentally. Clarifying the interaction of LC with NVU in AD pathogenesis may disclose potential therapeutic targets for AD.

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“…Several pieces of research indicate that activation of the BDNF/TrkB pathway upregulates HIF-1α expression even under normoxic conditions (Nakamura et al, 2006;Helan et al, 2014;Lin et al, 2014;Jin et al, 2019). BDNF is essential for the maintenance of cortical neurons, whose downregulation contributes to the initial loss of short-term memory in AD (Giuffrida et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, emerging evidence shows that the infusion of brain-derived neurotrophic factor (BDNF) improves glucose metabolism and cognitive function (Kuroda et al, 2003;Li et al, 2012;Kuipers et al, 2016). BDNF increased VEGF mRNA and protein expression via a HIF-1α signal transduction pathway (Lin et al, 2014), and the underlying mechanism was the activation of the BDNF/tyrosine Kinase receptor B (TrkB) pathway, which stimulate increases in HIF-1α (Nakamura et al, 2006;Helan et al, 2014;Jin et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

α-Lipoic Acid Maintains Brain Glucose Metabolism via BDNF/TrkB/HIF-1α Signaling Pathway in P301S Mice

Zhang

Yan

et al. 2020

Front. Aging Neurosci.

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The microtubule-associated protein tau is closely correlated with hypometabolism in Alzheimer's disease (AD). α-lipoic acid (LA), which is a naturally occurring cofactor in mitochondrial, has been shown to have properties that can inhibit the tau pathology and neuronal damage in our previous research. However, if LA affects glucose metabolism when it reverses tau pathology remains unclear, especially concerning the potential mechanism. Therefore, we make a further study using the P301S mouse model (a tauopathy and AD mouse model which overexpressing fibrillary tau) to gain a clear idea of the aforementioned problems. Here, we found chronic LA administration significantly increased glucose availability by elevating glucose transporter 3 (GLUT3), GLUT4, vascular endothelial growth factor (VEGF) protein and mRNA level, and heme oxygenase-1 (HO-1) protein level in P301S mouse brains. Meanwhile, we found that LA also promoted glycolysis by directly upregulating hexokinase (HK) activity, indirectly by increasing proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and DNA repair enzymes (OGG1/2 and MTH1). Further, we found the underlying mechanism of restored glucose metabolism might involve in the activation of brain-derived neurotrophic factor (BDNF)/tyrosine Kinase receptor B (TrkB)/hypoxia-inducible factor-1α (HIF-1α) signaling pathway by LA treatment.

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BDNF-mediated mitophagy alleviates high-glucose-induced brain microvascular endothelial cell injury

Cited by 71 publications

References 69 publications

Intracavernous Injection of Autologous Platelet-Rich Plasma Ameliorates Hyperlipidemia-Associated Erectile Dysfunction in a Rat Model

Intracavernous Injection of Autologous Platelet-Rich Plasma Ameliorates Hyperlipidemia-Associated Erectile Dysfunction in a Rat Model

Locus Coeruleus and neurovascular unit: From its role in physiology to its potential role in Alzheimer’s disease pathogenesis

α-Lipoic Acid Maintains Brain Glucose Metabolism via BDNF/TrkB/HIF-1α Signaling Pathway in P301S Mice

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