Gene expression and association analysis of vascular endothelial growth factor in major depressive disorder

Iga, Jun‐ichi; Ueno, Shu‐ichi; Yamauchi, Ken; Numata, Shusuke; Tayoshi-Shibuya, Surniko; Kinouchi, Sawako; Nakataki, Masahito; Song, Hongwei; Hokoishi, Kazuhiko; Tanabe, Hirotaka; Sano, Akira; Ohmori, Tetsuro

doi:10.1016/j.pnpbp.2006.12.011

Cited by 93 publications

(69 citation statements)

References 30 publications

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“…Chronic stress exposure has been shown to decrease and antidepressant administration to increase hippocampal VEGF [71,70]. Consistent with these results, it has been reported that VEGF expression and blood levels are increased in patients with depression and that antidepressant treatment reverses these effects [72,73]. …”

Section: Depression As a Cardiovascular Diseasementioning

confidence: 63%

Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies

Lang

Borgwardt²

2013

Cell Physiol Biochem

6,204

229

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Depression is a multicausal disorder and has been associated with the risk to develop cancer, dementia, diabetes, epilepsy and stroke. As a metabolic disorder depression has been associated with obesity, diabetes, insulin sensitivity, neuropeptide Y, glucose regulation, poor glycemic control, glucagone-like peptide-1, cholezystokinin, ghrelin, leptin, the endocannabinoid system, insulin-like growth factor and gastrin-releasing peptide. As a cardiovascular disease a close relationship exists between depression and blood pressure, heart rate, norepinephrine, sympathetic tone, vascular resistance, blood viscosity, plasma volume, intima thickness and atherosclerosis. Additionally blood coagulation, fibrinolysis, D-dimers, plasminogen activator inhibitor-1 protein, platelet activation, VEGF, plasma nitric oxide and its synthase are changed in depressed patients. As an endocrinological and stress disorder depression has been connected with the concentration of free T₄, TSH, CRH, arginine vasopressin, corticotrophin, corticosteroid release and ACTH. Depression as an inflammatory disorder is mediated by pro-inflammatory cytokines, interleukin-1, interleukin-6, TNF-alpha, soluble interleukin-2 receptors, interferon-alpha, interleukin 8, interleukin-10, hs-CRP, acute phase proteins, haptoglobin, toll like receptor 4, interleukin-1beta, mammalian target of rapamycin pathway, substance P, cyclooxygenase-2, prostaglandin-E2, lipid peroxidation levels and acid sphingomyelinase. Nutritional factors might influence depression risk, i.e. the consumption of folate, omega-3 fatty acids, monounsaturated fatty acids, olive oil, fish, fruits, vegetables, nuts, legumes, vitamin B6 and vitamin B12. The neurodegenerative hypothesis of depression explains decreased hippocampal volumes in depressed patients and changes of neurotrophic support by BDNF, erythropoietin, GDNF, FGF-2, NT3, NGF and growth hormone. In this context, a fast neuroprotective and antidepressant effect has also been observed by ketamine, which acts via the glutamatergic system. Hence, GABA, AMPA, EAAT, NMDA- and metabotropic glutamate receptors (mGluR1 to mGluR8) have gained interest in depression recently. Alternative, causative or also easy available treatment strategies beyond serotonin and noradrenaline reuptake inhibition might be a major topic of future psychiatric care. In this review, an attempt is made to overview concepts of the disease and search for perspectives on antidepressant treatment strategies beyond approved medications.

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Section: Depression As a Cardiovascular Diseasementioning

confidence: 63%

Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies

Lang

Borgwardt²

2013

Cell Physiol Biochem

6,204

229

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“…Kahl and colleagues found increased concentrations of VEGF in nonmedicated depressive patients with borderline personality disorder in comparison with healthy controls [Kahl et al 2009]. Iga and colleagues had previously suggested that a higher expression of VEGF mRNA in the peripheral leucocytes might be associated with the depressive state [Iga et al 2007]. Takebayashi and colleagues reported that plasma VEGF levels were increased significantly in MDD patients compared with matched controls [Takebayashi et al 2010].…”

Section: Discussionmentioning

confidence: 99%

Serum brain-derived neurotrophic factor, vascular endothelial growth factor and leptin levels in patients with a diagnosis of severe major depressive disorder with melancholic features

Kotan¹,

Sarandöl²,

Kırhan³

et al. 2012

Therapeutic Advances in Psychopharmacology

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Abstract:Objective: Brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF) and leptin have been hypothesized to be involved in the neurobiology of depression. The aim of this study was to investigate BDNF, VEGF and leptin levels in patients with severe melancholic depression. Methods: A total of 40 drug-free patients with major depressive disorder (MDD) with melancholic features and 40 healthy controls were included in the study. Demographic information, psychiatric evaluation and physical examination were documented for both groups. Serum BDNF, VEGF levels were determined by enzyme-linked immunosorbent assay and leptin with radioimmunoassay methods. The Hamilton Depression Rating Scale and Hamilton Anxiety Rating Scale were applied to the patients. Results: There were no significant differences in serum BDNF, VEGF and leptin levels between the patient and control groups. There was a negative correlation between BDNF levels and the number of depressive episodes. It was noted that VEGF levels decreased with increasing severity of depression. Conclusions: These findings suggest that BDNF levels might be associated with the recurrence of depression and VEGF levels might be a determinant of the severity of depression.

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“…The clinical data shed light to a more complex landscape. An eight-week treatment with paroxetine appeared to decrease VEGF mRNA levels in peripheral leukocytes of depressed patients in positive correlation with clinical improvement [125]. In the same class of antidepressants, escitalopram did not alter VEGF plasma levels in depressed patients after 12 weeks of treatment [129].…”

Section: Vascular Endothelial Growth Factor (Vegf)mentioning

confidence: 94%

“…However, data in human are more inconsistent [124]. In fact, while some authors observed higher serum or plasma VEGF concentrations in drug-free depressed patients [125][126][127] and in patients with acute episodes of MDD or bipolar disorders [128], others reported no significant difference compared to healthy controls [129]. It has been suggested that an elevation of VEGF expression may be a repair response to the neural damage that underlies the pathogenesis of depression [130].…”

Section: Vascular Endothelial Growth Factor (Vegf)mentioning

confidence: 99%

Neuroadaptations of the 5-HT System Induced by Antidepressant Treatments: Old and New Strategies

Haddjeri¹

2014

AAD

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Major Depressive Disorder (MDD) is a common illness worldwide with severe socioeconomic consequences. Several hypotheses have been formulated to explain the physiopathology of depression as well as the mechanism of action of antidepressants but two of them had attracted much attention. The dominant monoaminergic hypothesis of depression links the physiopathology of MDD to a deficiency on cerebral serotonin (5-HT) and/or Norepinephrine (NE) levels; however, the relatively new neurogenic and neurotrophic hypothesis raises the possibility of an impaired neuroplasticity and/or depletion of neurotrophic factors in specific networks resulting on their structural deformity and functional impairment. An enormous body of evidence reported particular neuroadaptations following chronic administration of antidepressant drugs. In this review, we describe major adaptive changes in pre-and post-synaptic 5-HT neurotransmission as well as alterations in gene transcription and neurotrophic factors in response to long-term treatment with conventional antidepressants, new putative ones or novel promising drug candidates, all acting via 5-HT system.

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Gene expression and association analysis of vascular endothelial growth factor in major depressive disorder

Cited by 93 publications

References 30 publications

Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies

Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies

Serum brain-derived neurotrophic factor, vascular endothelial growth factor and leptin levels in patients with a diagnosis of severe major depressive disorder with melancholic features

Neuroadaptations of the 5-HT System Induced by Antidepressant Treatments: Old and New Strategies

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