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APOE ε4-specific associations of VEGF gene family expression with cognitive aging and Alzheimer's disease.
Moore AM, Mahoney E, Dumitrescu L, De Jager PL, Koran MEI, Petyuk VA, Robinson RA, Ruderfer DM, Cox NJ, Schneider JA, Bennett DA, Jefferson AL, Hohman TJ
(2020) Neurobiol Aging 87: 18-25
MeSH Terms: Aged, Aged, 80 and over, Aging, Apolipoprotein E4, Cognitive Aging, Cognitive Dysfunction, Female, Gene Expression, Genetic Association Studies, Genetic Predisposition to Disease, Genotype, Humans, Male, Neovascularization, Physiologic, Neuropilin-1, Vascular Endothelial Growth Factor A
Show Abstract · Added March 30, 2020
Literature suggests vascular endothelial growth factor A (VEGFA) is protective among those at highest risk for Alzheimer's disease (AD). Apolipoprotein E (APOE) ε4 allele carriers represent a highly susceptible population for cognitive decline, and VEGF may confer distinct protection among APOE-ε4 carriers. We evaluated interactions between cortical expression of 10 VEGF gene family members and APOE-ε4 genotype to clarify which VEGF genes modify the association between APOE-ε4 and cognitive decline. Data were obtained from the Religious Orders Study and Rush Memory and Aging Project (N = 531). Linear regression assessed interactions on global cognition. VEGF genes NRP1 and VEGFA interacted with APOE-ε4 on cognitive performance (p.fdr < 0.05). Higher NRP1 expression correlated with worse outcomes among ε4 carriers but better outcomes among ε4 noncarriers, suggesting NRP1 modifies the risk for poor cognitive scores based on APOE-ε4 status. NRP1 regulates angiogenesis, and literature suggests vessels in APOE-ε4 brains are more prone to leaking, perhaps placing young vessels at risk for ischemia. Results suggest that future therapeutics targeting brain angiogenesis should also consider ε4 allele status.
Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.
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16 MeSH Terms
The 2019 Nobel Prize honors fundamental discoveries in hypoxia response.
Moslehi J, Rathmell WK
(2020) J Clin Invest 130: 4-6
MeSH Terms: Cell Hypoxia, History, 20th Century, Humans, Hypoxia-Inducible Factor 1, alpha Subunit, Nobel Prize, Vascular Endothelial Growth Factor A, Von Hippel-Lindau Tumor Suppressor Protein
Added November 27, 2019
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7 MeSH Terms
Cerebrospinal Fluid Ceruloplasmin, Haptoglobin, and Vascular Endothelial Growth Factor Are Associated with Neurocognitive Impairment in Adults with HIV Infection.
Kallianpur AR, Gittleman H, Letendre S, Ellis R, Barnholtz-Sloan JS, Bush WS, Heaton R, Samuels DC, Franklin DR, Rosario-Cookson D, Clifford DB, Collier AC, Gelman B, Marra CM, McArthur JC, McCutchan JA, Morgello S, Grant I, Simpson D, Connor JR, Hulgan T, CHARTER Study Group
(2019) Mol Neurobiol 56: 3808-3818
MeSH Terms: Adult, Antiretroviral Therapy, Highly Active, Biomarkers, Ceruloplasmin, Comorbidity, Female, HIV Infections, Haptoglobins, Humans, Inflammation, Iron, Male, Multivariate Analysis, Neurocognitive Disorders, Regression Analysis, Vascular Endothelial Growth Factor A
Show Abstract · Added December 11, 2019
Dysregulated iron transport and a compromised blood-brain barrier are implicated in HIV-associated neurocognitive disorders (HAND). We quantified the levels of proteins involved in iron transport and/or angiogenesis-ceruloplasmin, haptoglobin, and vascular endothelial growth factor (VEGF)-as well as biomarkers of neuroinflammation, in cerebrospinal fluid (CSF) from 405 individuals with HIV infection and comprehensive neuropsychiatric assessments. Associations with HAND [defined by a Global Deficit Score (GDS) ≥ 0.5, GDS as a continuous measure (cGDS), or by Frascati criteria] were evaluated for the highest versus lowest tertile of each biomarker, adjusting for potential confounders. Higher CSF VEGF was associated with GDS-defined impairment [odds ratio (OR) 2.17, p = 0.006] and cGDS in unadjusted analyses and remained associated with GDS impairment after adjustment (p = 0.018). GDS impairment was also associated with higher CSF ceruloplasmin (p = 0.047) and with higher ceruloplasmin and haptoglobin in persons with minimal comorbidities (ORs 2.37 and 2.13, respectively; both p = 0.043). In persons with minimal comorbidities, higher ceruloplasmin and haptoglobin were associated with HAND by Frascati criteria (both p < 0.05), and higher ceruloplasmin predicted worse impairment (higher cGDS values, p < 0.01). In the subgroup with undetectable viral load and minimal comorbidity, CSF ceruloplasmin and haptoglobin were strongly associated with GDS impairment (ORs 5.57 and 2.96, respectively; both p < 0.01) and HAND (both p < 0.01). Concurrently measured CSF IL-6 and TNF-α were only weakly correlated to these three biomarkers. Higher CSF ceruloplasmin, haptoglobin, and VEGF are associated with a significantly greater likelihood of HAND, suggesting that interventions aimed at disordered iron transport and angiogenesis may be beneficial in this disorder.
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MeSH Terms
Mechanisms of VEGF (Vascular Endothelial Growth Factor) Inhibitor-Associated Hypertension and Vascular Disease.
Pandey AK, Singhi EK, Arroyo JP, Ikizler TA, Gould ER, Brown J, Beckman JA, Harrison DG, Moslehi J
(2018) Hypertension 71: e1-e8
MeSH Terms: Angiogenesis Inhibitors, Animals, Humans, Hypertension, Signal Transduction, Vascular Diseases, Vascular Endothelial Growth Factor A
Added April 22, 2018
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7 MeSH Terms
Cardio-Oncology: Vascular Endothelial Growth Factor Inhibitors, Salt, and Macrophages: A Complicated Interaction.
Moslehi J, Pandey AK, Bhatia N
(2017) Hypertension 69: 785-786
MeSH Terms: Humans, Macrophages, Sodium Chloride, Sodium Chloride, Dietary, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factors
Added March 26, 2017
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1 Members
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6 MeSH Terms
Skeletal Colonization by Breast Cancer Cells Is Stimulated by an Osteoblast and β2AR-Dependent Neo-Angiogenic Switch.
Mulcrone PL, Campbell JP, Clément-Demange L, Anbinder AL, Merkel AR, Brekken RA, Sterling JA, Elefteriou F
(2017) J Bone Miner Res 32: 1442-1454
MeSH Terms: Animals, Bone and Bones, Breast Neoplasms, Cell Line, Tumor, Coculture Techniques, Female, Humans, Mice, Mice, Knockout, Neoplasm Metastasis, Neoplasm Proteins, Neovascularization, Pathologic, Osteoblasts, Receptors, Adrenergic, beta-2, Vascular Endothelial Growth Factor A
Show Abstract · Added April 26, 2017
The skeleton is a common site for breast cancer metastasis. Although significant progress has been made to manage osteolytic bone lesions, the mechanisms driving the early steps of the bone metastatic process are still not sufficiently understood to design efficacious strategies needed to inhibit this process and offer preventative therapeutic options. Progression and recurrence of breast cancer, as well as reduced survival of patients with breast cancer, are associated with chronic stress, a condition known to stimulate sympathetic nerve outflow. In this study, we show that stimulation of the beta 2-adrenergic receptor (β2AR) by isoproterenol, used as a pharmacological surrogate of sympathetic nerve activation, led to increased blood vessel density and Vegf-a expression in bone. It also raised levels of secreted Vegf-a in osteoblast cultures, and accordingly, the conditioned media from isoproterenol-treated osteoblast cultures promoted new vessel formation in two ex vivo models of angiogenesis. Blocking the interaction between Vegf-a and its receptor, Vegfr2, blunted the increase in vessel density induced by isoproterenol. Genetic loss of the β2AR globally, or specifically in type 1 collagen-expressing osteoblasts, diminished the increase in Vegf-positive osteoblast number and bone vessel density induced by isoproterenol, and reduced the higher incidence of bone metastatic lesions induced by isoproterenol after intracardiac injection of an osteotropic variant of MDA-MB-231 breast cancer cells. Inhibition of the interaction between Vegf-a and Vegfr2 with the blocking antibody mcr84 also prevented the increase in bone vascular density and bone metastasis triggered by isoproterenol. Together, these results indicate that stimulation of the β2AR in osteoblasts triggers a Vegf-dependent neo-angiogenic switch that promotes bone vascular density and the colonization of the bone microenvironment by metastatic breast cancer cells. © 2017 American Society for Bone and Mineral Research.
© 2017 American Society for Bone and Mineral Research.
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15 MeSH Terms
Associations between Tumor Vascularity, Vascular Endothelial Growth Factor Expression and PET/MRI Radiomic Signatures in Primary Clear-Cell-Renal-Cell-Carcinoma: Proof-of-Concept Study.
Yin Q, Hung SC, Wang L, Lin W, Fielding JR, Rathmell WK, Khandani AH, Woods ME, Milowsky MI, Brooks SA, Wallen EM, Shen D
(2017) Sci Rep 7: 43356
MeSH Terms: Adult, Aged, Carcinoma, Renal Cell, Female, Gene Expression, Humans, Image Interpretation, Computer-Assisted, Kidney Neoplasms, Magnetic Resonance Imaging, Male, Middle Aged, Neovascularization, Pathologic, Positron-Emission Tomography, Proof of Concept Study, Retrospective Studies, Tumor Burden, Vascular Endothelial Growth Factor A
Show Abstract · Added October 30, 2019
Studies have shown that tumor angiogenesis is an essential process for tumor growth, proliferation and metastasis. Also, tumor angiogenesis is an important prognostic factor of clear cell renal cell carcinoma (ccRCC), as well as a factor in guiding treatment with antiangiogenic agents. Here, we attempted to find the associations between tumor angiogenesis and radiomic imaging features from PET/MRI. Specifically, sparse canonical correlation analysis was conducted on 3 feature datasets (i.e., radiomic imaging features, tumor microvascular density (MVD), and vascular endothelial growth factor (VEGF) expression) from 9 patients with primary ccRCC. In order to overcome the potential bias of intratumoral heterogeneity of angiogenesis, this study investigated the relationship between regional expressions of angiogenesis and VEGF, and localized radiomic features from different parts within the tumors. Our study highlighted the significant strong correlations between radiomic features and MVD, and also demonstrated that the spatiotemporal features extracted from DCE-MRI provided stronger radiomic correlation to MVD than the textural features extracted from Dixon sequences and FDG PET. Furthermore, PET/MRI, which takes advantage of the combined functional and structural information, had higher radiomics correlation to MVD than solely utilizing PET or MRI alone.
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Novel Small Molecule JP-153 Targets the Src-FAK-Paxillin Signaling Complex to Inhibit VEGF-Induced Retinal Angiogenesis.
Toutounchian JJ, Pagadala J, Miller DD, Baudry J, Park F, Chaum E, Morales-Tirado , Yates CR
(2017) Mol Pharmacol 91: 1-13
MeSH Terms: Animals, Benzoxazines, Cell Movement, Cell Proliferation, Disease Models, Animal, Endothelial Cells, Focal Adhesion Protein-Tyrosine Kinases, Humans, Mice, Inbred C57BL, Models, Biological, Oxygen, Paxillin, Retinal Neovascularization, Signal Transduction, Small Molecule Libraries, Vascular Endothelial Growth Factor A, src-Family Kinases
Show Abstract · Added June 11, 2018
Targeting vascular endothelial growth factor (VEGF) is a common treatment strategy for neovascular eye disease, a major cause of vision loss in diabetic retinopathy and age-related macular degeneration. However, the decline in clinical efficacy over time in many patients suggests that monotherapy of anti-VEGF protein therapeutics may benefit from adjunctive treatments. Our previous work has shown that through decreased activation of the cytoskeletal protein paxillin, growth factor-induced ischemic retinopathy in the murine oxygen-induced retinopathy model could be inhibited. In this study, we demonstrated that VEGF-dependent activation of the Src/FAK/paxillin signalsome is required for human retinal endothelial cell migration and proliferation. Specifically, the disruption of focal adhesion kinase (FAK) and paxillin interactions using the small molecule JP-153 inhibited Src-dependent phosphorylation of paxillin (Y118) and downstream activation of Akt (S473), resulting in reduced migration and proliferation of retinal endothelial cells stimulated with VEGF. However, this effect did not prevent the initial activation of either Src or FAK. Furthermore, topical application of a JP-153-loaded microemulsion affected the hallmark features of pathologic retinal angiogenesis, reducing neovascular tuft formation and increased avascular area, in a dose-dependent manner. In conclusion, our results suggest that using small molecules to modulate the focal adhesion protein paxillin is an effective strategy for treating pathologic retinal neovascularization. To our knowledge, this is the first paradigm validating modulation of paxillin to inhibit angiogenesis. As such, we have identified and developed a novel class of small molecules aimed at targeting focal adhesion protein interactions that are essential for pathologic neovascularization in the eye.
Copyright © 2016 by The American Society for Pharmacology and Experimental Therapeutics.
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Plasma hepatocyte growth factor is a novel marker of AL cardiac amyloidosis.
Swiger KJ, Friedman EA, Brittain EL, Tomasek KA, Huang S, Su YR, Sawyer DB, Lenihan DJ
(2016) Amyloid 23: 242-248
MeSH Terms: Aged, Amyloidosis, Biomarkers, Cardiomyopathies, Cohort Studies, Diagnosis, Differential, Female, Galectin 3, Heart Failure, Systolic, Hepatocyte Growth Factor, Humans, Hypertrophy, Left Ventricular, Immunoglobulin Light Chains, Interleukin-6, Male, Middle Aged, Prealbumin, Registries, Survival Analysis, Vascular Endothelial Growth Factor A
Show Abstract · Added June 7, 2018
BACKGROUND - Cardiac amyloidosis is an infiltrative cardiomyopathy that is challenging to diagnose. We hypothesized that the novel biomarkers hepatocyte growth factor (HGF), galectin-3 (GAL-3), interleukin-6 (IL-6), and vascular endothelial growth factor (VEGF) would be elevated in cardiac amyloidosis and may be able to discriminate from non-cardiac systemic amyloidosis or other cardiomyopathies with similar clinical or morphologic characteristics.
METHODS - Patients were selected from the Vanderbilt Main Heart Registry according to the following groups: (1) amyloid light-chain (AL) cardiac amyloidosis (n = 26); (2) transthyretin (ATTR) cardiac amyloidosis (n = 7); (3) left ventricular hypertrophy (LVH) (n = 45); (4) systolic heart failure (n = 42); and (5) non-cardiac systemic amyloidosis (n = 7). Biomarkers were measured in stored plasma samples. Biomarkers' discrimination performance in predicting AL cardiac amyloidosis (i.e., Concordance index) was reported. A survival analysis was used to explore the relationship between HGF levels and mortality among AL cardiac amyloidosis patients.
RESULTS - HGF levels were markedly elevated in patients with AL cardiac amyloidosis (median = 622, interquartile range (IQR): 299-1228 pg/mL) compared with the other groups, including those with non-cardiac systemic amyloidosis (median = 134, IQR: 94-163 pg/mL, p < 0.001). HGF was not a specific marker for ATTR amyloidosis. Gal-3 was elevated in all groups with amyloidosis but could not differentiate between those with and without cardiac involvement. There was no difference in IL-6 or VEGF between those with AL cardiac amyloidosis compared to other groups (p = 0.13 and 0.057, respectively).
CONCLUSIONS - HGF may be a specific marker that distinguishes AL cardiac amyloidosis from other cardiomyopathies with similar clinical or morphologic characteristics. Further studies are necessary to determine whether HGF levels predict the likelihood of survival.
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Cardiovascular Toxic Effects of Targeted Cancer Therapies.
Moslehi JJ
(2016) N Engl J Med 375: 1457-1467
MeSH Terms: Antineoplastic Agents, Cardiovascular Diseases, Humans, Neoplasms, Protein Kinase Inhibitors, Protein-Tyrosine Kinases, Signal Transduction, Vascular Endothelial Growth Factor A
Added March 26, 2017
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8 MeSH Terms