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Total 79 results found since Jan 2013.

Aging decreases docosahexaenoic acid transport across the blood-brain barrier in C57BL/6J mice
by Takuro Iwao, Fuyuko Takata, Junichi Matsumoto, Hisataka Aridome, Miho Yasunaga, Miki Yokoya, Yasufumi Kataoka, Shinya Dohgu Nutrients are actively taken up by the brain via various transporters at the blood–brain barrier (BBB). A lack of specific nutrients in the aged brain, including decreased levels of docosahexaenoic acid (DHA), is associated with memory and cognitive dysfunction. To compensate for decreased brain DHA, orally supplied DHA must be transported from the circulating blood to the brain across the BBB through transport carriers, including major facilitator superfamily domain-containing protein 2a (MFSD2...
Source: PLoS One - February 16, 2023 Category: Biomedical Science Authors: Takuro Iwao Source Type: research

Gαq G proteins modulate MMP-9 gelatinase during remodeling of the murine femoral artery
Conclusions: These data demonstrate that femoral wire injury in the mouse is associated with a time-dependent increase in Gαq expression. Inhibition of Gαq alters cell proliferation and is associated with decreased MMP-9 expression and activity.
Source: Journal of Surgical Research - May 9, 2012 Category: Surgery Authors: Yiping Zou, Yuyang Fu, Mark G. Davies Tags: Association for Academic Surgery Source Type: research

T-cadherin Promotes Revascularization Cell Biology
Adipose tissue secretes protein factors that have systemic actions on cardiovascular tissues. Previous studies have shown that ablation of the adipocyte-secreted protein adiponectin leads to endothelial dysfunction, whereas its overexpression promotes wound healing. However, the receptor(s) mediating the protective effects of adiponectin on the vasculature is not known. Here we examined the role of membrane protein T-cadherin, which localizes adiponectin to the vascular endothelium, in the revascularization response to chronic ischemia. T-cadherin-deficient mice were analyzed in a model of hind limb ischemia where blood fl...
Source: Journal of Biological Chemistry - August 23, 2013 Category: Chemistry Authors: Parker-Duffen, J. L., Nakamura, K., Silver, M., Kikuchi, R., Tigges, U., Yoshida, S., Denzel, M. S., Ranscht, B., Walsh, K. Tags: Molecular Bases of Disease Source Type: research

Knockout of density-enhanced phosphatase-1 impairs cerebrovascular reserve capacity in an arteriogenesis model in mice.
Abstract Collateral growth, arteriogenesis, represents a proliferative mechanism involving endothelial cells, smooth muscle cells, and monocytes/macrophages. Here we investigated the role of Density-Enhanced Phosphatase-1 (DEP-1) in arteriogenesis in vivo, a protein-tyrosine-phosphatase that has controversially been discussed with regard to vascular cell biology. Wild-type C57BL/6 mice subjected to permanent left common carotid artery occlusion (CCAO) developed a significant diameter increase in distinct arteries of the circle of Willis, especially in the anterior cerebral artery. Analyzing the impact of loss of D...
Source: Biomed Res - September 18, 2013 Category: Research Authors: Hackbusch D, Dülsner A, Gatzke N, Krüger J, Hillmeister P, Nagorka S, Blaschke F, Ritter Z, Thöne-Reineke C, Böhmer FD, Buschmann I, Kappert K Tags: Biomed Res Int Source Type: research

In Barrett's Esophagus Patients and Barrett's Cell Lines, Ursodeoxycholic Acid Increases Antioxidant Expression and Prevents DNA Damage by Bile Acids.
Abstract Hydrophobic bile acids like deoxycholic acid (DCA), which cause oxidative DNA damage and activate NF-κB in Barrett's metaplasia, might contribute to carcinogenesis in Barrett's esophagus. We have explored mechanisms whereby ursodeoxycholic acid (UDCA, a hydrophilic bile acid) protects against DCA-induced injury in vivo in patients and in vitro using non-neoplastic, telomerase-immortalized Barrett's cell lines. We took biopsies of Barrett's esophagus from 21 patients before and after esophageal perfusion with DCA (250 µM) at baseline, and after 8 weeks of oral UDCA treatment. DNA damage was assessed by p...
Source: Am J Physiol Gastroi... - May 22, 2014 Category: Gastroenterology Authors: Peng S, Huo X, Rezaei D, Zhang Q, Zhang X, Yu C, Asanuma K, Cheng E, Pham TH, Wang DH, Chen M, Souza RF, Spechler SJ Tags: Am J Physiol Gastrointest Liver Physiol Source Type: research

Sphingosine kinase 1 expressed by endothelial colony-forming cells has a critical role in their revascularization activity
Conclusion The up-regulation of SphK1 and S1P-dependent pathways is critical for the angiogenic/vasculogenic activity of ECFCs. The identification of this pathway provides attractive targets to optimize cell-based therapy for revascularization in ischaemic diseases.
Source: Cardiovascular Research - June 20, 2014 Category: Cardiology Authors: Poitevin, S., Cussac, D., Leroyer, A. S., Albinet, V., Sarlon-Bartoli, G., Guillet, B., Hubert, L., Andrieu-Abadie, N., Couderc, B., Parini, A., Dignat-George, F., Sabatier, F. Tags: Vascular biology Source Type: research

In Barrett's esophagus patients and Barrett's cell lines, ursodeoxycholic acid increases antioxidant expression and prevents DNA damage by bile acids
Hydrophobic bile acids like deoxycholic acid (DCA), which cause oxidative DNA damage and activate NF-B in Barrett's metaplasia, might contribute to carcinogenesis in Barrett's esophagus. We have explored mechanisms whereby ursodeoxycholic acid (UDCA, a hydrophilic bile acid) protects against DCA-induced injury in vivo in patients and in vitro using nonneoplastic, telomerase-immortalized Barrett's cell lines. We took biopsies of Barrett's esophagus from 21 patients before and after esophageal perfusion with DCA (250 μM) at baseline and after 8 wk of oral UDCA treatment. DNA damage was assessed by phospho-H2AX expression,...
Source: AJP: Gastrointestinal and Liver Physiology - July 15, 2014 Category: Gastroenterology Authors: Peng, S., Huo, X., Rezaei, D., Zhang, Q., Zhang, X., Yu, C., Asanuma, K., Cheng, E., Pham, T. H., Wang, D. H., Chen, M., Souza, R. F., Spechler, S. J. Tags: CALL FOR PAPERS Source Type: research

Role ofTranscription Factor CCAAT/Enhancer Binding Protein Alphain Human Fetal LiverCell Typesin vitro
ConclusionsWe demonstrated that the effects of C/EBPα are specific for the different human fetal liver cell types, using an advanced three‐dimensional perfusion bioreactor as a humanin vivo‐like model.
Source: Hepatology Research - September 5, 2014 Category: Internal Medicine Authors: Jörg C. Gerlach, Patrick Over, Hubert G. Foka, Morris E. Turner, Robert L. Thompson, Bruno Gridelli, Eva Schmelzer Tags: Original Article Source Type: research

Role of transcription factor CCAAT/enhancer‐binding protein alpha in human fetal liver cell types in vitro
ConclusionWe demonstrated that the effects of C/EBPα are specific for the different human fetal liver cell types, using an advanced 3‐D perfusion bioreactor as a human in vivo‐like model.
Source: Hepatology Research - October 9, 2014 Category: Internal Medicine Authors: Jörg C. Gerlach, Patrick Over, Hubert G. Foka, Morris E. Turner, Robert L. Thompson, Bruno Gridelli, Eva Schmelzer Tags: Original Article Source Type: research

Pannexin 1 Channels Mediate the Release of ATP into the Lumen of the Rat Urinary Bladder.
This article is protected by copyright. All rights reserved. PMID: 25630792 [PubMed - as supplied by publisher]
Source: The Journal of Physiology - January 29, 2015 Category: Physiology Authors: Beckel JM, Daugherty SL, Tyagi P, Wolf-Johnston AS, Birder LA, Mitchell CH, de Groat WC Tags: J Physiol Source Type: research

Dopamine induces growth inhibition and vascular normalization through reprograming M2-polarized macrophages in rat C6 glioma.
Abstract Dopamine (DA), a monoamine catecholamine neurotransmitter with antiangiogenic activity, stabilizes tumor vessels in colon, prostate and ovarian cancer, thus increases chemotherapeutic efficacy. Here, in the rat C6 glioma models, we investigated the vascular normalization effects of DA and its mechanisms of action. DA (25, 50 mg/kg) inhibited tumor growth, while a precursor of DA (levodopa) prolonged the survival time of rats bearing orthotopic C6 glioma. DA improved tumor perfusion, with significant effects from day 3, and a higher level at day 5 to 7. In addition, DA decreased microvessel density and hyp...
Source: Toxicology and Applied Pharmacology - March 25, 2015 Category: Toxicology Authors: Qin T, Wang C, Chen X, Duan C, Zhang X, Zhang J, Chai H, Tang T, Chen H, Yue J, Li Y, Yang J Tags: Toxicol Appl Pharmacol Source Type: research

Abstract 1265: LAMP2 overexpression in the plasma membrane of breast cancer cells in response of chronic acidosis as a new imaging and therapeutic target
A combination of poor vasculature perfusion, hypoxia, and increased flux of carbons through fermentative glycolysis lead to extracellular acidosis in solid tumors; with extracellular pH values as low as 6.5. The proton concentration increases within the lumen due to diffusion limitations and increased production of acid from hypoxic-glycolytic cells, causing the interior of the lumen to become highly acidic. The glycolytic phenotype can become “hardwired” as Warburg proposed, leading to the continued generation of metabolic acids even in well-oxygenated conditions. This acidified habitat is constant and imparts a Darwi...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Damaghi, M., Sprung, R., Tafreshi, N., Estrella, V., Koomen, J., Morse, D., Gillies, R. Tags: Molecular and Cellular Biology Source Type: research

Abstract 5222: Endothelial plasticity generates aberrant angiogenesis and therapy resistance in glioblastoma
Overgrown, abnormal vasculature characterizes the microenvironment that fuels cancer progression and induces therapeutic resistance. Here we reveal that endothelial plasticity drives excessive and abnormal tumor angiogenesis. Glioblastoma multiforme (GBM) is among the most lethal of human malignancies, distinguished by prominent vascularity and extreme vascular abnormality. We identify endothelial fibro-transformation (Endo-FT) in GBM, contributing significantly to aberrant vascularization, tumor progression, and therapeutic resistance. Utilizing human GBM specimens and allograft and genetic murine GBM models driven by RCA...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Huang, M., Fan, Y. Tags: Tumor Biology Source Type: research

Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) Promotes Angiogenesis and Ischemia-Induced Neovascularization Via NADPH Oxidase 4 (NOX4) and Nitric Oxide-Dependent Mechanisms Coronary Heart Disease
Conclusions This is the first report demonstrating that TRAIL can promote angiogenesis following hindlimb ischemia in vivo. The angiogenic effect of TRAIL on human microvascular endothelial cell-1 cells is downstream of fibroblast growth factor-2, involving NOX4 and nitric oxide signaling. These data have significant therapeutic implications, such that TRAIL may improve the angiogenic response to ischemia and increase perfusion recovery in patients with cardiovascular disease and diabetes.
Source: JAHA:Journal of the American Heart Association - November 16, 2015 Category: Cardiology Authors: Di Bartolo, B. A., Cartland, S. P., Prado-Lourenco, L., Griffith, T. S., Gentile, C., Ravindran, J., Azahri, N. S. M., Thai, T., Yeung, A. W. S., Thomas, S. R., Kavurma, M. M. Tags: Coronary Heart Disease Source Type: research

Liraglutide protects cardiac microvascular endothelial cells against hypoxia/reoxygenation injury through the suppression of the SR-Ca(2+)-XO-ROS axis via activation of the GLP-1R/PI3K/Akt/Survivin pathways.
Abstract Microvascular endothelial cells (CMECs) oxidative damage resulting from hypoxia/reoxygenation (H/R) injury is responsible for microcirculation perfusion disturbances and the progression of cardiac dysfunction. However, few strategies are available to reverse such pathologies. Here, we studied the effects and mechanisms of liraglutide on CEMCs oxidative damage, focusing in particular on calcium overload-triggered free radical injury signals and the GLP-1R/PI3K/Akt/Survivin survival pathways. The results indicate that H/R increased IP3R expression but reduced SERCA2a expression, which rapidly raised intrace...
Source: Free Radical Biology and Medicine - March 29, 2016 Category: Biology Authors: Zhang Y, Zhou H, Wu W, Shi C, Hu S, Yin T, Ma Q, Han T, Zhang Y, Tian F, Chen Y Tags: Free Radic Biol Med Source Type: research