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albumin human [keywords]
- Human Serum Albumin Cys(34) Oxidative Modifications following Infiltration in the Carotid Atherosclerotic Plaque. [Journal Article]
- Oxid Med Cell Longev 2014.:690953.
Objectives.To evaluate if the prooxidant environment present in atherosclerotic plaque may oxidatively modify filtered albumin. Methods. Fluorescein-5-maleimide labelled plasma samples and plaque extracts from 27 patients who had undergone carotid endarterectomy were analysed through nonreducing SDS-PAGE for albumin-Cys(34) oxidation. Furthermore, degree and pattern of S-thiolation in both circulating and plaque-filtered albumin were assayed.
Results.Albumin filtered in the atherosclerotic plaque showed higher levels of Cys(34) oxidative modifications than the corresponding circulating form as well as different patterns of S-thiolation.
Conclusions.Data indicate that the circulating albumin, once filtered in plaque, undergoes Cys(34) oxidative modifications and demonstrate for the first time that albumin is a homocysteine and cysteinylglycine vehicle inside the plaque environment.
- Serum enhanced cytokine responses of macrophages to silica and iron oxide particles and nanomaterials: a comparison of serum to lung lining fluid and albumin dispersions. [JOURNAL ARTICLE]
- J Appl Toxicol 2014 Apr 16.
The potential hazard to humans exposed to nanomaterials such as silica and iron oxide was investigated using an in vitro macrophage cell culture system. Amorphous silica and iron oxide particles and nanomaterials (NMs) were dispersed in cell culture medium supplemented with either bovine serum albumin (BSA), lung lining fluid (LLF) or serum, in order to mimic the body fluids encountered during different routes of exposure in the body. End points investigated included macrophage viability and cytokine production. Silica NMs and particles (50 and 200 nm, respectively) were unmodified (plain) or aminated (NH2 ). Iron oxide NMs and particles, Fe3 O4 45 nm and Fe2 O3 280 nm were also used in this study. Silica particles and NMs induced a dose-dependent increase in cytotoxicity as measured by lactate dehydrogenase (LDH) release. Serum enhanced silica-induced interleukin (IL)-6, IL-10, IL-1β and MCP-1 release, whereas albumin partially inhibited MCP-1 release. Aminated silica, 50 nm was more potent than the 200-nm particles at inducing monocyte chemoattractant protein-1 (MCP-1) production when dispersed in medium or LLF, suggesting a size specific effect for these particles and this cytokine. Iron oxide particles were relatively inert compared with the silica particles and NMs; however, serum and albumin did affect cytokine release in some treatments. In conclusion, the data suggests that serum, compared with medium, BSA and LLF is very potent at enhancing macrophage responses to silica and iron oxide particles and NMs. Size was only influential in LLF for a limited number of parameters, whereas surface chemistry was not of consequence in this in vitro macrophage system. Copyright © 2014 John Wiley & Sons, Ltd.
- Spectroscopic investigations of the interaction of the anti‑hypertension drug valsartan with human serum albumin. [JOURNAL ARTICLE]
- Mol Med Rep 2014 Apr 9.
The aim of the present study was to investigate the interaction between valsartan, an anti‑hypertension drug, and human serum albumin (HSA) using spectroscopic techniques, including fluorescence, ultraviolet‑visible absorption, synchronous fluorescence and circular dichroism (CD). The results demonstrated that valsartan and HSA form a complex and that a static quenching mechanism occurs. In addition, the binding constant and the number of binding sites for valsartan on HSA were analyzed. Hydrophobic interactions and hydrogen bonds were the predominant forces in the association reaction based on thermodynamic parameters. The distance between the donor (HSA) and the acceptor (valsartan) was 1.994 nm as derived from Forster's theory. Alterations in the secondary structure of HSA in the presence of valsartan were assessed using synchronous fluorescence and CD. This study provides an enhanced understanding of the pharmacodynamic effects of valsartan on the physiologically important protein HSA.
- Engineering Theranostic Nanovehicles Capable of Targeting Cerebrovascular Amyloid Deposits. [JOURNAL ARTICLE]
- J Control Release 2014 Apr 12.
Cerebral amyloid angiopathy (CAA), is characterized by the deposition of amyloid beta (Aβ) proteins within the walls of the cerebral vasculature with subsequent aggressive vascular inflammation leading to recurrent hemorrhagic strokes. The objective of the study was to develop theranostic nanovehicles (TNVs) capable of a) targeting cerebovascular amyloid; b) providing magnetic resonance imaging (MRI) contrast for the early detection of CAA; and c) treating cerebrovascular inflammation resulting from CAA. The TNVs comprised of a polymeric nanocore made from Magnevist® (MRI contrast agent) conjugated chitosan. The nanocore was also loaded with cyclophosphamide (CYC), an immunosuppressant shown to reduce the cerebrovascular inflammation in CAA. Putrescine modified F(ab')2 fragment of anti-amyloid antibody, IgG4.1, (pF(ab')24.1) was conjugated to the surface of the nanocore to target cerebrovascular amyloid. The average size of the control chitosan nanoparticles (conjugated with albumin and are devoid of Magnevist®, CYC, and pF(ab')24.1) was 164±1.2nm and that of the TNVs was 239±4.1nm. The zeta potential values of the CCNs and TNVs were 21.6±1.7mV and 11.9±0.5mV, respectively. The leakage of Magnevist® from the TNVs was a modest 0.2% over 4days, and the CYC release from the TNVs followed Higuchi's model that describe sustained drug release from polymeric matrices. The studies conducted in polarized human microvascular endothelial cell monolayers (hCMEC/D3) in vitro as well as in mice in vivo have demonstrated the ability of TNVs to target cerebrovascular amyloid. In addition, the TNVs provided contrast for imaging cerebrovascular amyloid using MRI and single photon emission computed tomography. Moreover, the TNVs were shown to reduce pro-inflammatory cytokine production by the Aβ challenged blood brain barrier (BBB) endothelium more effectively than the cyclophosphamide alone.
- A Tumor Environment Responsive Doxorubicin-loaded Nanoparticle for Targeted Cancer Therapy. [JOURNAL ARTICLE]
- Mol Pharm 2014 Apr 15.
Doxorubicin (DOX) is a potent cancer chemotherapeutic agent but its clinical use is severely limited by potentially lethal cardiotoxicity. Delivery of DOX by particulate carriers can be an effective way to reduce its distribution in cardiac tissue. In the present study, we developed a self-assembled, tumor-microenvironment-responsive delivery system for DOX. The core of the carrier was built upon the DOX/DNA intercalation, which was further combined with cationic gelatin (C-gel) to form the complex GDD. GDD was then packaged into a complex, namely HDD, based on the electrostatic interactions between the positively charged C-gel and negatively charged human serum albumin (HSA). The HSA molecules on the surface of the complex HDD effectively helped the particle evade the filtration of the body when injected into the circulation and passively accumulate into the tumor sites. After entering the tumor tissue, where albumin is rapidly consumed, GDD was release from HDD and the C-gel was then digested by the tumor-specific matrix metalloproteinase (MMPs) to free the DOX/DNA intercalation. Deoxyribonucleases (DNases) in the tissue could completely destroy the DNA molecules to release DOX into the microenvironments. After a series of in vitro optimization tests, we evaluated the anti-cancer capacity and cardiac toxicity of HDD in two animal models with cancer. The results suggested that HDD had a higher anti-cancer efficacy and a significantly lower cardiotoxicity than free DOX. Additionally, the main components of the carrier are all clinically approved materials. Taken together, our present delivery system is safe, efficient and has high potential for further clinical trials.
- MicroRNA-122 Overexpression Promotes Hepatic Differentiation of Human Adipose Tissue-Derived Stem Cells. [JOURNAL ARTICLE]
- J Cell Biochem 2014 Apr 15.
MicroRNAs are the regulatory molecules in post-transcriptional regulation of gene expression, which affect diverse biological processes and have been found to play important roles in regulating stem cell character in plants and animals. The aim of this study was to identify the role of miR-122 during hepatic differentiation of human adipose tissue-derived stem cells (hADSCs), and also to investigate whether overexpression of miR-122 could enhance differentiation of ADSCs toward functional hepatocyte-like cells without any extrinsic factor. To investigate this, the level of miR-122 was monitored by quantitative real-time PCR (qRT-PCR) at specific time intervals following hepatic differentiation of hADSCs using growth factors. For the next step, lentiviral transduction was applied to overexpress miR-122 in hADSCs for up to 21 days. Hepatic functionality was evaluated by analyzing specific hepatocyte genes and biochemical markers at different time points of differentiation induction. The qRT-PCR results revealed that miR-122 was upregulated during hepatic differentiation of hADSCs. Additionally, the stable miR-122 overexpression in hADSCs resulted in increased expression of specific hepatocyte markers such as ALB, AFP, CK18, CK19, and HNF4a compared with the negative control cells. Moreover, urea and albumin production as well as glycogen deposits were observed in the treated cells. Therefore, our findings demonstrate that the hepatic differentiation process could be improved by the overexpression of miR-122 in hADSCs, making it a potential therapeutic resource for liver disorders. J. Cell. Biochem. © 2014 Wiley Periodicals, Inc.
- Transcompartmental Inflammatory Responses in Humans: IV Versus Endobronchial Administration of Endotoxin. [JOURNAL ARTICLE]
- Crit Care Med 2014 Apr 11.
Transcompartmental signaling during early inflammation may lead to propagation of disease to other organs. The time course and the mechanisms involved are still poorly understood. We aimed at comparing acute transcompartmental inflammatory responses in humans following lipopolysaccharide-induced pulmonary and systemic inflammation.Randomized, double-blind, placebo-controlled, crossover study.Healthy male volunteers.Fifteen volunteers (mean age, 23; SD, 2 yr) received Escherichia coli endotoxin (lipopolysaccharide, 4 ng/kg) IV or endobronchially on two different study days. Groups were evaluated by bronchoalveolar lavage at baseline (0 hr) and 2, 4, 6, 8, or 24 hours postchallenge. Cardiorespiratory variables were continuously recorded throughout the study day, and plasma and bronchoalveolar lavage fluid markers of inflammation were measured.IV endotoxin elicited a systemic inflammatory response with a time-dependent increase and peak in tumor necrosis factor-α, interleukin-6, and leukocyte counts (all p < 0.001). Furthermore, a delayed (6-8 hr) increase in bronchoalveolar lavage fluid interleukin-6 concentration (p < 0.001) and alveolar leukocyte count (p = 0.03) and a minor increase in bronchoalveolar lavage fluid tumor necrosis factor-α were observed (p = 0.06). Endobronchial endotoxin was followed by progressive alveolar neutrocytosis and increased bronchoalveolar lavage fluid tumor necrosis factor-α, interleukin-6, and albumin (all p < 0.001); a systemic inflammatory response was observed after 2-4 hours, with no change in plasma tumor necrosis factor-α.Acute lung or systemic inflammation in humans is followed by a transcompartmental proinflammatory response, the degree and differential kinetics of which suggests that the propagation of inflammation may depend on the primary site of injury.
- Vitamin D binding protein and vitamin D in human allergen-induced endobronchial inflammation. [JOURNAL ARTICLE]
- Clin Exp Immunol 2014 Apr 14.
Allergic asthma is a chronic disease of the airways associated with airway hyperresponsiveness, a variable degree of airflow obstruction, airway remodeling, and a characteristic airway inflammation. Factors of the vitamin D axis, which include vitamin D metabolites and vitamin D binding protein (VDBP), have been linked to asthma but only few data exist about their regulation in the lung during acute allergen-induced airway inflammation. Therefore, we analysed the regulation of factors of the vitamin D axis during the early and late-phase reaction of allergic asthma. 15 patients with mild allergic asthma underwent segmental allergen challenge. VDBP was analyzed in bronchoalveolar lavage fluid (BALF) and serum using ELISA technique. 25-hydroxyvitamin D3 (25(OH)D3 ) and 1,25-dihydroxyvitamin D3 (1,25(OH)2 D3 ) were analyzed by a commercial laboratory using LC/MS-technique. VDBP (median 2.3, range 0.2 - 7.1 μg/ml), 25(OH)D3 (median 0.060, range < 0.002 - 3.210 ng/ml), and 1,25(OH)2 D3 (median < 0.1, range < 0.1 - 2.8 pg/ml) were significantly elevated in BALF 24 hours but not 10 minutes after allergen challenge. After correction for plasma leakage using the plasma marker protein albumin, VDBP and 25(OH)D3 were still significantly increased while 1,25(OH)2 D3 was not. VDBP and 25(OH)D3 were correlated with each other and with the inflammatory response 24 hours after allergen challenge. Serum concentrations of all three factors were not influenced by allergen challenge. In conclusion, we report a significant increase in VDBP and 25(OH)D3 in human BALF 24 hours after allergen challenge suggesting a role for these factors in the asthmatic late-phase reaction.
- Phenotypic and in vivo functional characterization of immortalized human fetal liver cells. [JOURNAL ARTICLE]
- Scand J Gastroenterol 2014 Apr 15.
Abstract We report the establishment and characterization of immortalized human fetal liver progenitor cells by expression of the Simian virus 40 large T (SV40 LT) antigen. Well-characterized cells at various passages were transplanted into nude mice with acute liver injury and tested for functional capacity. The SV40LT antigen-immortalized fetal liver cells showed a morphology similar to primary cells. Cultured cells demonstrated stable phenotypic expression in various passages, of hepatic markers such as albumin, CK 8, CK18, transcription factors HNF-4α and HNF-1α and CYP3A/7. The cells did not stain for any of the tested cancer-associated markers. Albumin, HNF-4α and CYP3A7 expression was confirmed by reverse transcription polymerase chain reaction (RT-PCR). Flow cytometry showed expression of some progenitor cell markers. In vivo study showed that the cells expressed both fetal and differentiated hepatocytes markers. Our study suggests new approaches to expand hepatic progenitor cells, analyze their fate in animal models aiming at cell therapy of hepatic diseases.
- Carbon nanofibers and carbon nanotubes sensitize prostate and bladder cancer cells to platinum-based chemotherapeutics. [Journal Article]
- J Biomed Nanotechnol 2014 Mar; 10(3):463-77.
Recent data suggest that carbon nanomaterials can act as antitumor agents themselves by increasing the efficiency of cytotoxic agents when applied in combination. Here, carbon nanofibers (CNFs) and multi-walled carbon nanotubes (CNTs) were investigated regarding their impact on cellular function, cellular uptake and ability to sensitize cancer cells of urological origin to the conventional chemotherapeutics cisplatin and carboplatin. CNFs and CNTs (1-200 microg/ml) showed a low to moderate impairment of cellular function with CNFs being more deleterious than CNTs. Inhibition of cellular viability by the nanomaterials was about 20% at most. In combinatory treatments, CNFs and CNTs markedly enhanced the effects of cisplatin and carboplatin on cellular viability by 1.2- to 2.8-fold in prostate, bladder and cisplatin-resistant prostate cancer cells in comparison to the individual effects of the chemotherapeutics. Particularly the cell viability-diminishing effect of CNFs alone and in combination with the chemotherapeutics was more pronounced with dispersions prepared with human serum albumin than with phospholipid-polyethylene glycol. Albumin might mediate the cellular uptake of carbon nanomaterials which was underlined by the co-localization of albumin and carbon nanomaterials along the cellular surface as evidenced by fluorescence microscopy. Transmission electron microscopy revealed that both carbon nanomaterials were internalized by cancer cells, thereby possibly leading to an enhanced accumulation of the chemotherapeutic drugs. In fact, CNFs enhanced the cellular accumulation of carboplatin by 28% as compared to the single treatment with carboplatin. In conclusion, carbon nanomaterial-based applications could present a new strategy to overcome chemoresistance by sensitizing cancer cells to conventional chemotherapeutics.