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51.
Parisa Koutsifeli Upasna Varma Lorna J. Daniels Marco Annandale Xun Li Joshua P.H. Neale Sarah Hayes Kate L. Weeks Samuel James Lea M.D. Delbridge Kimberley M. Mellor 《The Journal of biological chemistry》2022,298(7)
Autophagy is an essential cellular process involving degradation of superfluous or defective macromolecules and organelles as a form of homeostatic recycling. Initially proposed to be a “bulk” degradation pathway, a more nuanced appreciation of selective autophagy pathways has developed in the literature in recent years. As a glycogen-selective autophagy process, “glycophagy” is emerging as a key metabolic route of transport and delivery of glycolytic fuel substrate. Study of glycophagy is at an early stage. Enhanced understanding of this major noncanonical pathway of glycogen flux will provide important opportunities for new insights into cellular energy metabolism. In addition, glycogen metabolic mishandling is centrally involved in the pathophysiology of several metabolic diseases in a wide range of tissues, including the liver, skeletal muscle, cardiac muscle, and brain. Thus, advances in this exciting new field are of broad multidisciplinary interest relevant to many cell types and metabolic states. Here, we review the current evidence of glycophagy involvement in homeostatic cellular metabolic processes and of molecular mediators participating in glycophagy flux. We integrate information from a variety of settings including cell lines, primary cell culture systems, ex vivo tissue preparations, genetic disease models, and clinical glycogen disease states. 相似文献
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Davoodi P Mahesh PA Holla AD Vijayakumar GS Jayaraj BS Chandrashekara S Ramachandra NB 《Cytokine》2012,60(2):431-437
Serum protein analysis for noninvasive quantification of airway inflammation in asthma is a promising research tool in the field of lung diseases. Cytokines are believed to have major role in inflammatory process of the airways of the lung. There is an imbalance between T-helper (Th)-2 cells, which secrete interleukin (IL)-4 and interleukin (IL)-13, and Th1 cells, which secrete interferon (IFN)-gamma in asthma. To test the hypothesis that serum IL-13 and IL-4 levels may be elevated whereas IFN-gamma would be decreased in this cohort of patients, a property that could make them possible candidate biomarkers in determining asthma occurrence and severity, we measured concentrations of IL-4, IL-13 and IFN-gamma in serum samples of 88 subjects (44 normal, 12 with mild asthma, 16 with moderate asthma, and 16 with severe asthma). Serum Levels of IL-4, IL-13, and IFN-gamma were determined by an enzyme-linked immune-sorbent assay (ELISA). Median serum level of IFN-gamma in asthmatic patients was 8.0pg/ml, while it was 11.4pg/ml in healthy controls. However, the difference was not significant. Among the different age groups in whom IFN-gamma was assessed, the highest median value in both cases and controls was observed in the age group of 31-40years. The median serum level of IL-13 was 40.0pg/ml in asthmatic patients and 58.25pg/ml in healthy controls. The difference was not significant. On subgroup analysis, no significant difference of IFN-gamma and IL-13 between asthma of different severities was observed. The study also revealed nonsignificant difference of serum cytokines with the duration of asthma, number of allergens, and severity of sensitization. Normal serum levels of IFN-gamma and IL-13 in asthmatic patients suggest their neutral role in the inflammatory process; however, more studies are required to establish the effect of these cytokines in adulthood asthma in different ethnic populations. 相似文献
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Parisa Teimoori Baghaee Atena Donya 《Journal of biomolecular structure & dynamics》2019,37(9):2254-2264
The binding of malathion to human serum albumin (HSA) in the presence of silver nanoparticles (AgNPs) was investigated for the first time by multiple spectroscopic methods such as fluorescence quenching, fluorescence resonance energy transfer (FRET), circular dichroism, red-edge excitation shift (REES), synchronous fluorescence and three dimensional fluorescence spectroscopy under physiological conditions .The results indicated that binding of malathion to HSA induced fluorescence quenching through static mechanism. The number of binding sites was calculated by double logarithmic equation. Changes in the micro-environment of the fluorophore residues were also probed by synchronous fluorescence spectroscopy and REES. Changes of secondary structure of HSA in HSA–malathion complex was verified by circular dichroism approach in the presence of AgNPs that showed the electrostatic interaction changes in the protein structure. The binding average distance (r) between the donor (HSA) and the acceptor (malathion) was measured and found to be 1.63?nm according to the Forster’s theory of non-radiation energy transfer which was <7?nm confirmed the existence of static quenching in the presence of AgNPs. The conformational changes of HSA by three-dimensional fluorescence spectroscopy were studied. By comparing the resonance light scattering in the binary and ternary systems, we could estimate the effect of AgNPs on the precipitation of the malathion on the HSA. Generally we have discussed the toxicity reduction effect of malathion in food industrial by the results of spectroscopy techniques. 相似文献
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Winkeler A Sena-Esteves M Paulis LE Li H Waerzeggers Y Rückriem B Himmelreich U Klein M Monfared P Rueger MA Heneka M Vollmar S Hoehn M Fraefel C Graf R Wienhard K Heiss WD Jacobs AH 《PloS one》2007,2(6):e528
Strategies for non-invasive and quantitative imaging of gene expression in vivo have been developed over the past decade. Non-invasive assessment of the dynamics of gene regulation is of interest for the detection of endogenous disease-specific biological alterations (e.g., signal transduction) and for monitoring the induction and regulation of therapeutic genes (e.g., gene therapy). To demonstrate that non-invasive imaging of regulated expression of any type of gene after in vivo transduction by versatile vectors is feasible, we generated regulatable herpes simplex virus type 1 (HSV-1) amplicon vectors carrying hormone (mifepristone) or antibiotic (tetracycline) regulated promoters driving the proportional co-expression of two marker genes. Regulated gene expression was monitored by fluorescence microscopy in culture and by positron emission tomography (PET) or bioluminescence (BLI) in vivo. The induction levels evaluated in glioma models varied depending on the dose of inductor. With fluorescence microscopy and BLI being the tools for assessing gene expression in culture and animal models, and with PET being the technology for possible application in humans, the generated vectors may serve to non-invasively monitor the dynamics of any gene of interest which is proportionally co-expressed with the respective imaging marker gene in research applications aiming towards translation into clinical application. 相似文献
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Botulinum neurotoxin type A modulates vesicular release of glutamate from satellite glial cells 下载免费PDF全文
Larissa Bittencourt da Silva Jeppe Nørgaard Poulsen Lars Arendt‐Nielsen Parisa Gazerani 《Journal of cellular and molecular medicine》2015,19(8):1900-1909
This study investigated the presence of cell membrane docking proteins synaptosomal‐associated protein, 25 and 23 kD (SNAP‐25 and SNAP‐23) in satellite glial cells (SGCs) of rat trigeminal ganglion; whether cultured SGCs would release glutamate in a time‐ and calcium‐dependent manner following calcium‐ionophore ionomycin stimulation; and if botulinum neurotoxin type A (BoNTA), in a dose‐dependent manner, could block or decrease vesicular release of glutamate. SGCs were isolated from the trigeminal ganglia (TG) of adult Wistar rats and cultured for 7 days. The presence of SNAPs in TG sections and isolated SGCs were investigated using immunohistochemistry and immunocytochemistry, respectively. SGCs were stimulated with ionomycin (5 μM for 4, 8, 12 and 30 min.) to release glutamate. SGCs were then pre‐incubated with BoNTA (24 hrs with 0.1, 1, 10 and 100 pM) to investigate if BoNTA could potentially block ionomycin‐stimulated glutamate release. Glutamate concentrations were measured by ELISA. SNAP‐25 and SNAP‐23 were present in SGCs in TG sections and in cultured SGCs. Ionomycin significantly increased glutamate release from cultured SGCs 30 min. following the treatment (P < 0.001). BoNTA (100 pM) significantly decreased glutamate release (P < 0.01). Results from this study demonstrated that SGCs, when stimulated with ionomycin, released glutamate that was inhibited by BoNTA, possibly through cleavage of SNAP‐25 and/or SNAP‐23. These novel findings demonstrate the existence of vesicular glutamate release from SGCs, which could potentially play a role in the trigeminal sensory transmission. In addition, interaction of BoNTA with non‐neuronal cells at the level of TG suggests a potential analgesic mechanism of action of BoNTA. 相似文献
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Ghabaee M Bayati A Amri Saroukolaei S Sahraian MA Sanaati MH Karimi P Houshmand M Sadeghian H Hashemi Chelavi L 《Cellular and molecular neurobiology》2009,29(1):109-114
Multiple sclerosis (MS) is prototype of inflammatory demyelinating disease of the central nervous system .The etiology of
MS remains unclear, but according to current data the disease develops in genetically susceptible individuals and may require
additional environmental triggers. The human leukocyte antigen (HLA) class II alleles (DRB1*1501, DQA1*0102, DQB1*0602) may
have the strongest genetic effect in MS. In this study, the role of these alleles were investigated in 183 Iranian patients
with multiple sclerosis and compared with 100 healthy individuals. HLA typing for DRB1*1501, DQA1*0102, DQB1*0602 was performed
by polymerase chain reaction (PCR) amplification with sequence-specific primers (PCR-SSP) method. The results show that, HLA
DR B1*1501 was significantly more frequent among MS patients (46% vs. 20%, PV = 0.0006) but DQA1*0102 haplotype was negatively
associated with MS (30% vs. 50%, PV = 0.0049) and no significant association was found with DQB1*0602 and MS patients in comparison
with control group (24% and 30%, PV = 0.43). No significant correlation was observed among these alleles with sex, type of
disease; initial symptoms, expanded disability status scale (EDSS), as well as age at onset and familial MS. This study therefore
indicates that there is no association of above HLA haplotypes with clinical presentation, disease duration, and disability
in Iranian patients with MS which is in line with other previous studies in different ethnic groups. 相似文献
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Runnels JM Zamiri P Spencer JA Veilleux I Wei X Bogdanov A Lin CP 《Molecular imaging》2006,5(1):31-40
Molecular expression on the vascular endothelium is critical in regulating the interaction of circulating cells with the blood vessel wall. Leukocytes as well as circulating cancer cells gain entry into tissue by interacting with adhesion molecules on the endothelial cells (EC). Molecular targets on the EC are increasingly being explored for tissue-specific delivery of therapeutic and imaging agents. Here we use in vivo immunofluorescence microscopy to visualize the endothelial molecular expression in the vasculature of live animals. High-resolution images are obtained by optical sectioning through the intact skin using in vivo confocal and multiphoton microscopy after in situ labeling of EC surface markers with fluorescent antibodies. Other vascular beds such as the bone marrow and ocular blood vessels can be imaged with little or no tissue manipulation. Live imaging is particularly useful for following the dynamic expression of inducible molecules such as E-selectin during an inflammatory response. 相似文献
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Sharif Moradi Parisa Torabi Saeed Mohebbi Sara Amjadian Piter Bosma Farnoush Faridbod Vahid Khoddami Morteza Hosseini Sadegh Babashah Maryam Ghotbaddini Arezoo Rasti Faezeh Shekari Hamid Sadeghi-Abandansari Jafar Kiani Mehdi Shamsara Mohammad Kazemi-Ashtiani Samira Gholami 《BioEssays : news and reviews in molecular, cellular and developmental biology》2020,42(6):2000042