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Renu Goel Krishna R Murthy Srinivas M Srikanth Sneha M Pinto Mitali Bhattacharjee Dhanashree S Kelkar Anil K Madugundu Gourav Dey Sujatha S Mohan Venkatarangaiah Krishna TS Keshava Prasad Shukti Chakravarti HC Harsha Akhilesh Pandey 《Clinical proteomics》2013,10(1):9
Background
The ciliary body is the circumferential muscular tissue located just behind the iris in the anterior chamber of the eye. It plays a pivotal role in the production of aqueous humor, maintenance of the lens zonules and accommodation by changing the shape of the crystalline lens. The ciliary body is the major target of drugs against glaucoma as its inhibition leads to a drop in intraocular pressure. A molecular study of the ciliary body could provide a better understanding about the pathophysiological processes that occur in glaucoma. Thus far, no large-scale proteomic investigation has been reported for the human ciliary body.Results
In this study, we have carried out an in-depth LC-MS/MS-based proteomic analysis of normal human ciliary body and have identified 2,815 proteins. We identified a number of proteins that were previously not described in the ciliary body including importin 5 (IPO5), atlastin-2 (ATL2), B-cell receptor associated protein 29 (BCAP29), basigin (BSG), calpain-1 (CAPN1), copine 6 (CPNE6), fibulin 1 (FBLN1) and galectin 1 (LGALS1). We compared the plasma proteome with the ciliary body proteome and found that the large majority of proteins in the ciliary body were also detectable in the plasma while 896 proteins were unique to the ciliary body. We also classified proteins using pathway enrichment analysis and found most of proteins associated with ubiquitin pathway, EIF2 signaling, glycolysis and gluconeogenesis.Conclusions
More than 95% of the identified proteins have not been previously described in the ciliary body proteome. This is the largest catalogue of proteins reported thus far in the ciliary body that should provide new insights into our understanding of the factors involved in maintaining the secretion of aqueous humor. The identification of these proteins will aid in understanding various eye diseases of the anterior segment such as glaucoma and presbyopia. 相似文献3.
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Sonya B Dumanis Kelly A Chamberlain Yoo Jin Sohn Young Jin Lee Suzanne Y Guénette Toshiharu Suzuki Paul M Mathews Daniel TS Pak G William Rebeck Yoo-hun Suh Hee-Sae Park Hyang-Sook Hoe 《Molecular neurodegeneration》2012,7(1):1-15
Background
Loss-of-function mutations in PTEN-induced kinase 1 (PINK1) have been linked to familial Parkinson??s disease, but the underlying pathogenic mechanism remains unclear. We previously reported that loss of PINK1 impairs mitochondrial respiratory activity in mouse brains.Results
In this study, we investigate how loss of PINK1 impairs mitochondrial respiration using cultured primary fibroblasts and neurons. We found that intact mitochondria in PINK1?/? cells recapitulate the respiratory defect in isolated mitochondria from PINK1?/? mouse brains, suggesting that these PINK1?/? cells are a valid experimental system to study the underlying mechanisms. Enzymatic activities of the electron transport system complexes are normal in PINK1?/? cells, but mitochondrial transmembrane potential is reduced. Interestingly, the opening of the mitochondrial permeability transition pore (mPTP) is increased in PINK1?/? cells, and this genotypic difference between PINK1?/? and control cells is eliminated by agonists or inhibitors of the mPTP. Furthermore, inhibition of mPTP opening rescues the defects in transmembrane potential and respiration in PINK1?/? cells. Consistent with our earlier findings in mouse brains, mitochondrial morphology is similar between PINK1?/? and wild-type cells, indicating that the observed mitochondrial functional defects are not due to morphological changes. Following FCCP treatment, calcium increases in the cytosol are higher in PINK1?/? compared to wild-type cells, suggesting that intra-mitochondrial calcium concentration is higher in the absence of PINK1.Conclusions
Our findings show that loss of PINK1 causes selective increases in mPTP opening and mitochondrial calcium, and that the excessive mPTP opening may underlie the mitochondrial functional defects observed in PINK1?/? cells. 相似文献5.
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The invasive freshwater snail Tarebia granifera (Lamarck, 1822) was first reported in South Africa in 1999 and it has become widespread across the country, with some evidence to suggest that it reduces benthic macroinvertebrate biodiversity. The current study aimed to identify the primary abiotic drivers behind abundance patterns of T. granifera, by comparing the current abundance of the snail in three different regions, and at three depths, of the highly modified Nseleni River in KwaZulu-Natal, South Africa. Tarebia granifera was well established throughout the Nseleni River system, with an overall preference for shallow waters and seasonal temporal patterns of abundance. Although it is uncertain what the ecological impacts of the snail in this system are, its high abundances suggest that it should be controlled where possible and prevented from invading other systems in the region. 相似文献
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Numerical and structural karyotypic variability was investigated in the NBL-3-17 and NBL-3-11 “markerless” rat kangaroo kidney cell lines cultivated on a fibronectin-coated surface. For the NBL-3-17 cell line grown on a fibronectin-coated surface for periods of 1, 2, 4 and 8 days, the chromosome number distribution changed. These changes involved a significant decrease in the frequency of cells with the modal chromosome number and an increase in the frequency of cells with a lower chromosome number. Many new additional structural variants of the karyotype (SVK) appeared. The observed alterations seem to be due to the predominant adhesion of cells with a lower chromosome number, disturbances of the mitotic apparatus and selection for SVK adapted to the changes in culture conditions. Detachment of cells from the fibronectin-coated surface followed by 5 days cultivation on a hydrophilic surface restored the control cell distribution. For the NBL-3-11 cell line cultured on the fibronectin-coated surface for 1, 2, 4 and 8 days, the numerical karyotypic variability did not change compared to control variants. For the NBL-3-17 cell line grown on a fibronectin-coated surface for 1, 2, 4 and 8 days, the frequency of chromosomal aberrations also did not change relatively to the control. In the NBL-3-11 cell line, the frequency of chromosomal aberrations under the same conditions significantly increased, mainly due to chromosome and chromatid breaks and dicentrics (telomeric associations). The differences in the numerical and structural karyotypic variability between NBL-3-17 (hypotriploid) and NBL-3-11 (hypodiploid) cell lines cultivated on fibronectin are discussed. It is assumed that the observed differences in the karyotypic variability between these cell lines were determined by the specific karyotypic structure of the NBL-3-11 cell line and the altered gene expression of the NBL-3-17 hypotriploid cell line caused by increased doses of certain functioning genes. 相似文献
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Sairah Y Malkin Alexandra MF Rao Dorina Seitaj Diana Vasquez-Cardenas Eva-Maria Zetsche Silvia Hidalgo-Martinez Henricus TS Boschker Filip JR Meysman 《The ISME journal》2014,8(9):1843-1854
Recently, a novel mode of sulphur oxidation was described in marine sediments, in which sulphide oxidation in deeper anoxic layers was electrically coupled to oxygen reduction at the sediment surface. Subsequent experimental evidence identified that long filamentous bacteria belonging to the family Desulfobulbaceae likely mediated the electron transport across the centimetre-scale distances. Such long-range electron transfer challenges some long-held views in microbial ecology and could have profound implications for sulphur cycling in marine sediments. But, so far, this process of electrogenic sulphur oxidation has been documented only in laboratory experiments and so its imprint on the seafloor remains unknown. Here we show that the geochemical signature of electrogenic sulphur oxidation occurs in a variety of coastal sediment environments, including a salt marsh, a seasonally hypoxic basin, and a subtidal coastal mud plain. In all cases, electrogenic sulphur oxidation was detected together with an abundance of Desulfobulbaceae filaments. Complementary laboratory experiments in intertidal sands demonstrated that mechanical disturbance by bioturbating fauna destroys the electrogenic sulphur oxidation signal. A survey of published geochemical data and 16S rRNA gene sequences identified that electrogenic sulphide oxidation is likely present in a variety of marine sediments with high sulphide generation and restricted bioturbation, such as mangrove swamps, aquaculture areas, seasonally hypoxic basins, cold sulphide seeps and possibly hydrothermal vent environments. This study shows for the first time that electrogenic sulphur oxidation occurs in a wide range of marine sediments and that bioturbation may exert a dominant control on its natural distribution. 相似文献
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V. E. Yurinskaya A. V. Moshkov T. S. Goryachaya A. A. Vereninov 《Cell and Tissue Biology》2014,8(1):80-90
Lithium transport across the cell membrane is interesting in the light of general cell physiology and because of its alteration during numerous human diseases. The mechanism of Li+ transfer has been studied mainly in erythrocytes with a slow kinetics of ion exchange and therefore under the unbalanced ion distribution. Proliferating cultured cells with a rapid ion exchange have not been used practically in study of Li+ transport. In the present paper, the kinetics of Li+ uptake and exit, as well as its balanced distribution across the plasma membrane of U937 cells, were studied at minimal external Li+ concentrations and after the whole replacement of external Na+ for Li+. It is found that a balanced Li+ distribution attained at a high rate similar to that for Na+ and Cl? and that Li+/Na+ discrimination under balanced ion distribution at 1–10 mM external Li+ stays on 3 and drops to 1 following Na, K-ATPase pump blocking by ouabain. About 80% of the total Li+ flux across the plasma membrane under the balanced Li+ distribution at 5 mM external Li+ accounts for the equivalent Li+/Li+ exchange. The majority of the Li+ flux into the cell down the electrochemical gradient is a flux through channels and its small part may account for the NC and NKCC cotransport influxes. The downhill Li+ influxes are balanced by the uphill Li+ efflux involved in Li+/Na+ exchange. The Na+ flux involved in the countertransport with the Li+ accounts for about 0.5% of the total Na+ flux across the plasma membrane. The study of Li+ transport is an important approach to understanding the mechanism of the equivalent Li+/Li+/Na+/Na+ exchange, because no blockers of this mode of ion transfer are known and it cannot be revealed by electrophysiological methods. Cells cultured in the medium where Na+ is replaced for Li+ are recommended as an object for studying cells without the Na,K-ATPase pump and with very low intracellular Na+ and K+ concentration. 相似文献
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V. E. Yurinskaya T. S. Goryachaya A. A. Rubashkin A. V. Shirokova A. A. Vereninov 《Cell and Tissue Biology》2010,4(5):457-463
The K+, Na+, and Cl− balance and K+ (Rb+) and 36Cl− fluxes in U937 cells induced to apoptosis by 0.2 or 1 μM staurosporine were studied using flame emission and radioisotope
techniques. It is found that two-thirds of the total decrease in the amount of intracellular osmolytes in apoptotic cells
is accounted for by monovalent ions and one-third consists of other intracellular osmolytes. A decrease in the amount of monovalent
ions results from a decrease in the amount of K+ and Cl− and an increase in the Na+ content. The rate of 36Cl−, Rb+ (K+), and 22Na+ equilibration between cells and the medium was found to significantly exceed the rate of apoptotic change in the cellular
ion content, which indicates that unidirectional influxes and effluxes during apoptosis may be considered as being in near
balance. The drift of the ion flux balance in apoptosis caused by 0.2 μM staurosporine was found to be associated with the
increased ouabain-resistant Rb+ (K+) channel influx and insignificantly altered the ouabain-sensitive pump influx. Severe apoptosis induced by 1 μM staurosporine
is associated with reduced pump fluxes and slightly changed channel Rb+ (K+) fluxes. In apoptotic cells, the 1.4–1.8-fold decreased Cl− level is accompanied by a 1.2–1.6-fold decreased flux. 相似文献