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281.
We sought to determine the mechanism by which angiotensin II (ANGII) stimulates NADPH oxidase‐mediated superoxide (O2.?) production in bovine pulmonary artery smooth muscle cells (BPASMCs). ANGII‐induced increase in phospholipase D (PLD) and NADPH oxidase activities were inhibited upon pretreatment of the cells with chemical and genetic inhibitors of PLD2, but not PLD1. Immunoblot study revealed that ANGII treatment of the cells markedly increases protein kinase C‐α (PKC‐α), ‐δ, ‐ε, and ‐ζ levels in the cell membrane. Pretreatment of the cells with chemical and genetic inhibitors of PKC‐ζ, but not PKC‐α, ‐δ, and ‐ε, attenuated ANGII‐induced increase in NADPH oxidase activity without a discernible change in PLD activity. Transfection of the cells with p47phox small interfering RNA inhibited ANGII‐induced increase in NADPH oxidase activity without a significant change in PLD activity. Pretreatment of the cells with the chemical and genetic inhibitors of PLD2 and PKC‐ζ inhibited ANGII‐induced p47phox phosphorylation and subsequently translocation from cytosol to the cell membrane, and also inhibited its association with p22phox (a component of membrane‐associated NADPH oxidase). Overall, PLD?PKCζ?p47phox signaling axis plays a crucial role in ANGII‐induced increase in NADPH oxidase‐mediated O2.? production in the cells. 相似文献
282.
Dipankar Chakraborti Anindya Sarkar Hossain Ali Mondal Sampa Das 《Transgenic research》2009,18(4):529-544
The phloem sap-sucking hemipteran insect, Aphis craccivora, commonly known as cowpea aphid, cause major yield loss of important food legume crop chickpea. Among different plant lectins
Allium sativum leaf agglutinin (ASAL), a mannose binding lectin was found to be potent antifeedant for sap sucking insect A. craccivora. Present study describes expression of ASAL in chickpea through Agrobacterium-mediated transformation of “single cotyledon with half embryo” explant. ASAL was expressed under the control of CaMV35S promoter for constitutive expression and phloem specific rolC promoter for specifically targeting the toxin at feeding site, using pCAMBIA2301 vector containing plant selection marker
nptII. Southern blot analysis demonstrated the integration and copy number of chimeric ASAL gene in chickpea and its inheritance in T1 and T2 progeny plants. Expression of ASAL in T0 and T1 plants was confirmed through northern and western blot analysis. The segregation pattern of ASAL transgene was observed in T1 progenies, which followed the 3:1 Mendelian ratio. Enzyme linked immunosorbant assay (ELISA) determined the level of ASAL
expression in different transgenic lines in the range of 0.08–0.38% of total soluble protein. The phloem tissue specific expression
of ASAL gene driven by rolC promoter has been monitored by immunolocalization analysis of mature stem sections. Survival and fecundity of A. craccivora decreased to 11–26% and 22–42%, respectively when in planta bioassay conducted on T1 plants compared to untransformed control plant which showed 85% survival. Thus, through unique approach of phloem specific
expression of novel insecticidal lectin (ASAL), aphid resistance has been successfully achieved in chickpea.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. 相似文献
283.
The present study was undertaken to test the hypothesis that activation of cell membrane associated protein kinase C (PKC) plays a role in stimulating cell membrane associated phospholipase A2 (PLA2) activity, and subsequent liberation of arachidonic acid (AA) under exposure of rabbit pulmonary arterial smooth muscle cells to the oxidant hydrogen peroxide (H2O2). Exposure of the smooth muscle cells to H2O2 dose-dependently stimulates [14C] AA release, and enhances the cell membrane associated PLA2 activity. Pretreatment of the cells with protein kinase C (PKC) inhibitors H7 and sphingosine prevent the cell membrane associated PLA2 activity, and AA release caused by H2O2. Treatment of the smooth muscle cells with H2O2 stimulates the cell membrane associated PKC activity. Pretreatment of the cells with an antioxidant vitamin E prevents H2O2 caused stimulation of the cell membrane associated PKC activity. The cell membrane associated PLA2 and PKC activities correlate linearly. These results suggest that H2O2 caused stimulation of the smooth muscle cell membrane associated PLA2 activity, and subsequent liberation of AA can occur through an increase in the activity of the cell membrane associated PKC. (Mol Cell Biochem122: 9–15, 1993)Abbreviations AA
Arachidonic Acid
- PLA2
Phospholipase A2
- PKC
Protein Kinase C
- PBS
Phosphate Buffered Saline
- HBPS
Hank's Buffered Physiological Saline
- HEPES
4-(2-Hydroxyethyl)-1-Piperazine N-2-Ethanesulfonate
- FCS
Fetal Calf Serum
- ATP
Adenosine Triphosphate
- H7
1-(5-isoquinolinesulfonyl)-2-methyl-piperazine
- DMEM
Dulbecco's Modified Eagles Medium
- TCA
Trichloroacetic Acid 相似文献
284.
Salil K. Ghosh Tapati Chakraborti Arun B. Banerjee Sujata Roychoudhury Sajal Chakraborti 《Journal of biosciences》1996,21(1):35-43
Treatment of bovine pulmonary artery smooth muscle microsomes with the superoxide radical generating system hypoxanthine plus
xanthine oxidase stimulated iron release, hydroxyl radical production and lipid peroxidation. Pretreatment of the microsomes
with deferoxamine or dime thy lthiourea markedly inhibited lipid peroxidation, and prevented hydroxyl radical production without
appreciably altering iron release. The superoxide radical generating system did not alter the ambient superoxide dismutase
activity. However,addition of exogenous superoxide dismutase prevented superoxide radical induced iron release,hydroxyl radical production and lipid peroxidation. Simultaneous treatment of the microsomes with deferoxamine, dimethylthiourea
or superoxide dismutase prevented hydroxyl radical production and liqid peroxidation. While deferoxamine or dimethylthiourea
did not appreciably alter iron release, superoxide dismutase prevented iron release. However, addition of deferoxamine, dimethylthiourea
or superoxide dismutase even 2 min after treatment did not significantly inhibit lipid peroxidation, hydroxyl radical production
and iron release. Pretreatment of microsomes with the anion channel blocker 4,4’- dithiocyano 2,′- disulphonic acid stilbine
did not cause any discernible change in chemiluminiscence induced by the superoxide radical generating system but markedly
inhibited lipid peroxidation without appreciably altering iron release and hydroxial radical production. 相似文献
285.
Friend spleen focus-forming virus induces factor independence in an erythropoietin-dependent erythroleukemia cell line 总被引:26,自引:10,他引:16
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S K Ruscetti N J Janesch A Chakraborti S T Sawyer W D Hankins 《Journal of virology》1990,64(3):1057-1062
Erythroid cells from mice infected with the polycythemia-inducing strain of Friend spleen focus-forming virus (SFFVP), unlike normal erythroid cells, can proliferate and differentiate in apparent absence of the erythroid hormone erythropoietin (Epo). The unique envelope glycoprotein encoded by SFFV has been shown to be responsible for this biological effect. The recent isolation of an Epo-dependent erythroleukemia cell line, HCD-57, derived from a mouse infected at birth with Friend murine leukemia virus, afforded us the opportunity to study the direct effect of SFFVP on a homogeneous population of factor-dependent cells. The introduction of SFFVP in complex with various helper viruses into these Epo-dependent cells efficiently and reproducibly gave rise to lines which expressed high levels of SFFV and were factor independent. SFFV appears to be unique in its ability to abrogate the factor dependence of Epo-dependent HCD-57 cells, since infection of these cells with retroviruses carrying a variety of different oncogenes had no effect. The induction of Epo independence by SFFV does not appear to involve a classical autocrine mechanism, since there is no evidence that the factor-independent cells synthesize or secrete Epo or depend on it for their growth. However, the SFFV-infected, factor-independent cells had significantly fewer receptors available for binding Epo than their factor-dependent counterparts had, raising the possibility that the induction of factor independence by the virus may be due to the interaction of an SFFV-encoded protein with the Epo receptor. 相似文献
286.
Degradation of phenanthrene by different bacteria: evidence for novel transformation sequences involving the formation of 1-naphthol 总被引:15,自引:0,他引:15
Four polycyclic aromatic hydrocarbon (PAH)- degrading bacteria, namely Arthrobacter sulphureus RKJ4, Acidovorax delafieldii P4-1, Brevibacterium sp. HL4 and Pseudomonas sp. DLC-P11, capable of utilizing phenanthrene as the sole source of carbon and energy, were tested for its degradation using
radiolabelled phenanthrene. [9-14C]Phenanthrene was incubated with microorganisms containing 100 mg/l unlabelled phenanthrene and the evolution of 14CO2 was monitored: within 18 h of incubation, 30.1, 35.6, 26.5 and 2.1% of the recovered radiolabelled carbon was degraded to
14CO2 by RKJ4, P4-1, HL4 and DLC-P11, respectively. When mixtures of other PAHs such as fluorene, fluoranthene and pyrene, in addition
to phenanthrene, were added as additional carbon sources, there was a 36.1 and 20.6% increase in 14CO2 production from [9-14C]phenanthrene in the cases of RKJ4 and HL4, respectively, whereas P4-1 and DLC-P11 did not show any enhancement in 14CO2 production. Although, a combination of many bacteria enhances the degradation of organic compounds, no enhancement in the
degradation of [9-14C]phenanthrene was observed in mixed culture involving all four microorganisms together. However, when different PAHs, as
indicated above, were used in mixed culture, there was a 68.2% increase in 14CO2 production. In another experiment, the overall growth rate of P4-1 on phenanthrene could be enhanced by adding the non-ionic
surfactant Triton X-100, whereas RKJ4, HL4 and DLC-P11 did not show any enhancement in growth. Pathways for phenanthrene degradation
were also analysed by thin-layer chromatography, gas chromatography and gas chromatography-mass spectrometry. Common intermediates
such as o-phthalic acid and protocatechuic acid were detected in the case of RKJ4 and o-phthalic acid was detected in the case of P4-1. A new intermediate, 1-naphthol, was detected in the cases of HL4 and DLC-P11.
HL4 degrades phenanthrene via 1-hydroxy-2-naphthoic acid, 1-naphthol and salicylic acid, whereas DLC-P11 degrades phenanthrene
via the formation of 1-hydroxy-2-naphthoic acid, 1-naphthol and o-phthalic acid. Both transformation sequences are novel and have not been previously reported in the literature. Mega plasmids
were found to be present in RKJ4, HL4 and DLC-P11, but their involvement in phenanthrene degradation could not be established.
Received: 25 May 1999 / Received revision: 16 July 1999 / Accepted: 1 August 1999 相似文献
287.
Oxidant, mitochondria and calcium: an overview 总被引:26,自引:0,他引:26
Mitochondria are active in the continuous generation of reactive oxygen species (ROS), (e.g., superoxide), thereby favouring a situation of mitochondrial oxidative stress. Under oxidative stress--for example, ischaemia-reoxygenation injury to cells--mitochondria form superoxide, which in turn is converted to hydrogen peroxide and the potent reactive species, hydroxyl radical. Alternatively, mitochondrial superoxide may react with nitric oxide to form potent oxidant peroxynitrite and as a consequence, mitochondrial function is altered. An increase in the release of calcium from mitochondria by oxidants stimulates calcium-dependent enzymes such as calcium-dependent proteases, nucleases, and phospholipases, which subsequently trigger apoptosis of the cells. In principle, calcium can leave mitochondria by different ways: by non-specific leakage through the inner membrane by "pore formation," by changes in the membrane lipid phase, by reversal of the uniport influx carrier, by the specific calcium/hydrogen (or sodium) antiport system, by channel-mediated release pathways, or by a combination of two or more of these pathways. Additionally, the release of calcium from mitochondria can also occur either by oxidation of internal nicotinamide adenine nucleotides to ADP ribose and nicotinamide or by oxidation of thiols in membrane proteins. Once calcium efflux has been triggered, a series of common pathways of apoptosis are initiated, each of which may be sufficient to destroy the cell. Apoptosis requires the active participation of cellular components, and several genes have been suggested to control apoptosis. The proto-oncogene bcl-2 suppresses apoptosis through mitochondrial effects. Overexpression of bcl-2 in the mitochondrial membrane inhibits calcium efflux, but the underlying mechanisms are not clearly known. Further studies are needed to explore the nature of the apoptosis-inducing pathways, the precise mechanisms of calcium efflux, the molecular partners of bcl-2 oncoproteins at the level of the outer-inner membrane contact sites, the molecular biology of the apoptosis-inducing factor formation and release, and the essential molecular targets of apoptosis-inducing proteases. Clarification of these issues might facilitate the understanding of mitochondrial response on cellular calcium dynamics under oxidant stress. 相似文献
288.
289.
Subha Manna Amaresh Sinha Ramkrishna Sadhukhan S. L. Chakrabarty 《Current microbiology》1995,30(5):291-298
An l-asparaginase produced by Pseudomonas stutzeri MB-405 was isolated and characterized. After initial ammonium sulfate fractionation, the enzyme was purified by consecutive column chromatography on Sephadex G-100, Ca-hydroxylapatite, and DEAE-Sephadex A-50. The 665.5-fold purified enzyme thus obtained has the specific activity of 732.3 units mg protein-1 with an overall recovery of 27.2%. The apparent M
r of the enzyme under nondenaturing and denaturing conditions was 34 kDa and 33 kDa respectively, and the isoelectric point was 6.38±0.02. It displayed optimum activity at pH 9.0 and 37°C. The enzyme was very specific for l-asparagine and did not hydrolyze L-glutaminate. The K
m of the l-asparaginase was found to be 1.45×10-4
m towards l-asparagine and was competitively inhibited by 5-diazo-4-oxo-l-norvaline (DONV) with a K
i of 0.03mm. Metal ions such as Mn2+, Zn2+, Hg2+, Fe3+, Ni2+, and Cd2+ potentially inhibited the enzyme activity. The activity was enhanced in the presence of thiol-protecting reagents such as DTT, 2-ME, and glutathione (reduced), but inhibited by PCMB and iodoacetamide. The tumor inhibition study with Dalton's lymphoma tumor cells in vivo indicated that this enzyme possesses antitumor properties. 相似文献
290.
Biswarup Ghosh Pulak Kar Amritlal Mandal Kuntal Dey Tapati Chakraborti Sajal Chakraborti 《Life sciences》2009,84(5-6):139-148
AimsWe sought to determine the mechanisms of an increase in Ca2+ level in caveolae vesicles in pulmonary smooth muscle plasma membrane during Na+/K+-ATPase inhibition by ouabain.Main methodsThe caveolae vesicles isolated by density gradient centrifugation were characterized by electron microscopic and immunologic studies and determined ouabain induced increase in Na+ and Ca2+ levels in the vesicles with fluorescent probes, SBFI-AM and Fura2-AM, respectively.Key findingsWe identified the α2β1 and α1β1 isozymes of Na+/K+-ATPase in caveolae vesicles, and only the α1β1 isozyme in noncaveolae fraction of the plasma membrane. The α2-isoform contributes solely to the enzyme inhibition in the caveolae vesicles at 40 nM ouabain. Methylisobutylamiloride (Na+/H+-exchange inhibitor) and tetrodotoxin (voltage-gated Na+-channel inhibitor) pretreatment prevented ouabain induced increase in Na+ and Ca2+ levels. Ouabain induced increase in Ca2+ level was markedly, but not completely, inhibited by KB-R7943 (reverse-mode Na+/Ca2+-exchange inhibitor) and verapamil (L-type Ca2+-channel inhibitor). However, pretreatment with tetrodotoxin in conjunction with KB-R7943 and verapamil blunted ouabain induced increase in Ca2+ level in the caveolae vesicles, indicating that apart from Na+/Ca+-exchanger and L-type Ca2+-channels, “slip-mode conductance” of Na+ channels could also be involved in this scenario.SignificanceInhibition of α2 isoform of Na+/K+-ATPase by ouabain plays a crucial role in modulating the Ca2+ influx regulatory components in the caveolae microdomain for marked increase in (Ca2+)i in the smooth muscle, which could be important for the manifestation of pulmonary hypertension. 相似文献