Biotechnological Implication with Azolla pinnata R.Br. for Metal Quenching Ability with Physiological Biomarkers.

2016 ◽  
Vol 1 (1) ◽  
Author(s):  
Arnab Kumar De ◽  
Narottam Dey ◽  
Malay Kumar Adak
Keyword(s):  
Higher Plants ◽  
Lead Toxicity ◽  
Threshold Value ◽  
Cellular Level ◽  
Dependent Manner ◽  
Azolla Pinnata ◽  
Concentration Dependent Manner ◽  
Aquatic Fern ◽  
Enzymatic Cascades ◽  
Net Assimilation

<p>The present paper holds the accountability of an aquatic fern R.Br. for biotechnological implication. Azolla pinnata In an artificial<br />laboratory condition Azolla plants responded well in hyper accumulation of lead in a concentration dependent manner however, within a<br />threshold value. In accompany with metal bioaccumulation plants responded a regulated growth performances with relative growth rate<br />(RGR) and net assimilation rate (NAR). The plants responded well with a chemical elicitors like polyamine in response to metal<br />quenching ability. At the cellular level the phytotoxicity of the plant is mitigated by both non-enzymatic and enzymatic cascades. It is an<br />advantage of the plants to down regulate reactive oxygen species (ROS) - superoxide (O ) and peroxide (H O ) in a moderate level as 2 2 2<br />-<br />compare to higher plants and modulated with polyamine. The diversity in this species was also recorded for few gene expression related to<br />antioxidation. Fern under lead toxicity displayed well in protein polymorphism for peroxides with variations. The responses of this<br />species for metal hyper accumulation and over expressed physiological traits are discussed in light of phytoremidiation.<br />Keywords: Azolla; Heavy Metals; Oxidative Stress; Antioxidative enzymes; Polyamine</p><p> </p><p><span>DOI: </span><a id="pub-id::doi" href="http://dx.doi.org/10.21756/cba.v1i1.10960">http://dx.doi.org/10.21756/cba.v1i1.10960</a></p>

Biotechnological Implication with R.Br. for Azolla pinnata Metal Quenching Ability with Physiological Biomarkers

2016 ◽  
Vol 1 (1) ◽  
Author(s):  
Malay Kumar Adak ◽  
Arnab Kumar De ◽  
Narottam Dey
Keyword(s):  
Higher Plants ◽  
Lead Toxicity ◽  
Threshold Value ◽  
Cellular Level ◽  
Dependent Manner ◽  
Azolla Pinnata ◽  
Concentration Dependent Manner ◽  
Aquatic Fern ◽  
Enzymatic Cascades ◽  
Net Assimilation

The present paper holds the accountability of an aquatic fern Azolla pinnata R.Br. for biotechnological implication. In an artificial laboratory condition Azolla plants responded well in hyper accumulation of lead in a concentration dependent manner however, within a threshold value. In accompany with metal bioaccumulation plants responded a regulated growth performances with relative growth rate (RGR) and net assimilation rate (NAR). The plants responded well with a chemical elicitors like polyamine in response to metal quenching ability. At the cellular level the phytotoxicity of the plant is mitigated by both non-enzymatic and enzymatic cascades. It is an advantage of the plants to down regulate reactive oxygen species (ROS) - superoxide (O2 ) and peroxide (H2O2) in a moderate level as - compare to higher plants and modulated with polyamine. The diversity in this species was also recorded for few gene expression related to antioxidation. Fern under lead toxicity displayed well in protein polymorphism for peroxides with variations. The responses of this species for metal hyper accumulation and over expressed physiological traits are discussed in light of phytoremidiation.

scholarly journals Using a Multi-Stage hESC Model to Characterize BDE-47 Toxicity During Neurogenesis

2019 ◽  
Vol 171 (1) ◽  
pp. 221-234 ◽  
Author(s):  
Hao Chen ◽  
Helia Seifikar ◽  
Nicholas Larocque ◽  
Yvonne Kim ◽  
Ibrahim Khatib ◽  
...  
Keyword(s):  
Neural Development ◽  
Polybrominated Diphenyl Ethers ◽  
Neuronal Development ◽  
Embryonic Stem ◽  
Cellular Level ◽  
Environmental Chemicals ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Neurodevelopmental Toxicity

Abstract Although the ramifications associated with polybrominated diphenyl ethers (PBDEs) exposures during human pregnancy have yet to be determined, increasing evidence in humans and animal models suggests that these compounds cause neurodevelopmental toxicity. Human embryonic stem cells (hESCs) models can be used to study the effects of environmental chemicals throughout the successive stages of neuronal development. Here, using a hESC differentiation model, we investigated the effects of common PBDE congeners (BDE-47 or -99) on the successive stages of early neuronal development. First, we determined the points of vulnerability to PBDEs across 4 stages of in vitro neural development by using assays to assess for cytotoxicity. Differentiated neural progenitors were identified to be more sensitive to PBDEs than their less differentiated counterparts. In follow-up investigations, we observed BDE-47 to inhibit functional processes critical for neurogenesis (eg, proliferation, expansion) in hESC-derived neural precursor cells (NPCs) at sub-lethal concentrations. Finally, to determine the mechanism(s) underlying PBDE-toxicity, we conducted global transcriptomic and methylomic analyses of BDE-47. We identified 589 genes to be differentially expressed due to BDE-47 exposure, including molecules involved in oxidative stress mediation, cell cycle, hormone signaling, steroid metabolism, and neurodevelopmental pathways. In parallel analyses, we identified a broad significant increase in CpG methylation. In summary our results suggest, on a cellular level, PBDEs induce human neurodevelopmental toxicity in a concentration-dependent manner and sensitivity to these compounds is dependent on the developmental stage of exposure. Proposed mRNA and methylomic perturbations may underlie toxicity in early embryonic neuronal populations.

scholarly journals Forced Expression of Keratin 16 Alters the Adhesion, Differentiation, and Migration of Mouse Skin Keratinocytes

2000 ◽  
Vol 11 (10) ◽  
pp. 3315-3327 ◽  
Author(s):  
Matthew Wawersik ◽  
Pierre A. Coulombe
Keyword(s):  
Mouse Skin ◽  
Cellular Level ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Keratin 16 ◽  
Skin Keratinocytes ◽  
Steady State Levels ◽  
And Migration ◽  
Mouse Skin Keratinocytes ◽  
The Impact

Injury to the skin results in an induction of keratins K6, K16, and K17 concomitant with activation of keratinocytes for reepithelialization. Forced expression of human K16 in skin epithelia of transgenic mice causes a phenotype that mimics several aspects of keratinocyte activation. Two types of transgenic keratinocytes, with forced expression of either human K16 or a K16-C14 chimeric cDNA, were analyzed in primary culture to assess the impact of K16 expression at a cellular level. High K16-C14-expressing and low K16-expressing transgenic keratinocytes behave similar to wild type in all aspects tested. In contrast, high K16-expressing transgenic keratinocytes show alterations in plating efficiency and calcium-induced differentiation, but proliferate normally. Migration of keratinocytes is reduced in K16 transgenic skin explants compared with controls. Finally, a subset of high K16-expressing transgenic keratinocytes develops major changes in the organization of keratin filaments in a time- and calcium concentration-dependent manner. These changes coincide with alterations in keratin content while the steady-state levels of K16 protein remain stable. We conclude that forced expression of K16 in progenitor skin keratinocytes directly impacts properties such as adhesion, differentiation, and migration, and that these effects depend upon determinants contained within its carboxy terminus.

scholarly journals LuxR Homologue SmcR Is Essential for Vibrio vulnificus Pathogenesis and Biofilm Detachment, and Its Expression is Induced by Host Cells

2013 ◽  
Vol 81 (10) ◽  
pp. 3721-3730 ◽  
Author(s):  
Seung Min Kim ◽  
Jin Hwan Park ◽  
Hyun Sung Lee ◽  
Won Bin Kim ◽  
Jung Min Ryu ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Vibrio Vulnificus ◽  
Cell Communication ◽  
Cellular Level ◽  
Host Cells ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Content Type ◽  
Biofilm Detachment

ABSTRACTQuorum sensing is a cell-to-cell communication system known to control many bacterial processes. In the present study, the functions of quorum sensing in the pathogenesis ofVibrio vulnificus, a food-borne pathogen, were assessed by evaluating the virulence of a mutant deficient in SmcR, a quorum-sensing regulator and homologue of LuxR. When biofilms were used as an inoculum, thesmcRmutant was impaired in virulence and colonization capacity in the infection of mice. The lack of SmcR also resulted in decreased histopathological damage in mouse jejunum tissue. These results indicated that SmcR is essential forV. vulnificuspathogenesis. Moreover, thesmcRmutant exhibited significantly reduced biofilm detachment. Upon exposure to INT-407 host cells, the wild type, but not thesmcRmutant, revealed accelerated biofilm detachment. The INT-407 cells increasedsmcRexpression by activating the expression of LuxS, an autoinducer-2 synthase, indicating that host cells manipulate the cellular level of SmcR through the quorum-sensing signaling ofV. vulnificus. A whole-genome microarray analysis revealed that the genes primarily involved in biofilm detachment and formation are up- and downregulated by SmcR, respectively. Among the SmcR-regulated genes,vvpEencoding an elastolytic protease was the most upregulated, and the purified VvpE appeared to dissolve established biofilms directly in a concentration-dependent mannerin vitro. These results suggest that the host cell-induced SmcR enhances the detachment ofV. vulnificusbiofilms entering the host intestine and thereby may promote the dispersal of the pathogen to new colonization loci, which is crucial for pathogenesis.

scholarly journals Graphene Enhances Actin Filament Assembly Kinetics and Modulates NIH-3T3 Fibroblast Cell Spreading

2022 ◽  
Vol 23 (1) ◽  
pp. 509
Author(s):  
Jinho Park ◽  
Pavlo Kravchuk ◽  
Adithi Krishnaprasad ◽  
Tania Roy ◽  
Ellen Hyeran Kang
Keyword(s):  
Actin Filament ◽  
Chemical Properties ◽  
Fibroblast Cell ◽  
Cellular Level ◽  
Dependent Manner ◽  
Cellular Functions ◽  
Concentration Dependent Manner ◽  
Filament Dynamics ◽  
Assembly Kinetics ◽  
Nih 3T3

Actin plays critical roles in various cellular functions, including cell morphogenesis, differentiation, and movement. The assembly of actin monomers into double-helical filaments is regulated in surrounding microenvironments. Graphene is an attractive nanomaterial that has been used in various biomaterial applications, such as drug delivery cargo and scaffold for cells, due to its unique physical and chemical properties. Although several studies have shown the potential effects of graphene on actin at the cellular level, the direct influence of graphene on actin filament dynamics has not been studied. Here, we investigate the effects of graphene on actin assembly kinetics using spectroscopy and total internal reflection fluorescence microscopy. We demonstrate that graphene enhances the rates of actin filament growth in a concentration-dependent manner. Furthermore, cell morphology and spreading are modulated in mouse embryo fibroblast NIH-3T3 cultured on a graphene surface without significantly affecting cell viability. Taken together, these results suggest that graphene may have a direct impact on actin cytoskeleton remodeling.

scholarly journals Tunable expression rate control of a growth-decoupled T7 expression system by l-arabinose only

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Patrick Stargardt ◽  
Gerald Striedner ◽  
Juergen Mairhofer
Keyword(s):  
Escherichia Coli ◽  
Fusion Proteins ◽  
Protein Production ◽  
Expression System ◽  
Regulation Of Gene Expression ◽  
Cellular Level ◽  
Fine Tuning ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Associated Production

Abstract Background Precise regulation of gene expression is of utmost importance for the production of complex membrane proteins (MP), enzymes or other proteins toxic to the host cell. In this article we show that genes under control of a normally Isopropyl β-d-1-thiogalactopyranoside (IPTG)-inducible PT7-lacO promoter can be induced solely with l-arabinose in a newly constructed Escherichia coli expression host BL21-AI<gp2>, a strain based on the recently published approach of bacteriophage inspired growth-decoupled recombinant protein production. Results Here, we show that BL21-AI<gp2> is able to precisely regulate protein production rates on a cellular level in an l-arabinose concentration-dependent manner and simultaneously allows for reallocation of metabolic resources due to l-arabinose induced growth decoupling by the phage derived inhibitor peptide Gp2. We have successfully characterized the system under relevant fed-batch like conditions in microscale cultivation (800 µL) and generated data proofing a relevant increase in specific yields for 6 different Escherichia coli derived MP-GFP fusion proteins by using online-GFP signals, FACS analysis, SDS-PAGE and western blotting. Conclusions In all cases tested, BL21-AI<gp2> outperformed the parental strain BL21-AI, operated in growth-associated production mode. Specific MP-GFP fusion proteins yields have been improved up to 2.7-fold. Therefore, this approach allows for fine tuning of MP production or expression of multi-enzyme pathways where e.g. particular stoichiometries have to be met to optimize product flux.

NaF-induced amylase release from rat parotid cells is mediated by PI breakdown leading to Ca2+ mobilization

1991 ◽  
Vol 260 (2) ◽  
pp. C194-C200 ◽  
Author(s):  
Y. Tojyo ◽  
A. Tanimura ◽  
S. Matsui ◽  
Y. Matsumoto ◽  
H. Sugiya ◽  
...  
Keyword(s):  
Inositol Phosphate ◽  
Protein S ◽  
Cellular Level ◽  
Dependent Manner ◽  
Slow Increase ◽  
Concentration Dependent Manner ◽  
Amylase Release ◽  
Parotid Cells ◽  
Muscarinic Cholinergic ◽  
Rat Parotid

We have examined the effects of sodium fluoride (NaF) on amylase release, cellular adenosine 3',5'-cyclic monophosphate (cAMP) level, inositol phosphate formation, and cytosolic free Ca2+ concentration ([Ca2+]i) in dispersed rat parotid acini or cells. At concentrations greater than 1 mM, NaF significantly increased amylase release. The maximum response was observed at 10 mM NaF and was comparable to that of the muscarinic-cholinergic agonist carbachol. Removal of extracellular Ca2+ with EGTA markedly suppressed the NaF-induced secretory response. At concentrations up to 10 mM, NaF did not increase the cellular level of cAMP, indicating that the NaF-induced amylase release is not mediated by cAMP. NaF (1-20 mM) caused a slow increase in [Ca2+]i in a concentration-dependent manner, as monitored with the fluorescent Ca2+ indicator fura-2, and the increased [Ca2+]i did not decline for at least 10 min after addition of NaF. In the absence of extracellular Ca2+, NaF evoked only a small and transient increase in [Ca2+]i. The addition of 10 mM NaF produced a significant accumulation of inositol monophosphate, inositol bisphosphate, and inositol trisphosphate. These results suggest that the NaF-induced amylase release is mediated by a breakdown of phosphoinositides leading to Ca2+ mobilization. The effects of fluoride may be through the action of F- on the GTP-binding protein(s) coupled to phospholipase C.

scholarly journals Effect of Auristatin PHE on Microtubule Integrity and Nuclear Localization in Cryptococcus neoformans

2002 ◽  
Vol 46 (12) ◽  
pp. 3802-3808 ◽  
Author(s):  
Tanja Woyke ◽  
Robert W. Roberson ◽  
George R. Pettit ◽  
Günther Winkelmann ◽  
Robin K. Pettit
Keyword(s):  
Cryptococcus Neoformans ◽  
Nuclear Localization ◽  
Cellular Level ◽  
Dependent Manner ◽  
Microtubule Organization ◽  
Concentration Dependent Manner ◽  
Cellular Division ◽  
Linear Peptide ◽  
Microtubule Disruption ◽  
Complete Disruption

ABSTRACT The mechanism of action of the fungicidal peptide auristatin PHE was investigated in Cryptococcus neoformans. Since auristatin PHE causes budding arrest in C. neoformans (T. Woyke, G. R. Pettit, G. Winkelmann, and R. K. Pettit, Antimicrob. Agents Chemother. 45:3580-3584, 2001), microtubule integrity and nuclear localization in auristatin PHE-treated cells were examined. Iterative deconvolution in conjunction with an optimized C. neoformans microtubule immunolabeling procedure enabled detailed visualization of the microtubule cytoskeleton in auristatin PHE-treated C. neoformans. The effect of auristatin PHE on C. neoformans microtubule organization was compared with that of the tubulin-binding agent nocodazole. Both drugs produced complete disruption first of cytoplasmic and then of spindle microtubules in a time- and concentration-dependent manner. Sub-MICs of auristatin PHE caused complete microtubule disruption within 4.5 h, while 1.5 times the nocodazole MIC was required for the same effect. For both drugs, disruption of microtubules was accompanied by blockage of nuclear migration and of nuclear and cellular division, resulting in cells arrested in a uninucleate, large-budded stage. Nocodazole and the linear peptide auristatin PHE are remarkably different in structure and spectrum of activity, yet on the cellular level, they have similar effects.

scholarly journals Characterization of preptin-induced insulin secretion in pancreatic β-cells

2012 ◽  
Vol 215 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Kai-Chun Cheng ◽  
Ying-Xiao Li ◽  
Akihiro Asakawa ◽  
Miharu Ushikai ◽  
Ikuo Kato ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Cellular Level ◽  
Dependent Manner ◽  
Acetoxymethyl Ester ◽  
Concentration Dependent Manner ◽  
Kinase C ◽  
Intracellular Ca ◽  
Dose Dependent ◽  
Pkc Activation

We aimed to characterize the effects of preptin on insulin secretion at the single-cell level, as well as the mechanisms underlying these changes, with respect to regulation by intracellular Ca2+[Ca2+]imobilization. This study assessed the effect of preptin on insulin secretion and investigated the link between preptin and the phospholipase C (PLC)/protein kinase C (PKC) pathway at the cellular level using fura-2 pentakis(acetoxymethyl) ester-loaded insulin-producing cells (Min 6 cells). Our results demonstrate that preptin promotes insulin secretion in a concentration-dependent manner. Using a PLC inhibitor (chelerythrine) or a PKC inhibitor (U73122) resulted in a concentration-dependent decrease in insulin secretion. Also, preptin mixed with IGF2 receptor (IGF2R) antibodies suppressed insulin secretion in a dose-dependent manner, which indicates that activation of IGF2R is mediated probably because preptin is a type of proIGF2. In addition, preptin stimulated insulin secretion to a similar level as did glibenclamide. The activation of PKC/PLC by preptin stimulation is highly relevant to the potential mechanisms for increase in insulin secretion. Our results provide new insight into the insulin secretion of preptin, a secreted proIGF2-derived peptide that can induce greater efficacy of signal transduction resulting from PLC and PKC activation through the IGF2R.

The Anti-Atherogenic Properties of Sesamin are Mediated via Improved Macrophage Cholesterol Efflux Through PPARγ1-LXRα and MAPK Signaling

2014 ◽  
Vol 84 (1-2) ◽  
pp. 79-91 ◽  
Author(s):  
Amin F. Majdalawieh ◽  
Hyo-Sung Ro
Keyword(s):  
Cholesterol Efflux ◽  
Transcriptional Activity ◽  
Molecular Mechanisms ◽  
Foam Cell ◽  
Mapk Signaling ◽  
Luciferase Reporter ◽  
Foam Cell Formation ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Macrophage Cholesterol Efflux

Background: Foam cell formation resulting from disrupted macrophage cholesterol efflux, which is triggered by PPARγ1 and LXRα, is a hallmark of atherosclerosis. Sesamin and sesame oil exert anti-atherogenic effects in vivo. However, the exact molecular mechanisms underlying such effects are not fully understood. Aim: This study examines the potential effects of sesamin (0, 25, 50, 75, 100 μM) on PPARγ1 and LXRα expression and transcriptional activity as well as macrophage cholesterol efflux. Methods: PPARγ1 and LXRα expression and transcriptional activity are assessed by luciferase reporter assays. Macrophage cholesterol efflux is evaluated by ApoAI-specific cholesterol efflux assays. Results: The 50 μM, 75 μM, and 100 μM concentrations of sesamin up-regulated the expression of PPARγ1 (p< 0.001, p < 0.001, p < 0.001, respectively) and LXRα (p = 0.002, p < 0.001, p < 0.001, respectively) in a concentration-dependent manner. Moreover, 75 μM and 100 μM concentrations of sesamin led to 5.2-fold (p < 0.001) and 6.0-fold (p<0.001) increases in PPAR transcriptional activity and 3.9-fold (p< 0.001) and 4.2-fold (p < 0.001) increases in LXR transcriptional activity, respectively, in a concentration- and time-dependent manner via MAPK signaling. Consistently, 50 μM, 75 μM, and 100 μM concentrations of sesamin improved macrophage cholesterol efflux by 2.7-fold (p < 0.001), 4.2-fold (p < 0.001), and 4.2-fold (p < 0.001), respectively, via MAPK signaling. Conclusion: Our findings shed light on the molecular mechanism(s) underlying sesamin’s anti-atherogenic effects, which seem to be due, at least in part, to its ability to up-regulate PPARγ1 and LXRα expression and transcriptional activity, improving macrophage cholesterol efflux. We anticipate that sesamin may be used as a therapeutic agent for treating atherosclerosis.

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