scholarly journals Comparative Proteomic Analysis of Two Ralstonia solanacearum Isolates Differing in Aggressiveness

2018 ◽  
Vol 19 (8) ◽  
pp. 2444 ◽  
Author(s):  
Guoping Wang ◽  
Jie Kong ◽  
Dandan Cui ◽  
Hongbo Zhao ◽  
Puyan Zhao ◽  
...  
Keyword(s):  
Ralstonia Solanacearum ◽  
Isocitrate Lyase ◽  
Extracellular Polysaccharide ◽  
Underlying Mechanism ◽  
Protein Abundance ◽  
Tomato Cultivar ◽  
Pronounced Difference ◽  
Glyoxylate Metabolism ◽  
Related Proteins ◽  
Number Of Plant Species

Ralstonia solanacearum is a soil-borne, plant xylem-infecting pathogen that causes the devastating bacterial wilt (BW) disease in a number of plant species. In the present study, two R. solanacearum strains with different degrees of aggressiveness―namely RsH (pathogenic to Hawaii 7996, a tomato cultivar resistant against most strains) and RsM (non-pathogenic to Hawaii 7996) were identified. Phylogenetic analysis revealed that both RsM and RsH belonged to phylotype I. To further elucidate the underlying mechanism of the different pathotypes between the two strains, we performed a comparative proteomics study on RsM and RsH in rich and minimal media to identify the change in the level of protein abundance. In total, 24 differential proteins were identified, with four clusters in terms of protein abundance. Further bioinformatics exploration allowed us to classify these proteins into five functional groups. Notably, the pathogenesis of RsM and RsH was particularly characterized by a pronounced difference in the abundance of virulence- and metabolism-related proteins, such as UDP-N-acetylglucosamine 2-epimerase (epsC) and isocitrate lyase (ICL), which were more abundant in the high pathogenicity strain RsH. Thus, we propose that the differences in pathogenicity between RsM and RsH can possibly be partially explained by differences in extracellular polysaccharide (EPS) and glyoxylate metabolism-related proteins.

scholarly journals SIRT1 attenuates sepsis-induced acute kidney injury via Beclin1 deacetylation-mediated autophagy activation

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Zhiya Deng ◽  
Maomao Sun ◽  
Jie Wu ◽  
Haihong Fang ◽  
Shumin Cai ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Protective Effect ◽  
Cell Model ◽  
Kidney Injury ◽  
Underlying Mechanism ◽  
Autophagy Induction ◽  
Promising Therapeutic Approach ◽  
Related Proteins ◽  
Caecal Ligation And Puncture

AbstractOur previous studies showed that silent mating-type information regulation 2 homologue-1 (SIRT1, a deacetylase) upregulation could attenuate sepsis-induced acute kidney injury (SAKI). Upregulated SIRT1 can deacetylate certain autophagy-related proteins (Beclin1, Atg5, Atg7 and LC3) in vitro. However, it remains unclear whether the beneficial effect of SIRT1 is related to autophagy induction and the underlying mechanism of this effect is also unknown. In the present study, caecal ligation and puncture (CLP)-induced mice, and an LPS-challenged HK-2 cell line were established to mimic a SAKI animal model and a SAKI cell model, respectively. Our results demonstrated that SIRT1 activation promoted autophagy and attenuated SAKI. SIRT1 deacetylated only Beclin1 but not the other autophagy-related proteins in SAKI. SIRT1-induced autophagy and its protective effect against SAKI were mediated by the deacetylation of Beclin1 at K430 and K437. Moreover, two SIRT1 activators, resveratrol and polydatin, attenuated SAKI in CLP-induced septic mice. Our study was the first to demonstrate the important role of SIRT1-induced Beclin1 deacetylation in autophagy and its protective effect against SAKI. These findings suggest that pharmacologic induction of autophagy via SIRT1-mediated Beclin1 deacetylation may be a promising therapeutic approach for future SAKI treatment.

scholarly journals Methionine and Arginine Supply Alters Abundance of Amino Acid, Insulin Signaling, and Glutathione Metabolism-Related Proteins in Bovine Subcutaneous Adipose Explants Challenged with N-Acetyl-d-sphingosine

Animals ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 2114
Author(s):  
Yusheng Liang ◽  
Nana Ma ◽  
Danielle N. Coleman ◽  
Fang Liu ◽  
Yu Li ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Amino Acid ◽  
Insulin Signaling ◽  
Elongation Factor ◽  
In Vivo Studies ◽  
Glutathione Metabolism ◽  
Protein Abundance ◽  
Related Proteins ◽  
Subcutaneous Adipose

The objective was to perform a proof-of-principle study to evaluate the effects of methionine (Met) and arginine (Arg) supply on protein abundance of amino acid, insulin signaling, and glutathione metabolism-related proteins in subcutaneous adipose tissue (SAT) explants under ceramide (Ce) challenge. SAT from four lactating Holstein cows was incubated with one of the following media: ideal profile of amino acid as the control (IPAA; Lys:Met 2.9:1, Lys:Arg 2:1), increased Met (incMet; Lys:Met 2.5:1), increased Arg (incArg; Lys:Arg 1:1), or incMet plus incArg (Lys:Met 2.5:1 Lys:Arg 1:1) with or without 100 μM exogenous cell-permeable Ce (N-Acetyl-d-sphingosine). Ceramide stimulation downregulated the overall abundance of phosphorylated (p) protein kinase B (AKT), p-mechanistic target of rapamycin (mTOR), and p-eukaryotic elongation factor 2 (eEF2). Without Ce stimulation, increased Met, Arg, or Met + Arg resulted in lower p-mTOR. Compared with control SAT stimulated with Ce, increased Met, Arg, or Met + Arg resulted in greater activation of mTOR (p-mTOR/total mTOR) and AKT (p-AKT/total AKT), with a more pronounced response due to Arg. The greatest protein abundance of glutathione S-transferase Mu 1 (GSTM1) was detected in response to increased Met supply during Ce stimulation. Ceramide stimulation decreased the overall protein abundance of the Na-coupled neutral amino acid transporter SLC38A1 and branched-chain alpha-ketoacid dehydrogenase kinase (BCKDK). However, compared with controls, increased Met or Arg supply attenuated the downregulation of BCKDK induced by Ce. Circulating ceramides might affect amino acid, insulin signaling, and glutathione metabolism in dairy cow adipose tissue. Further in vivo studies are needed to confirm the role of rumen-protected amino acids in regulating bovine adipose function.

scholarly journals Antiapoptosis and Antifibrosis Effects of Qishen Granules on Heart Failure Rats via Hippo Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Jian Zhang ◽  
Junjie Liu ◽  
Sheng Gao ◽  
Weili Lin ◽  
Pengrong Gao ◽  
...  
Keyword(s):  
Heart Failure ◽  
Hippo Pathway ◽  
Underlying Mechanism ◽  
Sprague Dawley ◽  
Artery Ligation ◽  
Regulatory Pathways ◽  
Sprague Dawley Rats ◽  
The Hippo Pathway ◽  
Related Proteins ◽  
P 53

Qishen granules (QSG) are a famous formula with cardioprotective properties to heart failure (HF). The aim of this study was to investigate the underlying mechanism of QSG on apoptosis and fibrosis in the treatment of HF. HF model was induced by left anterior descending artery ligation on Sprague-Dawley rats. Transcriptome analysis was used to investigate the regulatory pathways of QSG on HF. Interestingly, downregulated genes of QSG were significantly enriched in Hippo pathway which plays a crucial role in regulating cell apoptosis and proliferation. We found that QSG inhibited the expressions of proapoptotic key proteins P-53 and fibrosis-related proteins TGF-β1, SMAD3, and CTGF. Further, we conducted research on the key proteins in the Hippo pathway upstream of CTGF and P-53. The results showed that MST1, P-MST1, P-LATS1, and RASSF1A that exert proapoptotic function were downregulated after QSG intervention. Similarly, P-YAP and P-TAZ, mediating self-degradation and apoptosis, were both observably decreased after QSG administration. Taken together, QSG are shown to be likely to exert cardioprotective effects by inhibiting the progression of apoptosis and fibrosis through Hippo pathway.

scholarly journals The Role of Pathogenesis-Related Proteins in the Tomato-Rhizoctonia solani Interaction

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Parissa Taheri ◽  
Saeed Tarighi
Keyword(s):  
Rhizoctonia Solani ◽  
Rio Grande ◽  
Defense Responses ◽  
Structural Barriers ◽  
Tomato Cultivar ◽  
Potential Pathogen ◽  
Physical Barriers ◽  
Infected Tomato ◽  
Rot Disease ◽  
Related Proteins

Rhizoctonia solani is one of the most destructive pathogens causing foot rot disease on tomato. In this study, the molecular and cellular changes of a partially resistant (Sunny 6066) and a susceptible (Rio Grande) tomato cultivar after infection with necrotrophic soil-borne fungus R. solani were compared. The expression of defense-related genes such as chitinase (LOC544149) and peroxidase (CEVI-1) in infected tomato cultivars was investigated using semiquantitative reverse transcription-polymerase chain reaction (RT-PCR). This method revealed elevated levels of expression for both genes in the partially resistant cultivar compared to the susceptible cultivar. One of the most prominent facets of basal plant defense responses is the formation of physical barriers at sites of attempted fungal penetration. These structures are produced around the sites of potential pathogen ingress to prevent pathogen progress in plant tissues. We investigated formation of lignin, as one of the most important structural barriers affecting plant resistance, using thioglycolic acid assay. A correlation was found between lignification and higher level of resistance in Sunny 6066 compared to Rio Grande cultivar. These findings suggest the involvement of chitinase, peroxidase, and lignin formation in defense responses of tomato plants against R. solani as a destructive pathogen.

Extracellular polysaccharide from Ralstonia solanacearum ; A strong inducer of eggplant defense against bacterial wilt

2017 ◽  
Vol 110 ◽  
pp. 107-116 ◽  
Author(s):  
Avinash Prakasha ◽  
I. Darren Grice ◽  
K.S. Vinay Kumar ◽  
M.P. Sadashiva ◽  
H.N. Shankar ◽  
...  
Keyword(s):  
Bacterial Wilt ◽  
Ralstonia Solanacearum ◽  
Extracellular Polysaccharide

RBP4 induces pyroptosis in cardiomyocytes via activating NLRP3/Caspase-1/GSDMD pathway in acute myocardial infarction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
W Gao ◽  
K.Z Zhang
Keyword(s):  
Myocardial Infarction ◽  
Glucose Deprivation ◽  
Underlying Mechanism ◽  
Retinol Binding Protein ◽  
Inflammasome Activation ◽  
Funding Source ◽  
Cardiac Morbidity ◽  
Caspase 1 ◽  
Acute Mi ◽  
Related Proteins

Abstract Aims Myocardial infarction (MI) is the most common cause of cardiac morbidity and mortality worldwide. Pyroptosis is a novel form of inflammatory cell death that could be driven by the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation following MI. Retinol binding protein 4 (RBP4) is an pro-inflammatory adipokine with adverse effects on cardiovascular system. We investigated the role and underlying mechanism of RBP4 in inducing pyroptosis in cardiomyocytes in acute MI. Methods and results We established a mice MI model which ligated with the left anterior descending coronary artery and a cardiomyocytes injury model treated by oxygen-glucose deprivation (OGD). Western blot showed that RBP4 expression was exclusively increased in the heart following MI, as RBP4 expression remains unchanged in adipose tissues and liver. Cardicac pyroptosis was induced in MI mice as evidenced by increased expression of pyroptosis-related proteins, including NLRP3, Caspase-1, gasdermin D (GSDMD), IL-1β and IL-18. Moreover, increased cardiac RBP4 level was positively correlated with serum IL-1β and IL-18 levels in MI mice. Immunofluorescence identified that RBP4 was expressed in cardiomyocytes and was up-regulated along with increased pyroptosis-related proteins after treatment with OGD. Transfection of RBP4 adenovirus promoted pyroptosis while inhibition of RBP4 ameliorated OGD-induced pyroptosis in cardiomyocytes. Mechanically, transfection of NLRP3 siRNA or GSDMD siRNA along with RBP4 adenovirus could attenuate RBP4-induced pyroptosis in cardiomyocytes. Furthermore, in situ injection of adenovirus containing RBP4 siRNA could also attenuate pyroptosis and cardiac inflammation following MI in mice. Conclusion RBP4 is presented in cardiomyocytes and induces cardiac pyroptosis via activating NLRP3/Caspase-1/GSDMD pathway in acute MI Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): National Nature Science Foundation of China

scholarly journals Propofol Alleviates Neuropathic Pain in CCI Rat Model via the miR-140-3p/JAG1/Notch Signaling Pathway

2021 ◽  
Author(s):  
Fang Cheng ◽  
Wei Qin ◽  
Ai-xing Yang ◽  
Feng-feng Yan ◽  
Yu chen ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Notch Pathway ◽  
Thermal Hyperalgesia ◽  
Underlying Mechanism ◽  
Notch Signaling Pathway ◽  
Mechanical Threshold ◽  
Tnf Α ◽  
Related Proteins

Abstract As a renowned anesthetic, propofol exerts excellent analgesic function in nerve injury. However, the underlying mechanism of propofol on neuropathic pain (NP) remains unknown. The research aims to analyze propofol’s analgesia mechanism to alleviate NP in CCI rats. The chronic constriction injury (CCI) of sciatic nerve was used to established NP rat models. CCI rats were treated with propofol and its paw withdrawal mechanical threshold (PMWT) and paw withdraw thermal latency (PWTL) were measured. The expressions of TNF-α, IL-1β and IL-10 were detected. CCI rats with propofol treatment were injected with antagomiR-140-3p. After the targeting relationship between miR-140-3p and JAG1 was checked, JAG1 expression was detected. Propofol-treated CCI rats were further injected with Ad-JAG1. Finally, the levels of JAG1 and Notch pathway-related proteins were detected. As a result, propofol could alleviate NP, including thermal hyperalgesia and mechanical pain threshold, and ameliorate neuroinflammation. Mechanically, propofol enhanced the level of miR-140-3p in CCI rats. JAG1 was a direct target of miR-140-3p. The downregulation of miR-140-3p or upregulation of JAG1 could reduce the protective effect of propofol against NP. Propofol inhibited activation of Notch signaling via miR-140-3p/JAG1. Overall, Propofol could inhibit the neuroinflammation and Notch signaling pathway via miR-140-3p/JAG1 to alleviate NP.

scholarly journals LARP1 facilitates translational recovery after amino acid refeeding by preserving long poly(A)-tailed TOP mRNAs

2019 ◽  
Author(s):  
Koichi Ogami ◽  
Yuka Oishi ◽  
Takuto Nogimori ◽  
Kentaro Sakamoto ◽  
Shin-ichi Hoshino
Keyword(s):  
Amino Acid ◽  
Ribosomal Proteins ◽  
Rna Binding ◽  
Tail Length ◽  
Underlying Mechanism ◽  
Growth Conditions ◽  
Mtor Inhibition ◽  
Terminal Oligopyrimidine ◽  
Related Proteins

ABSTRACTOccasionally, cells must adapt to an inimical growth conditions like amino acid starvation (AAS) by downregulating protein synthesis. A class of transcripts containing 5’terminal oligopyrimidine (5’TOP) motif encodes translation-related proteins such as ribosomal proteins (RPs) and elongation factors, and therefore, their translation is severely repressed during AAS to conserve energy1. The RNA-binding protein LARP1 transduces amino acid signaling to TOP gene expression by controlling translation and stability of TOP mRNAs2-6. When released from AAS, translation machineries in turn have to be restored, however, the underlying mechanism of such re-adaptation is largely unknown. Here we show that LARP1 preserves TOP mRNAs in a long polyadenylated state during long-term AAS. We found that TOP mRNAs become highly polyadenylated when cells are in AAS or treated with the mTOR (mechanistic target of rapamycin) inhibitor Torin1. Importantly, depletion of LARP1 completely abrogated the polyadenylation of TOP mRNAs. Comprehensive analysis of poly(A) tail length using the Nanopore direct RNA sequencing revealed that TOP mRNAs are selectively polyadenylated under mTOR inhibition. Since a long poly(A) tail confers increased stability and polysome formation of TOP mRNAs, we predict that LARP1-dependent preservation of TOP mRNAs enables rapid translational resumption after the release from AAS.

scholarly journals Sodium Tanshinone IIA Sulfonate Improves Cognitive Impairment via Regulating Aβ Transportation in AD Transgenic Mouse Model

2021 ◽  
Author(s):  
shijie zhang ◽  
Hui-Han Ma ◽  
Can Wan ◽  
Lu-Ding Zhang ◽  
Rong-Rong Zhang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Underlying Mechanism ◽  
Transgenic Mouse Model ◽  
Tanshinone Iia ◽  
Potential Mechanism ◽  
Y Maze ◽  
Sodium Tanshinone Iia Sulfonate ◽  
Protein Expressions ◽  
Improved Learning ◽  
Related Proteins

Abstract Alzheimer’s disease (AD) is a most common neurodegenerative disease. Sodium Tanshinone IIA Sulfonate (STS) has been reported to ameliorate AD pathology. However, the underlying mechanism is still unclear. In this study, APP/PS1 mouse model was used to explore the potential mechanism of STS against AD. Morris water maze and Y-maze tests showed that administration of STS (10 or 20 mg/kg/day) improved learning and memory abilities of APP/PS1 mice. STS reduced the levels of ROS and MDA, while improved the activity of SOD in both hippocampus and cortex in APP/PS1 mice. STS inhibited the activity of AChE, while improved the activity of ChAT in APP/PS1 mice. In addition, STS elevated the protein expressions of neurotrophic factors (BDNF and NGF) and synapse-related proteins (PSD93, PSD95 and SYP) in both the hippocampus and cortex in APP/PS1 mice. At last, STS improved the protein expressions of GLUT1 and LRP1. These results indicated that the potential mechanism of STS on AD might be related to Aβ transportation function via GLUT1/LRP1 pathway.

Increasing Autophagy ameliorate all-trans-retinal-activated NLRP3 Inflammasome 2 in human THP-1 macrophage cells

2021 ◽  
Author(s):  
Qingqing Xia ◽  
Lvxing Huang ◽  
Hengyi Chen ◽  
Yingying Zhou ◽  
Lingmin Zhang ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Underlying Mechanism ◽  
Innate Immune ◽  
Cell Counting ◽  
Autophagic Flux ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation ◽  
Related Proteins ◽  
Excessive Activation ◽  
Insight Into

Abstract BackgroundProfound inflammation that mediated by innate immune sensors can be observed in retina, and is considered to play an important role in the pathogenesis of all-trans-retinal (atRAL)-caused retinal degeneration. However, the underlying mechanism remains elusive. MethodsCell viability was detected with Cell Counting Kit-8 (CCK-8). The concentration of IL-1β was evaluated using IL-1β ELISA Kits. The levels of autophagy-related proteins were measured by Western blotting. The measurement of autophagic flux was performed with virus vectors packing tandem monomeric mCherry-eGFP-tagged LC3B. ResultsWe focused on studying the effects of atRAL on macrophage cell line THP-1 and determining the underlying signal pathway through pharmacological and genetical manipulation. We first found the maturation and release of IL-1β was regulated by the activation of NLRP3 inflammasome. We secondly found that mitochondria-associated reactive oxygen species (ROS) were involved in the regulation of NLRP3 inflammasome activation and caspase 1 cleavage. Finally, we found that atRAL functionally activated autophagy in THP-1 cells, and atRAL-caused NLRP3 inflammasome activation is suppressed by autophagy. Overall, our results show atRAL simultaneously activates NLRP3 inflammasome and autophagy in THP-1 cells, and increasing autophagy leads to the inhibition of the excessive activation of NLRP3 inflammasome. Our study provides new insight into the pathogenesis of aging related retina degeneration.

Sign in / Sign up

Export Citation Format

Share Document