scholarly journals Regulation of Angiogenesis-Related Prostaglandin F2alpha-Induced Genes in the Bovine Corpus Luteum1

2012 ◽  
Vol 86 (3) ◽  
Author(s):  
Yulia Zalman ◽  
Eyal Klipper ◽  
Svetlana Farberov ◽  
Mohan Mondal ◽  
Gabbine Wee ◽  
...  
Keyword(s):  
Prostaglandin F2alpha ◽  
Induced Genes

Isolation of in planta-Induced Genes of Pseudomonas viridiflava

2004 ◽  
Vol 39 (4) ◽  
pp. 361-375 ◽  
Author(s):  
A. A. Czelleng ◽  
Z. Bozsó ◽  
P. G. Ott ◽  
E. Besenyei ◽  
G. J. Varga ◽  
...  
Keyword(s):  
In Planta ◽  
Pseudomonas Viridiflava ◽  
Induced Genes

scholarly journals Levosimendan as a therapeutic strategy to prevent neuroinflammation after aneurysmal subarachnoid hemorrhage?

2021 ◽  
pp. neurintsurg-2021-017504
Author(s):  
Stefan Wanderer ◽  
Lukas Andereggen ◽  
Jan Mrosek ◽  
Sepide Kashefiolasl ◽  
Gerrit Alexander Schubert ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Severe Heart Failure ◽  
Prostaglandin F2alpha ◽  
Sprague Dawley ◽  
Delayed Cerebral Vasospasm ◽  
Sprague Dawley Rats ◽  
Solvent Control ◽  
Anti Inflammatory

BackgroundPoor patient outcomes after aneurysmal subarachnoid hemorrhage (SAH) occur due to a multifactorial process, mainly involving cerebral inflammation (CI), delayed cerebral vasospasm (DCVS), and delayed cerebral ischemia, followed by neurodegeneration. CI is mainly triggered by enhanced synthesis of serotonin (5-HT), prostaglandin F2alpha (PGF2a), and cytokines such as interleukins. Levosimendan (LV), a calcium-channel sensitizer, has already displayed anti-inflammatory effects in patients with severe heart failure. Therefore, we wanted to elucidate its potential anti-inflammatory role on the cerebral vasculature after SAH.MethodsExperimental SAH was induced by using an experimental double-hemorrhage model. Sprague Dawley rats were harvested on day 3 and day 5 after the ictus. The basilar artery was used for isometric investigations of the muscular media tone. Vessel segments were either preincubated with LV or without, with precontraction performed with 5-HT or PGF2a followed by application of acetylcholine (ACh) or LV.ResultsAfter preincubation with LV 10−4 M and 5-HT precontraction, ACh triggered a strong vasorelaxation in sham segments (LV 10−4 M, Emax 65%; LV 10−5 M, Emax 48%; no LV, Emax 53%). Interestingly, SAH D3 (LV 10−4, Emax 76%) and D5 (LV 10−4, Emax 79%) segments showed greater vasorelaxation compared with sham. An LV series after PGF2a precontraction showed significantly enhanced relaxation in the sham (P=0.004) and SAH groups (P=0.0008) compared with solvent control vessels.ConclusionsLV application after SAH seems to beneficially influence DCVS by antagonizing 5-HT- and PGF2a-triggered vasoconstriction. Considering this spasmolytic effect, LV might have a role in the treatment of SAH, additionally in selected patients suffering takotsubo cardiomyopathy.

scholarly journals Analysis of Subcellular RNA Fractions Revealed a Transcription-Independent Effect of Tumor Necrosis Factor Alpha on Splicing, Mediated by Spt5

2016 ◽  
Vol 36 (9) ◽  
pp. 1342-1353 ◽  
Author(s):  
Gil Diamant ◽  
Tal Eisenbaum ◽  
Dena Leshkowitz ◽  
Rivka Dikstein
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Independent Effect ◽  
Necrosis Factor Alpha ◽  
Pol Ii ◽  
Tnf Α ◽  
Factor Alpha ◽  
Induced Genes ◽  
Necrosis Factor

The proinflammatory cytokine tumor necrosis factor alpha (TNF-α) modulates the expression of many genes, primarily through activation of NF-κB. Here, we examined the global effects of the elongation factor Spt5 on nascent and mature mRNAs of TNF-α-induced cells using chromatin and cytosolic subcellular fractions. We identified several classes of TNF-α-induced genes controlled at the level of transcription, splicing, and chromatin retention. Spt5 was found to facilitate splicing and chromatin release in genes displaying high induction rates. Further analysis revealed striking effects of TNF-α on the splicing of 25% of expressed genes; the vast majority were not transcriptionally induced. Splicing enhancement of noninduced genes by TNF-α was transient and independent of NF-κB. Investigating the underlying basis, we found that Spt5 is required for the splicing facilitation of the noninduced genes. In line with this, Spt5 interacts with Sm core protein splicing factors. Furthermore, following TNF-α treatment, levels of RNA polymerase II (Pol II) but not Spt5 are reduced from the splicing-induced genes, suggesting that these genes become enriched with a Pol II-Spt5 form. Our findings revealed the Pol II-Spt5 complex as a highly competent coordinator of cotranscriptional splicing.

scholarly journals Early auxin-induced genes encode short-lived nuclear proteins.

1994 ◽  
Vol 91 (1) ◽  
pp. 326-330 ◽  
Author(s):  
S. Abel ◽  
P. W. Oeller ◽  
A. Theologis
Keyword(s):  
Nuclear Proteins ◽  
Induced Genes

scholarly journals Trichoderma asperelloides Suppresses Nitric Oxide Generation Elicited by Fusarium oxysporum in Arabidopsis Roots

2014 ◽  
Vol 27 (4) ◽  
pp. 307-314 ◽  
Author(s):  
Kapuganti J. Gupta ◽  
Luis A. J. Mur ◽  
Yariv Brotman
Keyword(s):  
Nitric Oxide ◽  
Fusarium Oxysporum ◽  
No Production ◽  
Disease Development ◽  
Necrotrophic Pathogen ◽  
Trichoderma Spp ◽  
Promote Plant Growth ◽  
Induced Genes ◽  
Underlying Mechanisms ◽  
Lectin Protein

Inoculations with saprophytic fungus Trichoderma spp. are now extensively used both to promote plant growth and to suppress disease development. The underlying mechanisms for both roles have yet to be fully described so that the use of Trichoderma spp. could be optimized. Here, we show that Trichoderma asperelloides effects include the manipulation of host nitric oxide (NO) production. NO was rapidly formed in Arabidopsis roots in response to the soil-borne necrotrophic pathogen Fusarium oxysporum and persisted for about 1 h but is only transiently produced (approximately 10 min) when roots interact with T. asperelloides (T203). However, inoculation of F. oxysporum–infected roots with T. asperelloides suppressed F. oxysporum–initiated NO production. A transcriptional study of 78 NO-modulated genes indicated most genes were suppressed by single and combinational challenge with F. oxysporum or T. asperelloides. Only two F. oxysporum–induced genes were suppressed by T. asperelloides inoculation undertaken either 10 min prior to or after pathogen infection: a concanavlin A-like lectin protein kinase (At4g28350) and the receptor-like protein RLP30. Thus, T. asperelloides can actively suppress NO production elicited by F. oxysporum and impacts on the expression of some genes reported to be NO-responsive. Of particular interest was the reduced expression of receptor-like genes that may be required for F. oxysporum–dependent necrotrophic disease development.

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