An intronic endogenous retrovirus-like sequence attenuates human haptoglobin-related gene expression in an orientation-dependent manner

Gene ◽  
2003 ◽  
Vol 319 ◽  
pp. 55-63 ◽  
Author(s):  
Seigo Hatada ◽  
Delores J Grant ◽  
Nobuyo Maeda
HortScience ◽  
2016 ◽  
Vol 51 (2) ◽  
pp. 152-158 ◽  
Author(s):  
Ji-Lian Zheng ◽  
Lan-Ying Hu ◽  
Kang-Di Hu ◽  
Jun Wu ◽  
Feng Yang ◽  
...  

Hydrogen sulfide (H2S) has been identified as a multifunctional signaling molecule in plants. Here, we show that H2S delayed postharvest senescence of fresh-cut apples (Malus ×pumila) in a dose-dependent manner. Exogenous H2S application maintained significantly higher levels of ascorbic acid, flavonoids, total phenolics, reducing sugars and soluble proteins, and lower levels of free amino acids in apple slices compared with controls. Further investigations showed that H2S significantly reduced the accumulation of superoxide radicals, hydrogen peroxide (H2O2) and malondialdehyde (MDA). Apple fruits fumigated with H2S contained significantly higher activities of ascorbate peroxidase (APX), catalase (CAT), glutathione reductase (GR), guaiacol peroxidase (POD) and superoxide dismutase (SOD), and lower activities of lipoxygenase (LOX), phenylalanine ammonia lyase (PAL), polyphenol oxidase (PPO), and protease relative to controls. H2S also upregulated MdDHAR expression and downregulated the expression of MdLOX2, MdPG1, MdPPO, MdACO1, MdERS1, and MdETR1 in postharvest apple tissue. The present study indicates that H2S was involved in delaying postharvest senescence of apples by acting as an antioxidant and by regulating senescence-related gene expression.


Meat Science ◽  
2017 ◽  
Vol 124 ◽  
pp. 84-94 ◽  
Author(s):  
Joël D'Astous-Pagé ◽  
Claude Gariépy ◽  
Richard Blouin ◽  
Simon Cliche ◽  
Brian Sullivan ◽  
...  

2020 ◽  
Vol 59 (4) ◽  
pp. 669-676 ◽  
Author(s):  
Pedro Negri ◽  
Leonor Ramirez ◽  
Silvina Quintana ◽  
Nicolas Szawarski ◽  
Matías D. Maggi ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Temitayo O. Idowu ◽  
Valerie Etzrodt ◽  
Thorben Pape ◽  
Joerg Heineke ◽  
Klaus Stahl ◽  
...  

Abstract Background Reduced endothelial Tie2 expression occurs in diverse experimental models of critical illness, and experimental Tie2 suppression is sufficient to increase spontaneous vascular permeability. Looking for a common denominator among different critical illnesses that could drive the same Tie2 suppressive (thereby leak inducing) phenotype, we identified “circulatory shock” as a shared feature and postulated a flow-dependency of Tie2 gene expression in a GATA3 dependent manner. Here, we analyzed if this mechanism of flow-regulation of gene expression exists in vivo in the absence of inflammation. Results To experimentally mimic a shock-like situation, we developed a murine model of clonidine-induced hypotension by targeting a reduced mean arterial pressure (MAP) of approximately 50% over 4 h. We found that hypotension-induced reduction of flow in the absence of confounding disease factors (i.e., inflammation, injury, among others) is sufficient to suppress GATA3 and Tie2 transcription. Conditional endothelial-specific GATA3 knockdown (B6-Gata3tm1-Jfz VE-Cadherin(PAC)-cerERT2) led to baseline Tie2 suppression inducing spontaneous vascular leak. On the contrary, the transient overexpression of GATA3 in the pulmonary endothelium (jet-PEI plasmid delivery platform) was sufficient to increase Tie2 at baseline and completely block its hypotension-induced acute drop. On the functional level, the Tie2 protection by GATA3 overexpression abrogated the development of pulmonary capillary leakage. Conclusions The data suggest that the GATA3–Tie2 signaling pathway might play a pivotal role in controlling vascular barrier function and that it is affected in diverse critical illnesses with shock as a consequence of a flow-regulated gene response. Targeting this novel mechanism might offer therapeutic opportunities to treat vascular leakage of diverse etiologies.


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