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1.
Article in English | MEDLINE | ID: mdl-30041062

ABSTRACT

Hypoxia inducible factor-1 (HIF-1) is a transcriptional factor that induces genes involved in glucose metabolism. HIF-1 is formed by a regulatory α-subunit (HIF-1α) and a constitutive ß-subunit (HIF-1ß). The white spot syndrome virus (WSSV) induces a shift in glucose metabolism and oxidative stress. HIF-1α is associated with the induction of metabolic changes in tissues of WSSV-infected shrimp. However, the contributions of HIF-1 to viral load and antioxidant responses in WSSV-infected shrimp have been not examined. In this study, the effect of HIF-1 silencing on viral load and the expression and activity of antioxidant enzymes (superoxide dismutase-SOD, glutathione S-transferase-GST, and catalase) along with oxidative damage (lipid peroxidation and protein carbonyl) in tissues of white shrimp infected with the WSSV were studied. The viral load increased in hepatopancreas and muscle after WSSV infection, and the accumulative mortality was of 100% at 72 h post-infection. The expression and activity of SOD, catalase, and GST decreased in each tissue evaluated after WSSV infection. Protein carbonyl concentrations increased in each tissue after WSSV infection, while lipid peroxidation increased in hepatopancreas, but not in muscle. Silencing of HIF-1α decreased the WSSV viral load in hepatopancreas and muscle of infected shrimp along with shrimp mortality. Silencing of HIF-1α ameliorated the antioxidant response in a tissue-specific manner, which translated to a decrease in oxidative damage. These results suggest that HIF-1 is essential for restoring the antioxidant response, which counters the oxidative injury associated with WSSV infection.


Subject(s)
Gene Expression Regulation, Developmental , Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & inhibitors , Penaeidae/virology , White spot syndrome virus 1/pathogenicity , Animals , Aquaculture , DNA, Viral/isolation & purification , Gene Silencing , Hepatopancreas/growth & development , Hepatopancreas/metabolism , Hepatopancreas/virology , Hypoxia-Inducible Factor 1, alpha Subunit/genetics , Hypoxia-Inducible Factor 1, alpha Subunit/metabolism , Injections, Intramuscular , Lipid Peroxidation , Mexico , Muscles/metabolism , Muscles/virology , Organ Specificity , Oxidative Stress , Oxidoreductases/genetics , Oxidoreductases/metabolism , Penaeidae/growth & development , Penaeidae/metabolism , Protein Carbonylation , RNA Interference , RNA, Double-Stranded/administration & dosage , RNA, Double-Stranded/metabolism , Viral Load , White spot syndrome virus 1/isolation & purification , White spot syndrome virus 1/physiology
2.
Biomed Res Int ; 2014: 984785, 2014.
Article in English | MEDLINE | ID: mdl-25147829

ABSTRACT

The pathologic cardiac remodeling has been widely documented; however, the physiological cardiac remodeling induced by pregnancy and its reversion in postpartum are poorly understood. In the present study we investigated the changes in collagen I (Col I) and collagen III (Col III) mRNA and protein levels in left ventricle from rat heart during pregnancy and postpartum. Col I and Col III mRNA expression in left ventricle samples during pregnancy and postpartum were analyzed by using quantitative PCR. Data obtained from gene expression show that Col I and Col III in left ventricle are upregulated during pregnancy with reversion in postpartum. In contrast to gene expression, the protein expression evaluated by western blot showed that Col I is downregulated and Col III is upregulated in left ventricle during pregnancy. In conclusion, the pregnancy differentially regulates collagens types I and III in heart; this finding could be an important molecular mechanism that regulates the ventricular stiffness in response to blood volume overload present during pregnancy which is reversed in postpartum.


Subject(s)
Collagen Type III/genetics , Collagen Type III/metabolism , Collagen Type I/genetics , Collagen Type I/metabolism , Heart Ventricles/metabolism , Animals , Down-Regulation/genetics , Female , Gene Expression/genetics , Postpartum Period/genetics , Pregnancy , RNA, Messenger/genetics , Rats , Rats, Sprague-Dawley , Up-Regulation/genetics
3.
Protein Pept Lett ; 13(1): 71-5, 2006.
Article in English | MEDLINE | ID: mdl-16454673

ABSTRACT

Shrimp High Density Lipoprotein-beta-Glucan Binding Protein (HDL/BGBP) has been studied by its role in nutrition and innate defense. Although the mechanisms of lipid loading are still unknown, HDL-BGBP binds and aggregates phospholipids vesicles in vitro. To gain insights into the HDL-BGBP mechanism of interaction with membranes, we have used fluorescence spectroscopy and electron microscopy. Data show that HDL-BGBP does not induce membrane fusion, leakage nor lipid exchange, although microstructural changes are clearly observed. This work supports a model where protein aggregation leads to liposome clustering. Such interaction may be a critical factor for the activation of the shrimp blood cell in vivo.


Subject(s)
Carrier Proteins/chemistry , Cholesterol, HDL/chemistry , Lectins/chemistry , Animals , Biophysical Phenomena , Biophysics , Carrier Proteins/ultrastructure , Crustacea , Lectins/ultrastructure , Liposomes , Membrane Lipids/chemistry , Microscopy, Electron , Spectrometry, Fluorescence
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