Kim, S.H* Dotaz Zobrazit nápovědu
Heat shock proteins (HSPs) can be induced by various stresses and play an important role in cell cycle progression. HSP70 has been shown to act as an inhibitor of apoptosis. We studied HSP70 expression in bronchial epithelial cells of C57BL/6 mice and homozygous HPS70 knockout mice (hsp70.1–/–) exposed to chronic hypoxic stress. We also investigated changes in cellular proliferation and apoptosis in relation to HSP70. Lungs were removed from mice after a three-week period of exposure to 10 % O2. Immunoblots for HSP70 and immunohistochemical staining for HSP70 and Ki-67 were performed. Apoptosis was assessed using the TUNEL assay. The three-week period of hypoxic stress did not change HSP70 levels in total lung tissue, but a significant reduction in HSP70 expression was observed in bronchiolar epithelial cells. In wild type mice, both HSP70 and Ki-67 expression were significantly reduced in bronchiolar epithelial cells. In homozygous HPS70 knockout mice (hsp70.1–/–), apoptosis of bronchiolar epithelial cells was significantly increased. Our results suggest that HSP70 may exert anti-apoptotic effects in mouse bronchiolar epithelial cells.
- MeSH
- apoptóza genetika účinky léků MeSH
- epitelové buňky cytologie chemie MeSH
- hypoxie buňky fyziologie imunologie MeSH
- imunoblotting metody statistika a číselné údaje MeSH
- interpretace statistických dat MeSH
- myši inbrední C57BL MeSH
- proliferace buněk MeSH
- proteiny tepelného šoku HSC70 chemie MeSH
- proteiny tepelného šoku HSP70 fyziologie chemie MeSH
- respirační sliznice cytologie patofyziologie MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- srovnávací studie MeSH
Asian sand dust (ASD), also called China dust or yellow dust, mainly occurs in East Asia during spring and autumn. Because ASD enters the body mainly through the respiratory system, it can cause respiratory disorders or worsen underlying diseases. Because of this, it has become an important health concern that threatens the well-being of humans and animals. In this study, we investigated the effects of 15 and 30 mg/kg of Pycnogenol (PYC15 and 30 groups), a pine bark extract, on ASD-induced pulmonary inflammation in mice. We evaluated the inflammatory cell counts, inflammatory cytokines, and matrix-metalloproteinase (MMP)-9 expression in animal models. PYC administration significantly decreased inflammatory cell infiltration into lung tissue; this was accompanied by a reduction in the levels of proinflammatory mediators including interleukin (IL)-1β (P < 0.01), IL-6 (P < 0.01) and tumour necrosis factor-α (P < 0.01) in bronchoalveolar lavage fluids of ASD-exposed mice (ASD group). Histological analysis revealed that PYC suppressed ASD-induced pulmonary inflammation. Moreover, PYC suppressed the levels of matrix-metalloproteinase (MMP)-9 in the lung tissue of ASD-exposed mice, indicating that PYC reduced ASD-induced pulmonary inflammation by suppressing MMP-9. Together, these results indicate that PYC as the potential to treat ASD-driven pulmonary inflammation.
Attraction effects arise when a comprehender erroneously retrieves a distractor instead of a target item during memory retrieval operations. In Korean, considerable processing difficulties occur in the agreement relation checking between a subject and an honorific-marked predicate when an intervening distractor carries a non-honorific feature. We investigate how attraction effects are managed during the processing of Korean subject-predicate honorific agreement by two Korean-speaking groups with different language use experience backgrounds: college students and airline workers. Results showed that both groups demonstrated stable knowledge of the honorific agreement in the acceptability judgment task. In the self-paced reading task, the airline group, who used honorifics extensively in their workplace, was less affected by the attraction effect than the student group. Our findings suggest that long-term language use experience can modulate how language users manage potential influence from attraction effects in real-time sentence processing.
The Crb1 and 2 (Crumbs homolog 1 & 2) genes encode large, single-pass transmembrane proteins essential for the apicobasal polarity and adhesion of epithelial cells. Crb1 mutations cause degenerative retinal diseases in humans, including Leber congenital amaurosis type 8 (LCA8) and retinitis pigmentosa type 12 (RP12). In LCA8, impaired photoreceptor development and/or survival is thought to cause blindness during early infancy, whereas, in RP12, progressive photoreceptor degeneration damages peripheral vision later in life. There are multiple animal models of RP12 pathology, but no experimental model of LCA8 recapitulates the full spectrum of its pathological features. To generate a mouse model of LCA8 and identify the functions of Crb1/2 in developing ocular tissues, we used an mRx-Cre driver to generate allelic combinations that enabled conditional gene ablation from the optic vesicle stage. In this series only Crb1/2 double knockout (dKO) mice exhibited characteristics of human LCA8 disease: locally thickened retina with spots devoid of cells, aberrant positioning of retinal cells, severely disrupted lamination, and depigmented retinal-pigmented epithelium. Retinal defects antedated E12.5, which is far earlier than the stage at which photoreceptor cells mainly differentiate. Most remarkably, Crb1/Crb2 dKO showed a severely attenuated electroretinogram at the eye opening stage. These results suggest that human LCA8 can be modeled in the mouse by simultaneously ablating Crb1/2 from the beginning of eye development. Importantly, they also indicate that LCA8 is caused by malfunction of retinal progenitor cells during early ocular development rather than by defective photoreceptor-Muller glial interaction, a mechanism proposed for RP12.
- MeSH
- delece genu * MeSH
- dospělí MeSH
- elektroretinografie MeSH
- fotoreceptory obratlovců metabolismus MeSH
- Leberova kongenitální amauróza genetika patologie MeSH
- lidé MeSH
- membránové proteiny genetika metabolismus MeSH
- modely nemocí na zvířatech MeSH
- mutace genetika MeSH
- myši inbrední C57BL MeSH
- myši knockoutované MeSH
- oči metabolismus patologie MeSH
- orgánová specificita MeSH
- pigmentace MeSH
- proteiny nervové tkáně genetika metabolismus MeSH
- retinální pigmentový epitel metabolismus patologie MeSH
- zvířata MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Publikační typ
- abstrakt z konference MeSH
- MeSH
- HIV infekce diagnóza epidemiologie virologie MeSH
- HIV genetika klasifikace mikrobiologie MeSH
- lidé MeSH
- sekvence nukleotidů MeSH
- sérologické testy MeSH
- virové geny MeSH
- Check Tag
- lidé MeSH
- Geografické názvy
- Korea MeSH
Remifentanil is a commonly used opioid in anesthesia with cardioprotective effect in ischemia-reperfused (I/R) heart. We evaluated the influence of remifentanil on myocardial infarct size and expressions of proteins involved in apoptosis in I/R rat heart following various time protocols of remifentanil administration. Artificially ventilated anesthetized Sprague-Dawley rats were subjected to a 30 min of left anterior descending coronary artery occlusion followed by 2 h of reperfusion. Rats were randomly assigned to one of five groups; Sham, I/R only, remifentanil preconditioning, postconditioning and continuous infusion group. Myocardial infarct size, the phosphorylation of ERK1/2, Bcl2, Bax and cytochrome c and the expression of genes influencing Ca2+ homeostasis were assessed. In remifentanil-administered rat hearts, regardless of the timing and duration of administration, infarct size was consistently reduced compared to I/R only rats. Remifentanil improved expression of ERK 1/2 and anti-apoptotic protein Bcl2, and expression of sarcoplasmic reticulum genes which were significantly reduced in the I/R rats only. Remifentanil reduced expression of pro-apoptotic protein, Bax and cytochrome c. These suggested that remifentanil produced cardioprotective effect by preserving the expression of proteins involved in anti-apoptotic pathways, and the expression of sarcoplasmic reticulum genes in I/R rat heart, regardless of the timing of administration.
- MeSH
- adjuvancia anestetická MeSH
- apoptóza účinky léků MeSH
- časové faktory MeSH
- cytochromy c metabolismus MeSH
- financování organizované MeSH
- fosforylace MeSH
- hemodynamika účinky léků MeSH
- homeostáza MeSH
- infarkt myokardu MeSH
- krysa rodu rattus MeSH
- messenger RNA metabolismus MeSH
- mitogenem aktivovaná proteinkinasa 1 metabolismus MeSH
- mitogenem aktivovaná proteinkinasa 3 metabolismus MeSH
- modely nemocí na zvířatech MeSH
- myokard metabolismus patologie MeSH
- piperidiny aplikace a dávkování farmakologie MeSH
- polymerázová řetězová reakce s reverzní transkripcí MeSH
- potkani Sprague-Dawley MeSH
- protein X asociovaný s bcl-2 metabolismus MeSH
- protoonkogenní proteiny c-bcl-2 metabolismus MeSH
- regulace genové exprese účinky léků MeSH
- reperfuze myokardu MeSH
- sarkoplazmatické retikulum metabolismus MeSH
- vápník metabolismus MeSH
- viabilita buněk účinky léků MeSH
- western blotting MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
