Second messenger
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svazky
- MeSH
- fosfoproteiny MeSH
- metabolismus MeSH
- nukleotidy cyklické MeSH
- vápník MeSH
- Publikační typ
- periodika MeSH
- Konspekt
- Fyziologie člověka a srovnávací fyziologie
- NLK Obory
- biochemie
- NLK Publikační typ
- ročenky
Nitric oxide (NO) stimulated the activity of plasma membrane H+-ATPase, 5'-nucleotidase, peroxidase, ascorbate peroxidase and glutathione reductase in ultraviolet B (UV-B) irradiated Chlorella pyrenoidosa. It also boosted the activity of nitrogen-metabolism enzymes such as nitrate reductase, nitrite reductase, glutamine synthetase, which were inhibited by UV-B irradiation. The chlorophyll fluorescence ratio (Fv/Fm) of the UV-B irradiated algae and decreased continuously after the cells were transferred to UV-B irradiation. A continuing decrease of the Fv/Fm was observed even after the cells were transferred to photosynthetically active radiation (PAR). After adaptation for 8 h under PAR (after treatment with nitric oxide), Fv/Fm recovered to 55 % of normal levels--without NO the value approached zero. Exogenous NO stopped the decay of chlorophyll and thylakoid membrane in cells exposed to UV-B irradiation. NO plays probably a key role in damage induced by UV-B irradiation in green algae.
401 s. : il.
- MeSH
- energetický metabolismus fyziologie MeSH
- experimenty na zvířatech MeSH
- finanční podpora výzkumu jako téma MeSH
- guanosinmonofosfát cyklický fyziologie MeSH
- kosterní svaly metabolismus MeSH
- oxid dusnatý fyziologie MeSH
- potkani Wistar MeSH
- regionální krevní průtok MeSH
- spotřeba kyslíku fyziologie MeSH
- systémy druhého messengeru fyziologie MeSH
- techniky in vitro MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
We investigated the influence of membrane cholesterol content on preferential and non-preferential signaling through the M(2) muscarinic acetylcholine receptor expressed in CHO cells. Cholesterol depletion by 39% significantly decreased the affinity of M(2) receptors for [(3)H]-N-methylscopolamine ([(3)H]-NMS) binding and increased B(max) in intact cells and membranes. Membranes displayed two-affinity agonist binding sites for carbachol and cholesterol depletion doubled the fraction of high-affinity binding sites. In intact cells it also reduced the rate of agonist-induced receptor internalization and changed the profile of agonist binding from a single site to two affinity states. Cholesterol enrichment by 137% had no effects on carbachol E(max) of cAMP synthesis inhibition and on cAMP synthesis stimulation and inositolphosphates (IP) accumulation at higher agonist concentrations (non-preferred pathways). On the other hand, cholesterol depletion significantly increased E(max) of cAMP synthesis inhibition or stimulation without change in potency, and decreased E(max) of IP accumulation. Noteworthy, modifications of membrane cholesterol had no effect on membrane permeability, oxidative activity, protein content, or relative expression of G(s), G(i/o), and G(q/11) alpha subunits. These results demonstrate distinct changes of M(2) receptor signaling through both preferential and non-preferential G-proteins consequent to membrane cholesterol depletion that occur at the level of receptor/G-protein/effector protein interactions in the cell membrane. The significant decrease of IP accumulation by cholesterol depletion was also observed in cells expressing M(3) receptors and by both cholesterol depletion and enrichment in cells expressing M(1) receptors indicating relevance of reduced G(q/11) signaling for the pathogenesis of Alzheimer's disease.
- MeSH
- acetylcholin analogy a deriváty MeSH
- antagonisté muskarinových receptorů farmakologie MeSH
- beta-cyklodextriny farmakologie MeSH
- buněčná membrána metabolismus účinky léků MeSH
- CHO buňky MeSH
- cholesterol metabolismus MeSH
- Cricetulus MeSH
- karbachol analogy a deriváty farmakologie metabolismus MeSH
- křečci praví MeSH
- lidé MeSH
- N-methylskopolamin farmakologie metabolismus MeSH
- proteiny vázající GTP metabolismus MeSH
- receptor muskarinový M2 metabolismus MeSH
- systémy druhého messengeru účinky léků MeSH
- zvířata MeSH
- Check Tag
- křečci praví MeSH
- lidé MeSH
- zvířata MeSH
- Publikační typ
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
P53 controls the growth and survival of cells by acting in response to a multitude of cellular stresses. It is, however, not yet fully understood how different p53 activation pathways result in either cell cycle arrest or apoptosis. We and others have described an N-terminally truncated p53 protein (p53/47) originating from a second translation initiation site in the p53 messenger RNA (mRNA), which can interact with p53 and impose altered stability and transactivation properties to p53 complexes. Here we show that cap-dependent and cap-independent mechanisms of initiation govern the translation of the p53 mRNA. Changes in synthesis of full-length p53 or p53/47 are regulated through distinct cell stress-induced pathways acting through separate regions of the p53 mRNA. We also show that some cytotoxic drugs require the presence of full-length p53 to induce apoptosis, whereas for others p53/47 is sufficient. This indicates that by harbouring alternative translation initiation sites, the p53 mRNA gives rise to different levels of the p53 isoforms which help to orchestrate the cell biological outcome of p53 activation in response to different types of cell stress. This sheds new light into the way p53 can integrate and differentiate a large multiplicity of changes in the cellular environment.
- MeSH
- 5' nepřekládaná oblast MeSH
- exprese genu MeSH
- lidé MeSH
- messenger RNA * metabolismus MeSH
- nádorové buněčné linie MeSH
- nádorový supresorový protein p53 * genetika MeSH
- northern blotting MeSH
- polymerázová řetězová reakce s reverzní transkripcí MeSH
- protein - isoformy * genetika MeSH
- proteosyntéza * fyziologie MeSH
- průtoková cytometrie MeSH
- regulace genové exprese * genetika MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- práce podpořená grantem MeSH
UNLABELLED: Obesity and metabolic syndrome is increasing health problem worldwide. Among other ways, nutritional intervention using phytochemicals is important method for treatment and prevention of this disease. Recent studies have shown that certain phytochemicals could alter the expression of specific genes and microRNAs (miRNAs) that play a fundamental role in the pathogenesis of obesity. For study of the obesity and its treatment, monosodium glutamate (MSG)-injected mice with developed central obesity, insulin resistance and liver lipid accumulation are frequently used animal models. To understand the mechanism of phytochemicals action in obese animals, the study of selected genes expression together with miRNA quantification is extremely important. For this purpose, real-time quantitative PCR is a sensitive and reproducible method, but it depends on proper normalization entirely. The aim of present study was to identify the appropriate reference genes for mRNA and miRNA quantification in MSG mice treated with green tea catechins, potential anti-obesity phytochemicals. Two sets of reference genes were tested: first set contained seven commonly used genes for normalization of messenger RNA, the second set of candidate reference genes included ten small RNAs for normalization of miRNA. The expression stability of these reference genes were tested upon treatment of mice with catechins using geNorm, NormFinder and BestKeeper algorithms. Selected normalizers for mRNA quantification were tested and validated on expression of NAD(P)H: quinone oxidoreductase, biotransformation enzyme known to be modified by catechins. The effect of selected normalizers for miRNA quantification was tested on two obesity- and diabetes- related miRNAs, miR-221 and miR-29b, respectively. Finally, the combinations of B2M/18S/HPRT1 and miR-16/sno234 were validated as optimal reference genes for mRNA and miRNA quantification in liver and 18S/RPlP0/HPRT1 and sno234/miR-186 in small intestine of MSG mice. These reference genes will be used for mRNA and miRNA normalization in further study of green tea catechins action in obese mice.
- MeSH
- algoritmy MeSH
- geny * MeSH
- kvantitativní polymerázová řetězová reakce metody normy MeSH
- messenger RNA genetika metabolismus MeSH
- mikro RNA genetika metabolismus MeSH
- modely nemocí na zvířatech MeSH
- myši MeSH
- obezita genetika MeSH
- referenční standardy MeSH
- regulace genové exprese MeSH
- reprodukovatelnost výsledků MeSH
- software MeSH
- stanovení celkové genové exprese MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
222 s. : il.
