Myocardial perfusion and function imaging using single photon emission computed tomography (SPECT) plays the important role in coronary artery disease diagnostics and risk stratification, however, there is nowadays growing significance of the myocardial viability detection. A glucose metabolism assessment using positron emission tomography (PET) becomes accessible also. A brief review is given about the interpretation principle in the viable myocardium diagnosis and current progress in perfusion and metabolism defect severity quantification in patients with the left ventricular dysfunction.

• MeSH
• ischemická choroba srdeční diagnostické zobrazování   patofyziologie   MeSH
• jednofotonová emisní výpočetní tomografie * MeSH
• koronární cirkulace MeSH
• lidé MeSH
• pozitronová emisní tomografie * MeSH
• přežití tkáně MeSH
• srdce diagnostické zobrazování   MeSH
• zobrazování myokardiální perfuze * MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

The present study evaluated the impact of neonatal administration of capsaicin (neurotoxin from red hot pepper used for sensory denervation) on postnatal development of the heart rate and ventricular contractility. In the rats subjected to capsaicin administration (100 mg/kg) on postnatal days 2 and 3 and their vehicle-treated controls at the ages of 10 to 90 days, function of the sympathetic innervation of the developing heart was characterized by evaluation of chronotropic responses to metipranolol and atropine, norepinephrine concentrations in the heart, and norepinephrine release from the heart atria. Sensory denervation was verified by determination of calcitonin gene-related peptide levels in the heart. Direct cytotoxic effects of capsaicin were assessed on cultured neonatal cardiomyocytes. Capsaicin-treated rats displayed higher resting heart rates, lower atropine effect, but no difference in the effect of metipranolol. Norepinephrine tissue levels and release did not differ from controls. Contraction force of the right ventricular papillary muscle was lower till the age of 60 days. Significantly reduced viability of neonatal cardiomyocytes was demonstrated at capsaicin concentration 100 micromol/l. Our study suggests that neonatal capsaicin treatment leads to impaired maturation of the developing cardiomyocytes. This effect cannot be attributed exclusively to sensory denervation of the rat heart since capsaicin acts also directly on the cardiac cells.

• MeSH
• kapsaicin toxicita   MeSH
• kardiomyocyty účinky léků   fyziologie   MeSH
• kontrakce myokardu účinky léků   fyziologie   MeSH
• krysa rodu Rattus MeSH
• kultivované buňky MeSH
• novorozená zvířata MeSH
• potkani Wistar MeSH
• srdce účinky léků   růst a vývoj   MeSH
• srdeční frekvence účinky léků   fyziologie   MeSH
• viabilita buněk účinky léků   fyziologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• kapsaicin MeSH

The aim of this study was to find out whether opening of mitochondrial large-conductance Ca(2+)-activated potassium channels (BK(Ca)) protects cardiomyocytes against injury caused by simulated ischemia and reperfusion. This study also aimed to determine whether the protective mechanism involves signaling by reactive oxygen species (ROS) and phosphatidylinositol-3-kinase (PI3K). We used isolated ventricular myocytes, which are believed to contain no functional BK(Ca) channels in the sarcolemma. Cells were isolated from the left ventricles of adult male Wistar rats and subjected to 25-min metabolic inhibition with NaCN and 2-deoxyglucose followed by 30-min re-energization. NS11021 (0.1 μmol/L), a novel BK(Ca) channel opener, or hydrogen peroxide (2 μmol/L) added at re-energization, increased cell survival (the number of rod-shaped cells) and markedly reduced the release of lactate dehydrogenase (LDH). These cytoprotective effects of NS11021 were completely abolished by paxilline, a BK(Ca) inhibitor, or tempol, an antioxidant, but not by wortmannin, an inhibitor of PI3K. NS11021 slightly but significantly increased the fluorescence signal in 2'7'-dichlorodihydrofluorescein diacetate (DCF-DA)-loaded myocytes, indicating an increased ROS formation. The NS11021-induced ROS formation was abolished by paxilline or tempol. NS13558 (0.1 μmol/L), an inactive structural analogue of NS11021, affected neither cell survival/LDH release nor DCF-DA fluorescence. These results suggest that pharmacological activation of mitochondrial BK(Ca) channels effectively protects isolated cardiomyocytes against injury associated with simulated reperfusion. The mechanism for this form of protection requires ROS signaling, but not the activation of the PI3K pathway.

• MeSH
• kardiomyocyty účinky léků   fyziologie   MeSH
• kardiovaskulární látky metabolismus   MeSH
• krysa rodu Rattus MeSH
• L-laktátdehydrogenasa analýza   MeSH
• peroxid vodíku metabolismus   MeSH
• potkani Wistar MeSH
• reperfuzní poškození myokardu patologie   prevence a kontrola   MeSH
• tetrazoly metabolismus   MeSH
• thiomočovina analogy a deriváty   metabolismus   MeSH
• vápníkem aktivované draslíkové kanály s vysokou vodivostí - alfa-podjednotky agonisté   metabolismus   MeSH
• viabilita buněk účinky léků   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 1-(3,5-bis(trifluoromethyl)phenyl)-3-(4-bromo-2-(1H-tetrazol-5-yl)phenyl)thiourea MeSH Prohlížeč
• kardiovaskulární látky MeSH
• KCNMA1 protein, human MeSH Prohlížeč
• L-laktátdehydrogenasa MeSH
• peroxid vodíku MeSH
• tetrazoly MeSH
• thiomočovina MeSH
• vápníkem aktivované draslíkové kanály s vysokou vodivostí - alfa-podjednotky MeSH

Continuous normobaric hypoxia (CNH) renders the heart more tolerant to acute ischemia/reperfusion injury. Protein kinase C (PKC) is an important component of the protective signaling pathway, but the contribution of individual PKC isoforms under different hypoxic conditions is poorly understood. The aim of this study was to analyze the expression of PKCepsilon after the adaptation to CNH and to clarify its role in increased cardiac ischemic tolerance with the use of PKCepsilon inhibitory peptide KP-1633. Adult male Wistar rats were exposed to CNH (10 % O(2), 3 weeks) or kept under normoxic conditions. The protein level of PKCepsilon and its phosphorylated form was analyzed by Western blot in homogenate, cytosolic and particulate fractions; the expression of PKCepsilon mRNA was measured by RT-PCR. The effect of KP-1633 on cell viability and lactate dehydrogenase (LDH) release was analyzed after 25-min metabolic inhibition followed by 30-min re-energization in freshly isolated left ventricular myocytes. Adaptation to CNH increased myocardial PKCepsilon at protein and mRNA levels. The application of KP-1633 blunted the hypoxia-induced salutary effects on cell viability and LDH release, while control peptide KP-1723 had no effect. This study indicates that PKCepsilon is involved in the cardioprotective mechanism induced by CNH.

• MeSH
• fyziologická adaptace genetika   MeSH
• hypoxie enzymologie   genetika   patofyziologie   MeSH
• inhibitory proteinkinas farmakologie   MeSH
• kardiomyocyty účinky léků   metabolismus   MeSH
• krysa rodu Rattus MeSH
• L-laktátdehydrogenasa metabolismus   MeSH
• messenger RNA biosyntéza   genetika   MeSH
• potkani Wistar MeSH
• proteinkinasa C-epsilon antagonisté a inhibitory   biosyntéza   genetika   MeSH
• reperfuzní poškození myokardu enzymologie   genetika   MeSH
• viabilita buněk účinky léků   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• inhibitory proteinkinas MeSH
• L-laktátdehydrogenasa MeSH
• messenger RNA MeSH
• Prkce protein, rat MeSH Prohlížeč
• proteinkinasa C-epsilon MeSH

Chronic hypoxia protects the heart against injury caused by acute oxygen deprivation, but its salutary mechanism is poorly understood. The aim was to find out whether cardiomyocytes isolated from chronically hypoxic hearts retain the improved resistance to injury and whether the mitochondrial large-conductance Ca2+-activated K+ (BKCa) channels contribute to the protective effect. Adult male rats were adapted to continuous normobaric hypoxia (inspired O2 fraction 0.10) for 3 wk or kept at room air (normoxic controls). Myocytes, isolated separately from the left ventricle (LVM), septum (SEPM), and right ventricle, were exposed to 25-min metabolic inhibition with sodium cyanide, followed by 30-min reenergization (MI/R). Some LVM were treated with either 30 μM NS-1619 (BKCa opener), or 2 μM paxilline (BKCa blocker), starting 25 min before metabolic inhibition. Cell injury was detected by Trypan blue exclusion and lactate dehydrogenase (LDH) release. Chronic hypoxia doubled the number of rod-shaped LVM and SEPM surviving the MI/R insult and reduced LDH release. While NS-1619 protected cells from normoxic rats, it had no additive salutary effect in the hypoxic group. Paxilline attenuated the improved resistance of cells from hypoxic animals without affecting normoxic controls; it also abolished the protective effect of NS-1619 on LDH release in the normoxic group. While chronic hypoxia did not affect protein abundance of the BKCa channel regulatory β1-subunit, it markedly decreased its glycosylation level. It is concluded that ventricular myocytes isolated from chronically hypoxic rats retain the improved resistance against injury caused by MI/R. Activation of the mitochondrial BKCa channel likely contributes to this protective effect.

• MeSH
• benzimidazoly farmakologie   MeSH
• blokátory draslíkových kanálů farmakologie   MeSH
• chronická nemoc MeSH
• glykosylace MeSH
• hypoxie patofyziologie   MeSH
• indoly farmakologie   MeSH
• ischemické přivykání MeSH
• kardiomyocyty účinky léků   fyziologie   MeSH
• krysa rodu Rattus MeSH
• kultivované buňky MeSH
• L-laktátdehydrogenasa metabolismus   MeSH
• potkani Wistar MeSH
• reperfuzní poškození myokardu patofyziologie   prevence a kontrola   MeSH
• separace buněk MeSH
• srdeční mitochondrie účinky léků   fyziologie   MeSH
• vápníkem aktivované draslíkové kanály s vysokou vodivostí - beta-podjednotky fyziologie   MeSH
• vápníkem aktivované draslíkové kanály s vysokou vodivostí antagonisté a inhibitory   fyziologie   MeSH
• viabilita buněk MeSH
• western blotting MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Research Support, N.I.H., Extramural MeSH
• Názvy látek
• benzimidazoly MeSH
• blokátory draslíkových kanálů MeSH
• indoly MeSH
• L-laktátdehydrogenasa MeSH
• NS 1619 MeSH Prohlížeč
• paxilline MeSH Prohlížeč
• vápníkem aktivované draslíkové kanály s vysokou vodivostí - beta-podjednotky MeSH
• vápníkem aktivované draslíkové kanály s vysokou vodivostí MeSH

Ischemic postconditioning and remote conditioning are potentially useful tools for protecting ischemic myocardium. This study tested the hypothesis that 2,3-dehydrosilybin (DHS), a flavonolignan component of Silybum marianum, could attenuate cardiomyocyte damage following hypoxia/reoxygenation by decreasing the generation of reactive oxygen species (ROS). After 5-6 days of cell culture in normoxic conditions the rat neonatal cardiomyocytes were divided into four groups. Control group (9 h at normoxic conditions), hypoxia/reoxygenation group (3 h at 1 % O₂, 94 % N₂and 5 % CO₂followed by 10 min of 10 micromol·l⁻¹DHS and 6 h of reoxygenation in normoxia) and postconditioning group (3 h of hypoxia, three cycles of 5 min reoxygenation and 5 min hypoxia followed by 6 h of normoxia). Cell viability assessed by propidium iodide staining was decreased after DHS treatment consistent with increased levels of lactatedehydrogenase (LDH) after reoxygenation. LDH leakage was significantly reduced when cardiomyocytes in the H/Re group were exposed to DHS. DHS treatment reduced H₂O₂production and also decreased the generation of ROS in the H/Re group as evidenced by a fluorescence indicator. DHS treatment reduces reoxygenation-induced injury in cardiomyocytes by attenuation of ROS generation, H₂O₂and protein carbonyls levels. In addition, we found that both the postconditioning protocol and the DHS treatment are associated with restored ratio of phosphorylated/total protein kinase C epsilon, relative to the H/Re group. In conclusion, our data support the protective role of DHS in hypoxia/reperfusion injury and indicate that DHS may act as a postconditioning mimic.

• MeSH
• antioxidancia farmakologie   MeSH
• cytoprotekce MeSH
• fosforylace MeSH
• ischemické přivykání MeSH
• karbonylace proteinů účinky léků   MeSH
• kardiomyocyty účinky léků   metabolismus   patologie   MeSH
• kultivované buňky MeSH
• L-laktátdehydrogenasa metabolismus   MeSH
• novorozená zvířata MeSH
• oxidační stres účinky léků   MeSH
• peroxid vodíku metabolismus   MeSH
• potkani Wistar MeSH
• proteinkinasa C-epsilon metabolismus   MeSH
• reperfuzní poškození myokardu metabolismus   patologie   prevence a kontrola   MeSH
• signální transdukce účinky léků   MeSH
• silibinin MeSH
• silymarin farmakologie   MeSH
• viabilita buněk účinky léků   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• antioxidancia MeSH
• L-laktátdehydrogenasa MeSH
• peroxid vodíku MeSH
• Prkce protein, rat MeSH Prohlížeč
• proteinkinasa C-epsilon MeSH
• silibinin MeSH
• silymarin MeSH

Cardiac troponin T (cTnT) and troponin I (cTnI) are becoming acknowledged as useful biochemical markers of drug-induced cardiotoxicity. In this study we examined the release kinetics of cTnT and cTnI using an in vitro model of isolated rat neonatal ventricular cardiomyocytes (NVCM, 72h treatment with 0.1-3microM of daunorubicin) and compared it with data from a rabbit model of chronic anthracycline-induced cardiomyopathy in vivo (3mg/kg of daunorubicin weekly, 10 weeks). In cell-culture media, the cTnI and cTnT concentrations were concentration- and time-dependently increasing in response to daunorubicin exposure and were negatively exponentially related to cardiomyocyte viability. With 3microM daunorubicin, the relative increase of AUC of cTnT and cTnI was 2.4- and 5.3-fold higher than the increase of LDH activity, respectively. In rabbits, the daunorubicin-induced cardiomyopathy was associated with progressive increase of both cTnT and cTnI. Although the correlation between cTnT and cTnI cumulative release (AUCs) was found (R=0.81; P<0.01) and both cardiac troponins corresponded well with the echocardiographically-assessed systolic dysfunction (R=0.83 and 0.81 for cTnT and cTnI, respectively; P<0.001), the first significant increase in cTnI levels was observed earlier (at a cumulative daunorubicin dose of 200mg/m(2)) than with cTnT (350mg/m(2)). In conclusion, our study has confirmed cTnT and cTnI as very sensitive and specific markers of anthracycline-induced cardiotoxicity. The troponins can become not only the bridge between the clinical and experimental studies of drug-induced cardiotoxicity but also the linkage between the preclinical experiments in vitro and in vivo.

• MeSH
• biologické markery krev   MeSH
• daunomycin škodlivé účinky   MeSH
• kardiomyocyty * účinky léků   metabolismus   patologie   MeSH
• kardiomyopatie krev   chemicky indukované   metabolismus   MeSH
• králíci MeSH
• krysa rodu Rattus MeSH
• kultivované buňky MeSH
• novorozená zvířata MeSH
• protinádorová antibiotika škodlivé účinky   MeSH
• troponin I krev   MeSH
• troponin T krev   MeSH
• viabilita buněk účinky léků   MeSH
• western blotting MeSH
• zvířata MeSH
• Check Tag
• králíci MeSH
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• biologické markery MeSH
• daunomycin MeSH
• protinádorová antibiotika MeSH
• troponin I MeSH
• troponin T MeSH

Myocardial recovery from ischemia-reperfusion (IR) is shaped by the interaction of many signaling pathways and tissue repair processes, including the innate immune response. We and others previously showed that sustained expression of the transcriptional co-activator yes-associated protein (YAP) improves survival and myocardial outcome after myocardial infarction. Here, we asked whether transient YAP expression would improve myocardial outcome after IR injury. After IR, we transiently activated YAP in the myocardium with modified mRNA encoding a constitutively active form of YAP (aYAP modRNA). Histological studies 2 d after IR showed that aYAP modRNA reduced cardiomyocyte (CM) necrosis and neutrophil infiltration. 4 wk after IR, aYAP modRNA-treated mice had better heart function as well as reduced scar size and hypertrophic remodeling. In cultured neonatal and adult CMs, YAP attenuated H2O2- or LPS-induced CM necrosis. TLR signaling pathway components important for innate immune responses were suppressed by YAP/TEAD1. In summary, our findings demonstrate that aYAP modRNA treatment reduces CM necrosis, cardiac inflammation, and hypertrophic remodeling after IR stress.

• MeSH
• adaptorové proteiny signální transdukční aplikace a dávkování   genetika   MeSH
• apoptóza účinky léků   MeSH
• editace RNA MeSH
• infiltrace neutrofily účinky léků   MeSH
• injekce intramuskulární MeSH
• kardiomegalie farmakoterapie   etiologie   MeSH
• kardiomyocyty metabolismus   MeSH
• kultivované buňky MeSH
• lidé MeSH
• messenger RNA aplikace a dávkování   genetika   MeSH
• modely nemocí na zvířatech MeSH
• myokard imunologie   MeSH
• myokarditida farmakoterapie   etiologie   MeSH
• myši inbrední C57BL MeSH
• myši MeSH
• novorozená zvířata MeSH
• reperfuzní poškození myokardu komplikace   MeSH
• signální proteiny YAP MeSH
• transkripční faktory aplikace a dávkování   genetika   MeSH
• viabilita buněk účinky léků   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Research Support, N.I.H., Extramural MeSH
• Názvy látek
• adaptorové proteiny signální transdukční MeSH
• messenger RNA MeSH
• signální proteiny YAP MeSH
• transkripční faktory MeSH
• YAP1 protein, human MeSH Prohlížeč

Homeostasis of reactive oxygen species (ROS) in cardiomyocytes is critical for elucidation of normal heart physiology and pathology. Mitochondrial phospholipases A2 (mt-PLA2) have been previously suggested to be activated by ROS. Therefore, we have attempted to elucidate physiological role of such activation. We have found that function of a specific i-isoform of mitochondrial phospholipase A2 (mt-iPLA2) is activated by tert-butylhydroperoxide in isolated rat heart mitochondria. Isoform specificity was judged from the inhibition by bromoenol lactone (BEL), a specific iPLA2 inhibitor. Concomitant uncoupling has been caused by free fatty acids, since it was inhibited by bovine serum albumin. The uncoupling was manifested as a respiration burst accompanied by a slight decrease in mitochondrial inner membrane potential. Since this uncoupling was sensitive to carboxyatractyloside and purine nucleotide di- and tri-phosphates, we conclude that it originated from the onset of fatty acid cycling mediated by the adenine nucleotide translocase (major contribution) and mitochondrial uncoupling protein(s) (minor contribution), respectively. Such a mild uncoupling may provide a feedback downregulation of oxidative stress, since it can further attenuate mitochondrial production of ROS. In conclusion, ROS-induced function of cardiac mt-iPLA2 may stand on a pro-survival side of ischemia-reperfusion injury.

• MeSH
• aktivace enzymů účinky léků   fyziologie   MeSH
• fosfolipasy A2, skupina VI metabolismus   MeSH
• iontové kanály metabolismus   MeSH
• krysa rodu Rattus MeSH
• mastné kyseliny metabolismus   MeSH
• mitochondriální ADP/ATP-translokasy metabolismus   MeSH
• mitochondriální proteiny metabolismus   MeSH
• mitochondrie účinky léků   enzymologie   MeSH
• myokard enzymologie   patologie   MeSH
• oxidační stres účinky léků   fyziologie   MeSH
• oxidativní fosforylace MeSH
• potkani Wistar MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• reperfuzní poškození myokardu metabolismus   patologie   MeSH
• terc-butylhydroperoxid farmakologie   MeSH
• uncoupling protein 1 MeSH
• viabilita buněk fyziologie   MeSH
• zpětná vazba fyziologická fyziologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• fosfolipasy A2, skupina VI MeSH
• iontové kanály MeSH
• mastné kyseliny MeSH
• mitochondriální ADP/ATP-translokasy MeSH
• mitochondriální proteiny MeSH
• Pla2g6 protein, rat MeSH Prohlížeč
• reaktivní formy kyslíku MeSH
• terc-butylhydroperoxid MeSH
• uncoupling protein 1 MeSH

MicroRNAs are emerging as important regulators of cardiac function. This study investigated the role of microRNA-24 (miR-24) in ischemic cardiomyocytes, based on the observation that miR-24 expression was significantly enhanced in the ischemic myocardium of rats. Using primary cultured rat cardiomyocytes, cell injury was induced by ischemic conditions, and the cells were evaluated for changes in lactate dehydrogenase (LDH) release, cell viability, apoptosis and necrosis. The results showed that miR-24 was increased in myocytes exposed to ischemia. When miR-24 was further overexpressed in ischemic myocytes using the mimic RNA sequence, LDH release was reduced, cell viability was enhanced, and apoptosis and necrosis rates were both decreased. By contrast, a deficiency in miR-24 resulted in the largest LDH release, lowest cell viability and highest apoptosis and necrosis rates in normal and ischemic myocytes, with significant changes compared to that of non-transfected myocytes. Additionally, the mRNA and protein levels of the pro-apoptotic gene, BCL2L11, were down-regulated by miR-24 overexpression and up-regulated by miR-24 deficiency. The luciferase reporter assay confirmed BCL2L11 to be a target of miR-24. Overall, this study showed a protective role for miR-24 against myocardial ischemia by inhibiting BCL2L11, and may represent a potential novel treatment for ischemic heart disease.

• MeSH
• apoptóza genetika   MeSH
• faktor 1 indukovatelný hypoxií metabolismus   MeSH
• ischemická choroba srdeční genetika   metabolismus   patologie   MeSH
• kardiomyocyty metabolismus   MeSH
• krysa rodu Rattus MeSH
• L-laktátdehydrogenasa genetika   metabolismus   MeSH
• membránové proteiny genetika   metabolismus   MeSH
• mikro RNA genetika   metabolismus   MeSH
• nekróza genetika   MeSH
• ochranné látky metabolismus   MeSH
• potkani Sprague-Dawley MeSH
• protein BCL2L11 MeSH
• proteiny regulující apoptózu genetika   metabolismus   MeSH
• protoonkogenní proteiny genetika   metabolismus   MeSH
• upregulace MeSH
• viabilita buněk genetika   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• Bcl2l11 protein, rat MeSH Prohlížeč
• faktor 1 indukovatelný hypoxií MeSH
• L-laktátdehydrogenasa MeSH
• membránové proteiny MeSH
• mikro RNA MeSH
• MIRN24 microRNA, rat MeSH Prohlížeč
• ochranné látky MeSH
• protein BCL2L11 MeSH
• proteiny regulující apoptózu MeSH
• protoonkogenní proteiny MeSH