BMC Physiology最新文献

{"title":"Dual role of nNOS in ischemic injury and preconditioning.","authors":"Anupama Barua,&nbsp;Nicholas B Standen,&nbsp;Manuel Galiñanes","doi":"10.1186/1472-6793-10-15","DOIUrl":"https://doi.org/10.1186/1472-6793-10-15","url":null,"abstract":"<p><strong>Background: </strong>Nitric oxide (NO) is cardioprotective and a mediator of ischemic preconditioning (IP). Endothelial nitric oxide synthase (eNOS) is protective against myocardial ischemic injury and a component of IP but the role and location of neuronal nitric oxide synthase (nNOS) remains unclear. Therefore, the aims of these studies were to: (i) investigate the role of nNOS in ischemia/reoxygenation-induced injury and IP, (ii) determine whether its effect is species-dependent, and (iii) elucidate the relationship of nNOS with mitoKATP channels and p38MAPK, two key components of IP transduction pathway.</p><p><strong>Results: </strong>Ventricular myocardial slices from rats and wild and nNOS knockout mice, and right atrial myocardial slices from human were subjected to 90 min ischemia and 120 min reoxygenation (37 degrees C). Specimens were randomized to receive various treatments (n = 6/group). Both the provision of exogenous NO and the inhibition of endogenous NO production significantly reduced tissue injury (creatine kinase release, cell necrosis and apoptosis), an effect that was species-independent. The cardioprotection seen with nNOS inhibition was as potent as that of IP, however, in nNOS knockout mice the cardioprotective effect of non-selective NOS (L-NAME) and selective nNOS inhibition and also that of IP was blocked while the benefit of exogenous NO remained intact. Additional studies revealed that the cardioprotection afforded by exogenous NO and by inhibition of nNOS were unaffected by the mitoKATP channel blocker 5-HD, although it was abrogated by p38MAPK blocker SB203580.</p><p><strong>Conclusions: </strong>nNOS plays a dual role in ischemia/reoxygenation in that its presence is necessary to afford cardioprotection by IP and its inhibition reduces myocardial ischemic injury. The role of nNOS is species-independent and exerted downstream of the mitoKATP channels and upstream of p38MAPK.</p>","PeriodicalId":35905,"journal":{"name":"BMC Physiology","volume":"10 ","pages":"15"},"PeriodicalIF":0.0,"publicationDate":"2010-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1472-6793-10-15","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29187079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peristalsis in the junction region of the Drosophila larval midgut is modulated by DH31 expressing enteroendocrine cells.","authors":"Dennis R LaJeunesse,&nbsp;Brooke Johnson,&nbsp;Jason S Presnell,&nbsp;Kathleen Kay Catignas,&nbsp;Grzegorz Zapotoczny","doi":"10.1186/1472-6793-10-14","DOIUrl":"https://doi.org/10.1186/1472-6793-10-14","url":null,"abstract":"<p><strong>Background: </strong>The underlying cellular and molecular mechanisms that coordinate the physiological processes in digestion are complex, cryptic, and involve the integration of multiple cellular and organ systems. In all intestines, peristaltic action of the gut moves food through the various stages of digestion from the anterior end towards the posterior, with the rate of flow dependent on signals, both intrinsic and extrinsic to the gut itself.</p><p><strong>Results: </strong>We have identified an enteroendocrine cell type that regulates gut motility in the Drosophila melanogaster larval midgut. These cells are located at the junction of the anterior and the acidic portions of the midgut and are a group of enteroendocrine cells that express the peptide hormone Diuretic Hormone 31 in this region of the gut. Using cell ablation and ectopic activation via expression of the Chlamydomonas reinhardtii blue light-activated channelopsin, we demonstrate that these enteroendocrine cells are both necessary and sufficient for the peristalsis in the junction region of the midgut and require the Diuretic Hormone 31 to affect normal peristalsis in this region. Within the same junction region of the midgut, we have also identified morphological features suggesting that this region acts as a valve that regulates the transit of food from the anterior midgut into the acidic portion of the gut.</p><p><strong>Conclusions: </strong>We have characterized and described a set of enteroendocrine cells called the Midgut Junction DH31 expressing cells that are required for peristaltic movement in the junction region between the anterior portion and acidic region of the larval midgut of Drosophila melanogaster. We have shown that the Midgut Junction DH31 expressing cells are necessary and sufficient for motility and that the peptide hormone DH31 is required for peristalsis in the junction region of the midgut. The Drosophila model system will allow for a further dissection of the digestion process and provide a better understanding of the mechanisms that regulate digestion in all organisms.</p>","PeriodicalId":35905,"journal":{"name":"BMC Physiology","volume":"10 ","pages":"14"},"PeriodicalIF":0.0,"publicationDate":"2010-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1472-6793-10-14","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29181543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular pathology of vertebral deformities in hyperthermic Atlantic salmon (Salmo salar).","authors":"Elisabeth Ytteborg,&nbsp;Grete Baeverfjord,&nbsp;Jacob Torgersen,&nbsp;Kirsti Hjelde,&nbsp;Harald Takle","doi":"10.1186/1472-6793-10-12","DOIUrl":"https://doi.org/10.1186/1472-6793-10-12","url":null,"abstract":"<p><strong>Background: </strong>Hyperthermia has been shown in a number of organisms to induce developmental defects as a result of changes in cell proliferation, differentiation and gene expression. In spite of this, salmon aquaculture commonly uses high water temperature to speed up developmental rate in intensive production systems, resulting in an increased frequency of skeletal deformities. In order to study the molecular pathology of vertebral deformities, Atlantic salmon was subjected to hyperthermic conditions from fertilization until after the juvenile stage.</p><p><strong>Results: </strong>Fish exposed to the high temperature regime showed a markedly higher growth rate and a significant higher percentage of deformities in the spinal column than fish reared at low temperatures. By analyzing phenotypically normal spinal columns from the two temperature regimes, we found that the increased risk of developing vertebral deformities was linked to an altered gene transcription. In particular, down-regulation of extracellular matrix (ECM) genes such as col1a1, osteocalcin, osteonectin and decorin, indicated that maturation and mineralization of osteoblasts were restrained. Moreover, histological staining and in situ hybridization visualized areas with distorted chondrocytes and an increased population of hypertrophic cells. These findings were further confirmed by an up-regulation of mef2c and col10a, genes involved in chondrocyte hypertrophy.</p><p><strong>Conclusion: </strong>The presented data strongly indicates that temperature induced fast growth is severely affecting gene transcription in osteoblasts and chondrocytes; hence change in the vertebral tissue structure and composition. A disrupted bone and cartilage production was detected, which most likely is involved in the higher rate of deformities developed in the high intensive group. Our results are of basic interest for bone metabolism and contribute to the understanding of the mechanisms involved in development of temperature induced vertebral pathology. The findings may further conduce to future molecular tools for assessing fish welfare in practical farming.</p>","PeriodicalId":35905,"journal":{"name":"BMC Physiology","volume":"10 ","pages":"12"},"PeriodicalIF":0.0,"publicationDate":"2010-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1472-6793-10-12","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29102831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morphological and molecular characterization of developing vertebral fusions using a teleost model.","authors":"Elisabeth Ytteborg, Jacob Torgersen, Grete Baeverfjord, Harald Takle","doi":"10.1186/1472-6793-10-13","DOIUrl":"10.1186/1472-6793-10-13","url":null,"abstract":"<p><strong>Background: </strong>Spinal disorders are a major cause of disability for humans and an important health problem for intensively farmed animals. Experiments have shown that vertebral deformities present a complex but comparable etiology across species. However, the underlying molecular mechanisms involved in bone deformities are still far from understood. To further explicate the mechanisms involved, we have examined the fundamental aspects of bone metabolism and pathogenesis of vertebral fusions in Atlantic salmon (Salmo salar).</p><p><strong>Results: </strong>Experimentally, juvenile salmon were subjected to hyperthermic conditions where more than 28% developed fused vertebral bodies. To characterize the fusion process we analyzed an intermediate and a terminal stage of the pathology by using x-ray, histology, immunohistochemistry, real-time quantitative PCR and in situ hybridization. At early stage in the fusion process, disorganized and proliferating osteoblasts were prominent at the growth zones of the vertebral body endplates. PCNA positive cells further extended along the rims of fusing vertebral bodies. During the developing pathology, the marked border between the osteoblast growth zones and the chondrocytic areas connected to the arches became less distinct, as proliferating cells and chondrocytes blended through an intermediate zone. This cell proliferation appeared to be closely linked to fusion of opposing arch centra. During the fusion process a metaplastic shift appeared in the arch centra where cells in the intermediate zone between osteoblasts and chondrocytes co-expressed mixed signals of chondrogenic and osteogenic markers. A similar shift also occurred in the notochord where proliferating chordoblasts changed transcription profile from chondrogenic to also include osteogenic marker genes. In progressed fusions, arch centra and intervertebral space mineralized.</p><p><strong>Conclusion: </strong>Loss of cell integrity through cell proliferation and metaplastic shifts seem to be key events in the fusion process. The fusion process involves molecular regulation and cellular changes similar to those found in mammalian deformities, indicating that salmon is suitable for studying general bone development and to be a comparative model for spinal deformities.</p>","PeriodicalId":35905,"journal":{"name":"BMC Physiology","volume":"10 ","pages":"13"},"PeriodicalIF":0.0,"publicationDate":"2010-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909226/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29102832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resveratrol suppresses body mass gain in a seasonal non-human primate model of obesity.","authors":"Alexandre Dal-Pan,&nbsp;Stéphane Blanc,&nbsp;Fabienne Aujard","doi":"10.1186/1472-6793-10-11","DOIUrl":"https://doi.org/10.1186/1472-6793-10-11","url":null,"abstract":"<p><strong>Background: </strong>Resveratrol, a natural polyphenolic compound, was shown to protect rodents against high-fat-diet induced diabesity by boosting energy metabolism. To the best of our knowledge, no data is yet available on the effects of resveratrol in non-human primates. Six non-human heterotherm primates (grey mouse lemurs, Microcebus murinus) were studied during four weeks of dietary supplementation with resveratrol (200 mg/kg/day) during their winter body-mass gain period. Body mass, spontaneous energy intake, resting metabolic rate, spontaneous locomotor activity and daily variations in body temperature were measured. In addition, the plasma levels of several gut hormones involved in satiety control were evaluated.</p><p><strong>Results: </strong>Resveratrol reduced the seasonal body-mass gain by concomitantly decreasing energy intake by 13% and increasing resting metabolic rate by 29%. Resveratrol supplementation inhibited the depth of daily torpor, an important energy-saving process in this primate. The daily amount of locomotor activity remained unchanged. Except for an increase in the glucose-dependent insulinotropic polypeptide, a gut hormone known to promote mobilization of fat stores, no major change in satiety hormone plasma levels was observed under resveratrol supplementation.</p><p><strong>Conclusions: </strong>These results suggest that in a non-human primate, resveratrol reduces body-mass gain by increasing satiety and resting metabolic rate, and by inhibiting torpor expression. The measured anorectic gut hormones did not seem to play a major role in these observations.</p>","PeriodicalId":35905,"journal":{"name":"BMC Physiology","volume":"10 ","pages":"11"},"PeriodicalIF":0.0,"publicationDate":"2010-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1472-6793-10-11","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29071047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sinoatrial tissue of crucian carp heart has only negative contractile responses to autonomic agonists.","authors":"Matti Vornanen,&nbsp;Mervi Hälinen,&nbsp;Jaakko Haverinen","doi":"10.1186/1472-6793-10-10","DOIUrl":"https://doi.org/10.1186/1472-6793-10-10","url":null,"abstract":"<p><strong>Background: </strong>In the anoxia-tolerant crucian carp (Carassius carassius) cardiac activity varies according to the seasons. To clarify the role of autonomic nervous control in modulation of cardiac activity, responses of atrial contraction and heart rate (HR) to carbacholine (CCh) and isoprenaline (Iso) were determined in fish acclimatized to winter (4 degrees C, cold-acclimated, CA) and summer (18 degrees C, warm-acclimated, WA) temperatures.</p><p><strong>Results: </strong>Inhibitory action of CCh was much stronger on atrial contractility than HR. CCh reduced force of atrial contraction at an order of magnitude lower concentrations (EC50 2.75-3.5.10-8 M) in comparison to its depressive effect on HR (EC50 1.23-2.02.10-7 M) (P < 0.05) without differences between winter and summer acclimatized fish. Inhibition of nitric oxide synthase with 100 microM L-NMMA did not change the response of the sinoatrial tissue to CCh. Reduction of atrial force was associated with a strong shortening of action potential (AP) duration to approximately 50% (48 +/- 10 and 50 +/- 6% for CA and WA fish, respectively) and 11% (11 +/- 3 and 11 +/- 2% for CA and WA fish, respectively) of the control value at 3.10-8 M and 10-7 M CCh, respectively (P < 0.05). In atrial myocytes, CCh induced an inwardly rectifying K+ current, IK,CCh, with an EC50 value of 3-4.5.10-7 M and inhibited Ca2+ current (ICa) by 28 +/- 8% and 51 +/- 6% at 10-7 M and 10-6 M, respectively. These currents can explain the shortening of AP. Iso did not elicit any responses in crucian carp sinoatrial preparations nor did it have any effect on atrial ICa, probably due to the saturation of the beta-adrenergic cascade in the basal state.</p><p><strong>Conclusion: </strong>In the crucian carp, HR and force of atrial contraction show cardio-depressive responses to the cholinergic agonist, but do not have any responses to the beta-adrenergic agonist. The scope of inhibitory regulation by CCh is increased by the high basal tone of the adenylate cyclase-cAMP cascade. Higher concentrations of CCh were required to induce IK,CCh and inhibit ICa than was needed for CCh's negative inotropic effect on atrial muscle suggesting that neither IK,CCh nor ICa alone can mediate CCh's actions but they might synergistically reduce AP duration and atrial force production. Autonomic responses were similar in CA winter fish and WA summer fish indicating that cardiac sensitivity to external modulation by the autonomic nervous system is not involved in seasonal acclimatization of the crucian carp heart to cold and anoxic winter conditions.</p>","PeriodicalId":35905,"journal":{"name":"BMC Physiology","volume":"10 ","pages":"10"},"PeriodicalIF":0.0,"publicationDate":"2010-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1472-6793-10-10","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29049252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sterol carrier protein-x gene and effects of sterol carrier protein-2 inhibitors on lipid uptake in Manduca sexta.","authors":"Min-Sik Kim, Que Lan","doi":"10.1186/1472-6793-10-9","DOIUrl":"10.1186/1472-6793-10-9","url":null,"abstract":"<p><strong>Background: </strong>Cholesterol uptake and transportation during the feeding larval stages are critical processes in insects because they are auxotrophic for exogenous (dietary) cholesterol. The midgut is the main site for cholesterol uptake in many insects. However, the molecular mechanism by which dietary cholesterol is digested and absorbed within the midgut and then released into the hemolymph for transportation to utilization or storage sites is poorly understood. Sterol carrier proteins (SCP), non-specific lipid transfer proteins, have been speculated to be involved in intracellular cholesterol transfer and metabolism in vertebrates. Based on the high degree of homology in the conserved sterol transfer domain to rat and human SCP-2, it is supposed that insect SCP-2 has a parallel function to vertebrate SCP-2.</p><p><strong>Results: </strong>We identified the Manduca sexta sterol carrier protein-x and the sterol carrier protein-2 (MsSCP-x/SCP-2) gene from the larval fat body and the midgut cDNAs. The MsSCP-x/SCP-2 protein has a high degree of homology in the SCP-2 domain to other insects' SCP-2. Transcripts of MsSCP-2 were detected at high levels in the midgut and the fat body of M. sexta during the larval stages. Recombinant MsSCP-2 bound to NBD-cholesterol with high affinity, which was suppressed by sterol carrier protein-2 inhibitors.</p><p><strong>Conclusions: </strong>The results suggest that MsSCP-2 may function as a lipid carrier protein in vivo, and targeting insect SCP-2 may be a viable approach for the development of new insecticides.</p>","PeriodicalId":35905,"journal":{"name":"BMC Physiology","volume":"10 ","pages":"9"},"PeriodicalIF":0.0,"publicationDate":"2010-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903571/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29042690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia modifies the feeding preferences of Drosophila. Consequences for diet dependent hypoxic survival.","authors":"Paul Vigne,&nbsp;Christian Frelin","doi":"10.1186/1472-6793-10-8","DOIUrl":"https://doi.org/10.1186/1472-6793-10-8","url":null,"abstract":"<p><strong>Background: </strong>Recent attention has been given to the relationships between diet, longevity, aging and resistance to various forms of stress. Flies do not simply ingest calories. They sense different concentrations of carbohydrate and protein macronutrients and they modify their feeding behavior in response to changes in dietary conditions. Chronic hypoxia is a major consequence of cardiovascular diseases. Dietary proteins have recently been shown to decrease the survival of chronically hypoxic Drosophila. Whether flies modify their feeding behavior in response to hypoxia is not currently known. This study uses the recently developed capillary feeding assay to analyze the feeding behavior of normoxic and chronically hypoxic Drosophila melanogaster.</p><p><strong>Results: </strong>The intakes rates of sucrose and yeast by normoxic or chronically hypoxic flies (5% O2) were analyzed under self selecting and \"no choice\" conditions. Chronically hypoxic flies fed on pure yeast diets or mixed diets under self selection conditions stopped feeding on yeast. Flies fed on mixed diets under \"no choice\" conditions reduced their food intakes. Hypoxia did not modify the adaptation of flies to diluted diets or to imbalanced diets. Mortality was assessed in parallel experiments. Dietary yeast had two distinct effects on hypoxic flies (i) a repellent action which eventually led to starvation and which was best observed in the absence of dietary sucrose and (ii) a toxic action which led to premature death. Finally we determined that hypoxic survivals were correlated to the intakes of sucrose, which suggested that dietary yeast killed flies by reducing their intake of sucrose. The feeding preferences of adult Drosophila were insensitive to NO scavengers, NO donor molecules and inhibitors of phosphodiesterases which are active on Drosophila larvae.</p><p><strong>Conclusion: </strong>Chronically hypoxic flies modify their feeding behavior. They avoid dietary yeast which appears to be toxic. Hypoxic survival is dependent on a source of exogenous sucrose. Ultimately, dietary yeast reduces hypoxic survival by reducing the intake of sucrose. The results highlight the importance of behavioral mechanisms in the responses of Drosophila to chronic hypoxic conditions.</p>","PeriodicalId":35905,"journal":{"name":"BMC Physiology","volume":"10 ","pages":"8"},"PeriodicalIF":0.0,"publicationDate":"2010-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1472-6793-10-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28984898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of marathon on mRNA expression of anti-apoptotic and pro-apoptotic proteins and sirtuins family in male recreational long-distance runners.","authors":"Gabriella Marfe,&nbsp;Marco Tafani,&nbsp;Bruna Pucci,&nbsp;Carla Di Stefano,&nbsp;Manuela Indelicato,&nbsp;Angela Andreoli,&nbsp;Matteo Antonio Russo,&nbsp;Paola Sinibaldi-Salimei,&nbsp;Vincenzo Manzi","doi":"10.1186/1472-6793-10-7","DOIUrl":"https://doi.org/10.1186/1472-6793-10-7","url":null,"abstract":"<p><strong>Background: </strong>A large body of evidence shows that a single bout of strenuous exercise induces oxidative stress in circulating human lymphocytes leading to lipid peroxidation, DNA damage, mitochondrial perturbations, and protein oxidation.In our research, we investigated the effect of physical load on the extent of apoptosis in primary cells derived from blood samples of sixteen healthy amateur runners after marathon (a.m.).</p><p><strong>Results: </strong>Blood samples were collected from ten healthy amateur runners peripheral blood mononuclear cells (PBMCs) were isolated from whole blood and bcl-2, bax, heat shock protein (HSP)70, Cu-Zn superoxide dismutase (SOD), Mn-SOD, inducible nitric oxide synthase (i-NOS), SIRT1, SIRT3 and SIRT4 (Sirtuins) RNA levels were determined by Northern Blot analysis. Strenuous physical load significantly increased HSP70, HSP32, Mn-SOD, Cu-Zn SOD, iNOS, GADD45, bcl-2, forkhead box O (FOXO3A) and SIRT1 expression after the marathon, while decreasing bax, SIRT3 and SIRT4 expression (P < 0.0001).</p><p><strong>Conclusion: </strong>These data suggest that the physiological load imposed in amateur runners during marathon attenuates the extent of apoptosis and may interfere with sirtuin expression.</p>","PeriodicalId":35905,"journal":{"name":"BMC Physiology","volume":"10 ","pages":"7"},"PeriodicalIF":0.0,"publicationDate":"2010-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1472-6793-10-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28982402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gene expression and activity of digestive proteases in Daphnia: effects of cyanobacterial protease inhibitors.","authors":"Anke Schwarzenberger, Anja Zitt, Peter Kroth, Stefan Mueller, Eric Von Elert","doi":"10.1186/1472-6793-10-6","DOIUrl":"10.1186/1472-6793-10-6","url":null,"abstract":"<p><strong>Background: </strong>The frequency of cyanobacterial blooms has increased worldwide, and these blooms have been claimed to be a major factor leading to the decline of the most important freshwater herbivores, i.e. representatives of the genus Daphnia. This suppression of Daphnia is partly attributed to the presence of biologically active secondary metabolites in cyanobacteria. Among these metabolites, protease inhibitors are found in almost every natural cyanobacterial bloom and have been shown to specifically inhibit Daphnia's digestive proteases in vitro, but to date no physiological responses of these serine proteases to cyanobacterial protease inhibitors in Daphnia have been reported in situ at the protein and genetic levels.</p><p><strong>Results: </strong>Nine digestive proteases were detected in D. magna using activity-stained SDS-PAGE. Subsequent analyses by LC-MS/MS and database search led to the identification of respective protease genes. D. magna responded to dietary protease inhibitors by up-regulation of the expression of these respective proteases at the RNA-level and by the induction of new and less sensitive protease isoforms at the protein level. The up-regulation in response to dietary trypsin- and chymotrypsin-inhibitors ranged from 1.4-fold to 25.6-fold. These physiological responses of Daphnia, i.e. up-regulation of protease expression and the induction of isoforms, took place even after feeding on 20% cyanobacterial food for only 24 h. These physiological responses proved to be independent from microcystin effects.</p><p><strong>Conclusion: </strong>Here for the first time it was shown in situ that a D. magna clone responds physiologically to dietary cyanobacterial protease inhibitors by phenotypic plasticity of the targets of these specific inhibitors, i.e. Daphnia gut proteases. These regulatory responses are adaptive for D. magna, as they increase the capacity for protein digestion in the presence of dietary protease inhibitors. The type and extent of these responses in protease expression might determine the degree of growth reduction in D. magna in the presence of cyanobacterial protease inhibitors. The rapid response of Daphnia to cyanobacterial protease inhibitors supports the assumption that dietary cyanobacterial protease inhibitors exert a strong selection pressure on Daphnia proteases themselves.</p>","PeriodicalId":35905,"journal":{"name":"BMC Physiology","volume":"10 ","pages":"6"},"PeriodicalIF":0.0,"publicationDate":"2010-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2873468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28965407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}