Open neuroendocrinology journal (Online)最新文献

{"title":"Atrial Natriuretic Peptide and Acute Changes in Central Blood Volume by Hyperthermia in Healthy Humans","authors":"T. Vogelsang, J. Marving, C. Crandall, Chad E. Wilson, C. Yoshiga, N. Secher, B. Hesse, A. Kjær","doi":"10.2174/1876528901205010001","DOIUrl":"https://doi.org/10.2174/1876528901205010001","url":null,"abstract":"Background Hyperthermia induces vasodilatation that reduces central blood volume (CBV), central venous pressure (CVP) and mean arterial pressure (MAP). Inhibition of atrial natriuretic peptide (ANP) could be a relevant homeostatic defense mechanism during hyperthermia with a decrease in CBV. The present study evaluated how changes in plasma ANP reflect the changes in CBV during hyperthermia. Methods Ten healthy subjects provided with a water perfused body suit increased body core temperature 1 °C. In situ labeled autologous red blood cells were used to measure the CBV with a gamma camera. Regions of interest were traced manually on the images of the whole body blood pool scans. Two measures of CBV were used: Heart/whole body ratio and thorax/whole body ratio. CVP and MAP were recorded. Arterial (ANPart) and venous plasma ANP were determined by radioimmunoassay. Results The ratio thorax/whole body and heart/whole body decreased 7 % and 11 %, respectively (p<0.001). MAP and CVP decreased during hyperthermia by 6.8 and 5.0 mmHg, respectively (p<0.05; p<0.001). Changes in both thorax/whole body (R=0.80; p<0.01) and heart/whole body ratios (R=0.78; p<0.01) were correlated with changes in ANPart. However, there was no correlation between venous ANP and changes in CBV, nor between ANPart and MAP or CVP. Conclusion Arterial but not venous plasma concentration of ANP, is correlated to changes in CBV, but not to pressures. We suggest that plasma ANPart may be used as a surrogate marker of acute CBV changes.","PeriodicalId":88291,"journal":{"name":"Open neuroendocrinology journal (Online)","volume":"64 1","pages":"1 - 4"},"PeriodicalIF":0.0,"publicationDate":"2012-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87832140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Misfolding of Mutated Vasopressin Causes ER-Retention and Activation of ER-Stress Markers in Neuro-2a Cells.","authors":"Zhongyu Yan,&nbsp;Andrea Hoffmann,&nbsp;Erin Kelly Kaiser,&nbsp;William C Grunwald,&nbsp;David R Cool","doi":"10.2174/1876528901104010136","DOIUrl":"https://doi.org/10.2174/1876528901104010136","url":null,"abstract":"<p><p>Arginine-vasopressin (AVP) is a peptide hormone normally secreted from neuroendocrine cells via the regulated secretory pathway. In Familial Neurohypophyseal Diabetes Insipidus (FNDI), an autosomal dominant form of central diabetes insipidus, mutations of pro-vasopressin appear to accumulate in the endoplasmic reticulum (ER) causing a lack of biologically active AVP in the blood. To investigate the effect of pro-vasopressin mutations regarding intracellular functions of protein targeting and secretion, we created two FNDI-associated amino acid substitution mutants, e.g., G14R, and G17V in frame with green fluorescent protein (GFP) and pro-vasopressin (VP) in frame with red fluorescent protein (VP-RFP). Fluorescence microscopy of Neuro-2a cells expressing these constructs revealed co-localization of VP-GFP and VP-RFP to punctate granules along the length and accumulating at the tips of neurites, characteristic of regulated secretory granules. In contrast, the two FNDI-associated amino acid substitution mutants, e.g., G14R-GFP, and G17VGFP, were localized to a perinuclear region of the Neuro-2a cells characteristic of the endoplasmic reticulum. Co-expression of these mutants with VP-RFP showed VP-RFP was retained in the ER, co-localized with the mutants suggesting the formation of heterodimers as found in FNDI. Stimulated secretion experiments indicated that VP-GFP was secreted in an inducible manner whereas, G14R-GFP and G17V-GFP were retained to nearly 100% within the cells. Analysis by western blotting and semi-quantitative RT-PCR indicated an increased protein and mRNA expression for an ER resident molecular chaperone, BiP. Further analysis of ER-storage disease-associated proteins such as caspase 12 and CHOP showed an increase in these as well. The results suggest that G14R-GFP and G17V-GFP are retained in the ER of Neuro-2a cells, resulting in up-regulation of the molecular chaperone BiP, and activation of the ER-storage disease-associated caspase cascade system.</p>","PeriodicalId":88291,"journal":{"name":"Open neuroendocrinology journal (Online)","volume":"4 ","pages":"136-146"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/64/e0/nihms-545682.PMC3932059.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32151510","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 Local Control of the Pituitary by Activin Signaling and Modulation.","authors":"Louise M Bilezikjian, Wylie W Vale","doi":"10.2174/1876528901104010090","DOIUrl":"10.2174/1876528901104010090","url":null,"abstract":"<p><p>The pituitary gland plays a prominent role in the control of many physiological processes. This control is achieved through the actions and interactions of hormones and growth factors that are produced and secreted by the endocrine cell types and the non-endocrine constituents that collectively and functionally define this complex organ. The five endocrine cell types of the anterior lobe of the pituitary, somatotropes, lactotropes, corticotropes, thyrotropes and gonadotropes, are defined by their primary product, growth hormone (GH), prolactin (PRL), adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH) and follicle stimulating hormone (FSH)/luteinizing hormone (LH). They are further distinguishable by the presence of cell surface receptors that display high affinity and selectivity for specific hypothalamic hormones and couple to appropriate downstream signaling pathways involved in the control of cell type specific responses, including the release and/or synthesis of pituitary hormones. Central control of the pituitary via the hypothalamus is further fine-tuned by the positive or negative actions of peripheral feedback signals and of a variety of factors that originate from sources within the pituitary. The focus of this review is the latter category of intrinsic factors that exert local control. Special emphasis is given to the TGF-β family of growth factors, in particular activin effects on the gonadotrope population, because a considerable body of evidence supports their contribution to the local modulation of the embryonic and postnatal pituitary as well as pituitary pathogenesis. A number of other substances, including members of the cytokine and FGF families, VEGF, IGF1, PACAP, Ghrelin, adenosine and nitric oxide have also been shown or implicated to function as autocrine/paracrine factors, though, definitive proof remains lacking in some cases. The ever-growing list of putative autocrine/paracrine factors of the pituitary nevertheless has highlighted the complexity of the local network and its impact on pituitary functions.</p>","PeriodicalId":88291,"journal":{"name":"Open neuroendocrinology journal (Online)","volume":"4 ","pages":"90-101"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3173763/pdf/nihms323299.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30005385","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 Role of the Y Chromosome in Brain Function.","authors":"Eleni Kopsida, Evangelia Stergiakouli, Phoebe M Lynn, Lawrence S Wilkinson, William Davies","doi":"10.2174/1876528900902010020","DOIUrl":"10.2174/1876528900902010020","url":null,"abstract":"<p><p>In mammals, sex differences are evident in many aspects of brain development, brain function and behaviour. Ultimately, such differences must arise from the differential sex chromosome complements in males and females: males inherit a single X chromosome and a Y chromosome, whilst females inherit two X chromosomes. One possible mechanism for sexual differentiation of the brain is via male-limited expression of genes on the small Y chromosome. Many Y-linked genes have been implicated in the development of the testes, and therefore could theoretically contribute to sexual differentiation of the brain indirectly, through influencing gonadal hormone production. Alternatively, Y-linked genes that are expressed in the brain could directly influence neural masculinisation. The present paper reviews evidence from human genetic studies and animal models for Y-linked effects (both direct and indirect) on neurodevelopment, brain function and behaviour. Besides enhancing our knowledge of the mechanisms underlying mammalian neural sexual differentiation, studies geared towards understanding the role of the Y chromosome in brain function will help to elucidate the molecular basis of sex-biased neuropsychiatric disorders, allowing for more selective sex-specific therapies.</p>","PeriodicalId":88291,"journal":{"name":"Open neuroendocrinology journal (Online)","volume":"2 ","pages":"20-30"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854822/pdf/ukmss-29103.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28925412","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":"Structural Requirements for Sorting Pro-Vasopressin to the Regulated Secretory Pathway in a Neuronal Cell Line.","authors":"David R Cool,&nbsp;Steven B Jackson,&nbsp;Karen S Waddell","doi":"10.2174/1876528900801010001","DOIUrl":"10.2174/1876528900801010001","url":null,"abstract":"<p><p>Vasopressin is a peptide hormone normally secreted via the regulated secretory pathway in neuro-endocrine cells. In an effort to determine which region of vasopressin contains sufficient information for sorting, we created five constructs with the cDNA for vasopressin or regions of vasopressin in frame with the gene for green fluorescent protein (GFP). Fluorescence microscopy of Neuro-2a cells expressing the constructs revealed full-length vasopressin-GFP (VP-GFP), neurophysin-GFP (NP-GFP) and arginine-vasopressin/neurophysin-GFP (AN-GFP), were localized to punctate granules in the neurites and accumulated at the tips of neurites, characteristic of regulated secretory granules. These fusion proteins were secreted in a regulated manner as determined by pulse-chase labeling experiments. Two other chimeric proteins, signalpeptide-GFP and AVP-GFP were localized to a perinuclear region, characteristic of the endoplasmic reticulum. Pulse/chase [(35)S]labeling followed by immunoprecipitation using anti-GFP antibody indicated that these two fusion proteins were constitutively secreted. We conclude that the neurophysin region of pro-vasopressin contains information that is both sufficient and necessary for sorting GFP into the regulated secretory pathway.</p>","PeriodicalId":88291,"journal":{"name":"Open neuroendocrinology journal (Online)","volume":"1 ","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1876528900801010001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28059819","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}