GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Early Effects of Lipopolysaccharide-Induced Inflammation on Foetal Brain Development in Rat
    SAGE Publications ; 2011
    In:  ASN Neuro Vol. 3, No. 4 ( 2011-09-07), p. AN20110027-
    Details
    In: ASN Neuro, SAGE Publications, Vol. 3, No. 4 ( 2011-09-07), p. AN20110027-
    Abstract: Studies in humans and animal models link maternal infection and imbalanced levels of inflammatory mediators in the foetal brain to the aetiology of neuropsychiatric disorders. In a number of animal models, it was shown that exposure to viral or bacterial agents during a period that corresponds to the second trimester in human gestation triggers brain and behavioural abnormalities in the offspring. However, little is known about the early cellular and molecular events elicited by inflammation in the foetal brain shortly after maternal infection has occurred. In this study, maternal infection was mimicked by two consecutive intraperitoneal injections of 200 μg of LPS (lipopolysaccharide)/kg to timed-pregnant rats at GD15 (gestational day 15) and GD16. Increased thickness of the CP (cortical plate) and hippocampus together with abnormal distribution of immature neuronal markers and decreased expression of markers for neural progenitors were observed in the LPS-exposed foetal forebrains at GD18. Such effects were accompanied by decreased levels of reelin and the radial glial marker GLAST (glial glutamate transporter), and elevated levels of pro-inflammatory cytokines in maternal serum and foetal forebrains. Foetal inflammation elicited by maternal injections of LPS has discrete detrimental effects on brain development. The early biochemical and morphological changes described in this work begin to explain the sequelae of early events that underlie the neurobehavioural deficits reported in humans and animals exposed to prenatal insults.
    Type of Medium: Online Resource
    ISSN: 1759-0914 , 1759-0914
    URL: Article
    DOI: 10.1042/AN20110027
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2011
    detail.hit.zdb_id: 2485467-0
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Retinoic Acid Regulation of the VIP and PACAP Autocrine Ligand and Receptor System in Human Neuroblastoma Cell Lines 1 and 2
    Elsevier BV ; 1997
    In:  Peptides Vol. 18, No. 6 ( 1997), p. 835-841
    Details
    In: Peptides, Elsevier BV, Vol. 18, No. 6 ( 1997), p. 835-841
    Type of Medium: Online Resource
    ISSN: 0196-9781
    URL: Article
    DOI: 10.1016/S0196-9781(97)00015-6
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1997
    detail.hit.zdb_id: 2019194-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Comparative distributions of pituitary adenylyl cyclase-activating polypeptide and its selective type I receptor mRNA in the frog (Xenopus laevis) brain
    Elsevier BV ; 2002
    In:  Regulatory Peptides Vol. 109, No. 1-3 ( 2002-11), p. 15-26
    Details
    In: Regulatory Peptides, Elsevier BV, Vol. 109, No. 1-3 ( 2002-11), p. 15-26
    Type of Medium: Online Resource
    ISSN: 0167-0115
    URL: Article
    DOI: 10.1016/S0167-0115(02)00166-0
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2002
    detail.hit.zdb_id: 1498712-0
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Lack of vasoactive intestinal peptide reduces testosterone levels and reproductive aging in mouse testis
    Bioscientifica ; 2007
    In:  Journal of Endocrinology Vol. 194, No. 1 ( 2007-07), p. 153-160
    Details
    In: Journal of Endocrinology, Bioscientifica, Vol. 194, No. 1 ( 2007-07), p. 153-160
    Abstract: The neuropeptides vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide have long been considered as putative regulators of testicular functions. In vitro evidence suggests that VIP could play an important role in testosterone biosynthesis. However, the endogenous role of VIP on testicular functions remained to be demonstrated. In C57BL/6 mice exhibiting a complete disruption of the VIP gene, we first observed here that serum testosterone levels were lower than those of WT littermates. At the age of 4 months, this phenotype was accompanied with a reduction of expression of StAR and 3-β-hydroxysteroid dehydrogenase (3β-HSD) in the testis. In addition, serum levels of FSH but not LH were reduced in young knock-out (KO) males. Testicular anatomy also revealed a higher percentage of degenerated seminiferous tubules in the 4-month-old VIP KO animals when compared with WT. In 15-month-old animals, control males showed typical testicular aging, including a severe degeneration of seminiferous tubules, a dramatic decrease in serum levels of testosterone, and a reduction in StAR and 3 β -HSD gene expression. In age-matching VIP KO males, the levels of serum testosterone and steroidogenic enzymes were still very low. Interestingly, in contrast to that observed in young mice, testicular degeneration at 15 months was significantly less severe in VIP KO than WT mice. All together, these results suggest that 1) VIP is an important factor for regulating testosterone biosynthesis and FSH secretion and 2) VIP may influence testicular aging.
    Type of Medium: Online Resource
    ISSN: 0022-0795 , 1479-6805
    URL: Article
    DOI: 10.1677/JOE-07-0102
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 2007
    detail.hit.zdb_id: 1474892-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Small molecule blockers reveal an important role for Orai1-NFAT-orphan receptor pathway in Th17 differentiation (P5169)
    The American Association of Immunologists ; 2013
    In:  The Journal of Immunology Vol. 190, No. 1_Supplement ( 2013-05-01), p. 68.12-68.12
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 190, No. 1_Supplement ( 2013-05-01), p. 68.12-68.12
    Abstract: Orai1 is the pore subunit of the Calcium Release Activated Channels (CRAC) that activate downstream calcineurin-NFAT pathway. Loss of function mutation in Orai1 causes lethality due to severe defects in immune system, which can be rescued by bone marrow transplantation. Using a high throughput chemical library screening, we have identified a class of small molecule blockers that inhibit Orai1. One of the small molecules, compound 5D blocked the activity of a constitutively active mutant of Orai1, suggesting a direct block of ion permeation via Orai1. Primary murine Th17 cells showed highest sensitivity to block by this compound. Treatment with compound 5D not only suppressed cytokine production, but also inhibited differentiation of Th17 cells by suppression of the retinoic-acid-receptor-related orphan receptors RORα and RORγt. Exogenous expression of RORα, RORγt or a constitutive active mutant of NFAT (CA-NFAT) rescued the blocking effect, identifying the Orai1-NFAT- ROR signaling pathway to be important for Th17 differentiation. The defects in cytokine production and differentiation were recapitulated in Th17 cells from Orai1-deficient mice suggesting Orai1 as a specific target of the blockers. In vivo administration of Orai1 blockers effectively delayed the onset and reduced the severity of autoimmune disease in mice. These data indicate that derivatives of compound 5D can be used as chemical templates for development of therapeutic agents to alleviate autoimmune diseases.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.190.Supp.68.12
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2013
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    Targeted STAT3 disruption in myeloid cells alters immunosuppressor cell abundance in a murine model of spontaneous medulloblastoma
    Oxford University Press (OUP) ; 2013
    In:  Journal of Leukocyte Biology Vol. 95, No. 2 ( 2013-09-25), p. 357-367
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 95, No. 2 ( 2013-09-25), p. 357-367
    Abstract: Although the immune system may provide early protection against cancer, tumors may exploit the healing arm of the immune system to enhance their growth and metastasis. For example, myeloid derived suppressor cells (MDSCs) are thought to promote tumor growth by several mechanisms, including the suppression of T cell activity. It has been suggested that STAT3 activation in myeloid cells modulates multiple aspects of MDSC physiology, including their expansion and activity. Whereas most animal studies investigating tumor immunology have used tumor implants, we used transgenic mice (Smo*) that spontaneously develop medulloblastoma brain tumors to investigate the temporal accumulation of MDSCs within tumors and how myeloid STAT3 disruption affects MDSC and other immune cell types. We found distinct populations of MDSC in medulloblastoma tumors, with a high prevalence of CD11b+Ly6G+Ly6Clow/− cells, described previously by others as G-MDSCs. These were found early in tumor development, in premalignant lesions located on the surface of the cerebellum of 28-day-old mice. In fully developed tumors, pSTAT3 was found in the majority of these cells. Conditional STAT3 gene disruption in myeloid cells resulted in an enhanced proinflammatory phenotype of macrophages in Smo* mice. Moreover, a significant reduction in the abundance of G-MDSCs and Tregs was observed within tumors along with an increased presence of CD4+ and CD8+ cells. Despite these alterations in immune cells induced by myeloid STAT3 disruption, we found no effect on tumor incidence in Smo* mice with this deletion.
    Type of Medium: Online Resource
    ISSN: 0741-5400 , 1938-3673
    URL: Article
    DOI: 10.1189/jlb.1012531
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2013
    detail.hit.zdb_id: 2026833-6
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Pharmacology and functions of receptors for vasoactive intestinal peptide and pituitary adenylate cyclase‐activating polypeptide: IUPHAR Review 1
    Wiley ; 2012
    In:  British Journal of Pharmacology Vol. 166, No. 1 ( 2012-05), p. 4-17
    Details
    In: British Journal of Pharmacology, Wiley, Vol. 166, No. 1 ( 2012-05), p. 4-17
    Abstract: Vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase‐activating polypeptide (PACAP) are members of a superfamily of structurally related peptide hormones that includes glucagon, glucagon‐like peptides, secretin, gastric inhibitory peptide (GIP) and growth hormone‐releasing hormone (GHRH). VIP and PACAP exert their actions through three GPCRs – PAC 1 , VPAC 1 and VPAC 2 – belonging to class B (also referred to as class II, or secretin receptor‐like GPCRs). This family comprises receptors for all peptides structurally related to VIP and PACAP, and also receptors for parathyroid hormone, corticotropin‐releasing factor, calcitonin and related peptides. PAC 1 receptors are selective for PACAP, whereas VPAC 1 and VPAC 2 respond to both VIP and PACAP with high affinity. VIP and PACAP play diverse and important roles in the CNS, with functions in the control of circadian rhythms, learning and memory, anxiety and responses to stress and brain injury. Recent genetic studies also implicate the VPAC 2 receptor in susceptibility to schizophrenia and the PAC 1 receptor in post‐traumatic stress disorder. In the periphery, VIP and PACAP play important roles in the control of immunity and inflammation, the control of pancreatic insulin secretion, the release of catecholamines from the adrenal medulla and as co‐transmitters in autonomic and sensory neurons. This article, written by members of the International Union of Basic and Clinical Pharmacology Committee on Receptor Nomenclature and Drug Classification (NC‐IUPHAR) subcommittee on receptors for VIP and PACAP, confirms the existing nomenclature for these receptors and reviews our current understanding of their structure, pharmacology and functions and their likely physiological roles in health and disease. More detailed information has been incorporated into newly revised pages in the IUPHAR database ( http://www.iuphar‐db.org/DATABASE/FamilyMenuForward?familyId=67 ). LINKED ARTICLES This article is part of a themed section on Secretin Family (Class B) G Protein‐Coupled Receptors. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2012.166.issue‐1
    Type of Medium: Online Resource
    ISSN: 0007-1188 , 1476-5381
    URL: Issue
    URL: Article
    DOI: 10.1111/bph.2012.166.issue-1
    DOI: 10.1111/j.1476-5381.2012.01871.x
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 2029728-2
    SSG: 15,3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    Pituitary adenylyl cyclase activating polypeptide inhibits gli1 gene expression and proliferation in primary medulloblastoma derived tumorsphere cultures
    Springer Science and Business Media LLC ; 2010
    In:  BMC Cancer Vol. 10, No. 1 ( 2010-12)
    Details
    In: BMC Cancer, Springer Science and Business Media LLC, Vol. 10, No. 1 ( 2010-12)
    Abstract: Hedgehog (HH) signaling is critical for the expansion of granule neuron precursors (GNPs) within the external granular layer (EGL) during cerebellar development. Aberrant HH signaling within GNPs is thought to give rise to medulloblastoma (MB) - the most commonly-observed form of malignant pediatric brain tumor. Evidence in both invertebrates and vertebrates indicates that cyclic AMP-dependent protein kinase A (PKA) antagonizes HH signalling. Receptors specific for the neuropeptide pituitary adenylyl cyclase activating polypeptide (PACAP, gene name ADCYAP1) are expressed in GNPs. PACAP has been shown to protect GNPs from apoptosis in vitro , and to interact with HH signaling to regulate GNP proliferation. PACAP/ ptch1 double mutant mice exhibit an increased incidence of MB compared to ptch1 mice, indicating that PACAP may regulate HH pathway-mediated MB pathogenesis. Methods Primary MB tumorsphere cultures were prepared from thirteen ptch1 +/- /p53 +/- double mutant mice and treated with the smoothened (SMO) agonist purmorphamine, the SMO antagonist SANT-1, the neuropeptide PACAP, the PKA activator forskolin, and the PKA inhibitor H89. Gene expression of gli1 and [ 3 H]-thymidine incorporation were assessed to determine drug effects on HH pathway activity and proliferation, respectively. PKA activity was determined in cell extracts by Western blotting using a phospho-PKA substrate antibody. Results Primary tumor cells cultured for 1-week under serum-free conditions grew as tumorspheres and were found to express PAC1 receptor transcripts. Gli1 gene expression was significantly reduced by SANT-1, PACAP and forskolin, but was unaffected by purmorphamine. The attenuation of gli1 gene expression by PACAP was reversed by the PKA inhibitor H89, which also blocked PKA activation. Treatment of tumorsphere cultures with PACAP, forskolin, and SANT-1 for 24 or 48 hours reduced proliferation. Conclusions Primary tumorspheres derived from ptch1 +/- /p53 +/- mice exhibit constitutive HH pathway activity. PACAP antagonizes HH signalling in these cells in a manner blocked by the PKA antagonist H89. PACAP and pharmacological activation of PKA also inhibited proliferation. Our data suggests that regulation of HH signaling by PACAP/PKA signaling may provide an alternative to SMO inhibition for the treatment of MB.
    Type of Medium: Online Resource
    ISSN: 1471-2407
    URL: Article
    DOI: 10.1186/1471-2407-10-676
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2010
    detail.hit.zdb_id: 2041352-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Targeting VIP and PACAP Receptor Signalling: New Therapeutic Strategies in Multiple Sclerosis
    SAGE Publications ; 2011
    In:  ASN Neuro Vol. 3, No. 4 ( 2011-09-07), p. AN20110024-
    Details
    In: ASN Neuro, SAGE Publications, Vol. 3, No. 4 ( 2011-09-07), p. AN20110024-
    Abstract: MS (multiple sclerosis) is a chronic autoimmune and neurodegenerative pathology of the CNS (central nervous system) affecting approx. 2.5 million people worldwide. Current and emerging DMDs (disease-modifying drugs) predominantly target the immune system. These therapeutic agents slow progression and reduce severity at early stages of MS, but show little activity on the neurodegenerative component of the disease. As the latter determines permanent disability, there is a critical need to pursue alternative modalities. VIP (vasoactive intestinal peptide) and PACAP (pituitary adenylate cyclase-activating peptide) have potent anti-inflammatory and neuroprotective actions, and have shown significant activity in animal inflammatory disease models including the EAE (experimental autoimmune encephalomyelitis) MS model. Thus, their receptors have become candidate targets for inflammatory diseases. Here, we will discuss the immunomodulatory and neuroprotective actions of VIP and PACAP and their signalling pathways, and then extensively review the structure–activity relationship data and biophysical interaction studies of these peptides with their cognate receptors.
    Type of Medium: Online Resource
    ISSN: 1759-0914 , 1759-0914
    URL: Article
    DOI: 10.1042/AN20110024
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2011
    detail.hit.zdb_id: 2485467-0
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...