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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

J Neurochem. 2002 May;81(3):449-61.
Group IB secretory phospholipase A2 induces neuronal cell death via apoptosis.

Yagami T, Ueda K, Asakura K, Hayasaki-Kajiwara Y, Nakazato H, Sakaeda T, Hata S, Kuroda T, Takasu N, Hori Y.

Discovery Research Laboratories and Developmental Research Laboratories, Shionogi and Co., Ltd, Osaka, Japan. tatsurou.yagamhionogi.co.jp

Group IB secretory phospholipase A2 (sPLA2-IB) mediates cell proliferation, cell migration, hormone release and eicosanoid production via its receptor in peripheral tissues. In the CNS, high-affinity binding sites of sPLA2-IB have been documented. However, it remains obscure whether sPLA2-IB causes biologic or pathologic response in the CNS. To this end, we examined effects of sPLA2-IB on neuronal survival in primary cultures of rat cortical neurons. sPLA2-IB induced neuronal cell death in a concentration-dependent manner. This death was a delayed response requiring a latent time for 6 h; sPLA2-IB-induced neuronal cell death was accompanied with apoptotic blebbing, condensed chromatin, and fragmented DNA, exhibiting apoptotic features. Before cell death, sPLA2-IB liberated arachidonic acid (AA) and generated prostaglandin D2 (PGD2) from neurons. PGD2 and its metabolite, Delta12-PGJ2, exhibited neurotoxicity. Inhibitors of sPLA2 and cyclooxygenase-2 (COX-2) significantly suppressed not only AA release, but also PGD2 generation. These inhibitors significantly prevented neurons from sPLA2-IB-induced neuronal cell death. In conclusion, we demonstrate a novel biological response, apoptosis, of sPLA2-IB in the CNS. Furthermore, the present study suggests that PGD2 metabolites, especially Delta12-PGJ2, might mediate sPLA2-IB-induced apoptosis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12065654&dopt=Abstract

J Neurochem. 2002 May;81(3):565-74.
Isolation and characterization of VGF peptides in rat brain. Role of PC1/3 and PC2 in the maturation of VGF precursor.

Trani E, Giorgi A, Canu N, Amadoro G, Rinaldi AM, Halban PA, Ferri GL, Possenti R, Schinina ME, Levi A.

Istituto di Neurobiologia e Medicina Molecolare, CNR, Roma, Italy.

The neurotrophin responsive gene vgf is widely expressed in central and peripheral neurones, and in certain neuroendocrine cell populations. Its encoded VGF precursor protein (proVGF1: 617 amino acids in rat, 615 in man, > 85% homology) gives rise to several low molecular weight species. We studied a range of neuroendocrine and neuronal cells, in which VGF-processing products were prominent with an apparent molecular weight of 20 and 10 kDa (VGF20 and VGF10, respectively). Such peptides were recognized by antibodies specific for the C-terminal rat VGF nonapeptide, thus indicating that they included the C-terminus of proVGF. Ectopic expression of the neuroendocrine-specific prohormone convertases PC1/3 or PC2 in GH3 cells showed that both could generate VGF20, while VGF10 was preferentially produced by PC1/3. Site-directed mutagenesis was used to identify the KRKRKK(488) motif as the target within VGF sequence which leads to the production of VGF20. Molecular characterization of rat VGF10, on the other hand, revealed that this peptide is produced by cleavage at the RPR(555) site. By the combined use of high-resolution separation techniques, matrix-assisted laser desorption/ionization time of flight (MALDI-ToF) mass spectrometry and manual Edman degradation we identified in rat brain a VGF fragment analogous to bovine peptide V and two novel peptides also derived from the C-terminal region of proVGF.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12065665&dopt=Abstract

J Pharmacol Exp Ther. 2002 Jul;302(1):80-7.
Bisphenol A inhibits Cl(-) secretion by inhibition of basolateral K+ conductance in human airway epithelial cells.

Ito Y, Sato S, Son M, Kondo M, Kume H, Takagi K, Yamaki K.

Division II (Respiratory Division), Internal Medicine II, University of Nagoya School of Medicine, Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.

There has been growing concern about the potential threat of hormone-disrupting chemicals like bisphenol A to various aspects of animal and human health. We studied the effects of bisphenol A on the Cl(-) secretion in human airway epithelial Calu-3 cells. Pretreatment with bisphenol A (IC(50) = 60 microM, for 30 min) prevented isoproterenol (10 nM)-generated short-circuit current (I(sc)) more potently than 17beta-estradiol or tamoxifen (IC(50) = 1 mM). 5'-Nitro-2-(3-phenylpropylamino) benzoate-sensitive apical conductance potentiated by isoproterenol was not affected by the pretreatment with either of these estrogenic compounds. The effects of bisphenol A were simulated in I(sc) responses to forskolin (10 microM) and 8-bromo-cAMP (1 mM). Nystatin permeabilization of Calu-3 monolayers revealed that bisphenol A attenuated 8-bromo-cAMP-induced basolateral K+ current, which is sensitive to clotrimazole (30 microM) and insensitive to charybdotoxin (100 nM), without affecting the apical Cl(-) current. Bisphenol A, but neither 17beta-estradiol nor tamoxifen, interrupted the charybdotoxin-sensitive component of I(sc) stimulated by 1-ethyl-2-benzimidazolinone (1-EBIO; 500 microM). The inhibitory effects of bisphenol A on these Cl(-) secretory stimuli were remarkable when applied to the apical rather than the basolateral membrane. Alternatively, long-term incubation of bisphenol A (1 microM; 12-72 h) had no discernible effect on isoproterenol- and 1-EBIO-induced Cl(-) secretion. These findings indicate that short-term exposure to bisphenol A attenuates transepithelial Cl(-) secretion through inhibition of both cAMP- and Ca(2+)-activated K+ channels on the basolateral membrane, interacting from the cytosolic surface in Calu-3 cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12065703&dopt=Abstract

J Pharmacol Exp Ther. 2002 Jul;302(1):145-52.
Pharmacological evidence supporting a role for central corticotropin-releasing factor(2) receptors in behavioral, but not endocrine, response to environmental stress.

Pelleymounter MA, Joppa M, Ling N, Foster AC.

Department of Neuroscience, Neurocrine Biosciences, Inc., San Diego, CA 92121, USA.

Corticotropin-releasing factor (CRF) is one of the principle components of the stress response. The physiological effects of CRF are mediated by two receptor subtypes, CRF(1) and CRF(2). Recent data obtained with the selective CRF(2) antagonist antisauvagine-30 (ASV-30) has begun to suggest that both CRF receptor subtypes may play a role in stress-related behaviors. Exactly how these two receptor subtypes interact to modulate the behavioral and endocrine responses to stress is not clear, however. We have attempted to understand the role of the CRF(2) receptor in the behavioral and endocrine responses to stress by comparing the effects of ASV-30 with the mixed CRF(1)/CRF(2) receptor antagonist astressin. Centrally administered ASV-30 reduced anxiety-like behavior in BALB/c mice in three models of anxiety: marble burying [minimal effective dose (MED) = 3 nmol], open field (MED = 3 nmol), and elevated plus maze (MED = 0.1 nmol). ASV-30 did not change locomotor activity or the adrenocorticotropic hormone (ACTH) response to restraint stress. The potent mixed CRF(1)/CRF(2) antagonist astressin not only reduced anxiety-like behavior in all three models with equivalent potency but also blunted the ACTH response to restraint stress. Finally, the new selective CRF(2) receptor agonist urocortin-II produced a dose-dependent increase in anxiety-like behavior in the plus maze test. Therefore, our data suggest that the CRF(2) receptor plays a role in the behavioral, but not the hypothalamic-pituitary-adrenal axis, response to stress.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12065711&dopt=Abstract

J Pharmacol Exp Ther. 2002 Jul;302(1):205-11.
Rapid inhibition of thyroxine-induced bone resorption in the rat by an orally active vitronectin receptor antagonist.

Hoffman SJ, Vasko-Moser J, Miller WH, Lark MW, Gowen M, Stroup G.

Department of Musculoskeletal Diseases, GlaxoSmithKline, Mail Code UW2109, 709 Swedeland Road, PO Box 1539, King of Prussia, PA 19406, USA. Sandra_J_Hoffmask.com

An excess of thyroid hormone results in increased bone turnover and loss of bone mass in humans. Exogenous administration of thyroid hormone to rats has served as a model of human hyperthyroidism in which antiresorptive therapies have been tested. We have further refined this model of thyroxine (T4)-induced turnover in the rat. Daily administration of T4 to aged rats for as short as 1 week resulted in elevated bone resorption determined by significantly higher urinary deoxypyridinoline (Dpd) compared with vehicle controls or animals receiving T4 plus estradiol. Three weeks of daily administration of T4 led to significantly lower bone mineral density compared with untreated controls or animals receiving T4 plus estradiol. In a follow-up study, a depot formulation of T4 caused an increase in Dpd identical to that achieved with a bolus dose. SB-273005 [(4S)-2,3,4,5-tetrahydro-8-[2-[6-(methylamino)-2-pyridinyl] ethoxy]-3-oxo-2-(2,2,2-trifluoroethyl)-1H-2-benzazepine-4- acetic acid] a potent antagonist of the integrins alpha(v)beta(3) and alpha(v)beta(5), has been shown previously to inhibit bone resorption in cultures of human osteoclasts and to protect bone in ovariectomized rats. The effect of SB-273005 by oral administration was evaluated in this thyroxine-induced turnover model. Dose-dependent inhibition of resorption was seen with SB-273005 after 7 days of dosing using Dpd as a measure of bone resorption. In summary, it has been demonstrated that the antiresorptive activity of a vitronectin receptor antagonist can be measured after only 7 days of treatment in this refined rat model of thyroxine-induced bone turnover. These data suggest that SB-273005 may be useful for the treatment of metabolic bone diseases, including those resulting from hyperthyroidism.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12065718&dopt=Abstract

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