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Search Results: 1 - 10 of 249 matches for " Enri Borda "
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Differential β1 Cardiac Adrenoceptor Modulation of Nitric Oxide Isoforms by β1 IgG from Patients with Periodontitis during Short-Term Hypoxia  [PDF]
Sabrina Ganzinelli, Enri Borda
Pharmacology & Pharmacy (PP) , 2015, DOI: 10.4236/pp.2015.612057
Abstract: Background: We demonstrated previously that serum IgG from periodontitis patients interacting with the second extracellular loop of the human cardiac β1 adrenoreceptors triggers the production of second messengers. In this paper we quantified the production of nitrates/nitrites and nitric oxide (NO), which in turn induces nitric oxide synthase (NOS) mRNA expression. Methods: We determined using β1 IgG, NOS activity isoforms, NOS expression, nitrate/nitrite assay, cGMP accumulation and PKC activity. Results: We established that serum β1 IgG autoantibodies and NO might be considered as early markers in normoxia/hypoxia system in rat isolated atria. The β1 IgG autoantibodies from periodontitis patients, while stimulating myocardial atria β1 adrenoreceptors, exert an increase on NO levels indirectly quantified as nitrite/nitrate, which acts as NO-storage molecules with significant increase in neuronal NOS (nNOS) and inducible NOS (iNOS) mRNA levels in hypoxia conditions. The significant increase in nNOS/iNOS mRNA and NOS activity as well as in NO levels after short-time hypoxia in rat isolated atria was detected. The expression of these genes are related with the increase in atria dF/dt, cyclic GMP (cGMP) and protein kinase C (PKC) activity and resemble the results obtained by Isoproterenol, an β1 adrenoreceptor agonist. Conclusion: These findings indicate that short-term hypoxia up-regulated rat atria NO/NOS system in the presence of β1 IgG autoantibodies shows that an antibody interacting with rat atria β1 adrenoreceptor can act as expression inducer of proinflammatory NO and its metabolites and that it might be useful and helps to maintain heart function and to prevent necrosis and subsequent loss of heart function during hypoxia.
Lidocaine-Induced Cell Growth of Human Gingival Fibroblasts. Role of Na+-K+-ATPase and PKC Activities  [PDF]
Emmanuel Quinteros Villarruel, Betina Orman, Enri Borda
Pharmacology & Pharmacy (PP) , 2014, DOI: 10.4236/pp.2014.58090
Abstract:

Background: Evidences have shown that local anaesthetics are clinically useful compounds that exert a pharmacological effect by blocking nerve impulse propagation and also it is able to provoke proliferation and cell growth. Aims: The aim of this study was to investigate the proliferation and cell growth capacity of lidocaine on human gingival fibroblast cells and the different signal pathways involved in its effect. Method: For this purpose in vitro cultures of human gingival fibroblasts were assayed and the effects of lidocaine on proliferation and cell DNA synthesis, Na+-K+-ATPase and PKC activities and K+ efflux were also evaluated. Results: Lidocaine stimulated in a concentration-dependent manner proliferation and cell growth of human gingival cells and the mechanism involve an increment in Na+-K+-ATPase and PKC activities, which led to an increase in K+ release. All of these effects were blocked by tetrodotoxin, ouabain and calphostin C. In addition, PMA (activator of PKC)

Modulation of c-Jun NH2-Terminal (JNK) by Cholinergic Autoantibodies from Patients with Sjögren’s Syndrome  [PDF]
Enri Borda, Daniela Passafaro, Silvia Reina, Leonor Sterin-Borda
Pharmacology & Pharmacy (PP) , 2011, DOI: 10.4236/pp.2011.24033
Abstract: Background: We wanted to determine (via an immunopharmacological approach) whether the c-Jun NH2 terminal kinase (JNK) cascade is phosphorylated in the submandibular gland by carbachol and cholinergic autoantibodies (IgG) present in the sera of patients with primary Sjögren’s syndrome (pSS) by interaction and activation of salivary gland muscarinic acetylcholine receptors (mAChRs). Methods: The JNK, PGE2 and NOS assays were measured in rat sub- mandibular gland with pSS IgG and carbachol alone or in the presence of different blocker agents. Results: pSS IgG- activated M3 mAChRs stimulated JNK phosphorylation whereas the activation of M1 mAChRs by carbachol stimulated JNK phosphorylation involving calcium-activated mechanism. The intracellular pathway leading to pSS IgG-induced biological effects on JNK activity involved activation of protein kinase C (PKC), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) enzymes. Also, activation of COX-2 and COX-1 by pSS IgG and carbachol-induced PGE2 generation were involved. Conclusion: These results may contribute to better understanding the modulatory role of JNK enzymes by cholinergic autoantibodies from pSS patients acting on mAChR in rat submandibular gland.
Role of M3 Muscarinic Acethylcholine Receptor Antibodies as a New Marker in Primary Sj?gren Syndrome  [PDF]
Silvia Reina, Cecilia Pisoni, Roberto Arana, Sabrina Ganzinelli, Enri Borda
Pharmacology & Pharmacy (PP) , 2017, DOI: 10.4236/pp.2017.87017
Abstract: Aims: This paper investigates the presence of M3 muscarinic acetylcholine receptor autoantibody present in the serum of patients with primary Sj?gren syndrome (pSS). Main methods: We detected the levels of M3mAChR peptide IgG, PGE2, IL-1β in serum of SS patients using the enzyme-linked immune sorbent assay (ELISA). To measure the quantity of nitrite/nitrate, we used Griess reagent system. Key findings: Titres of M3mAChR antibody in sera from SS patients are significantly enhanced compared to healthy subjects (control). The enhancement of these autoantibodies is accompanied by the increase of the levels of PGE2, IL-1β and nitrite/nitrate in serum. Under in vitro conditions, the synthetic human M3 peptide impaires the increment of M3mAChR antibody but not that of nati-Ro/SSA antibody. In positive anti-Ro/SSA antibody patients, the increment of M3mAChR peptide IgG and the measured pro-inflammatory substances is related. Significance: On this basis, anti M3mAChR peptide IgG can be said to act as a modulator of the immune system and to play a role in the host-chronic increment of proinflammatory substances in SS patients with positive Ro/SSA antibody. This association between the antibody and the pathogenesis of SS disease may result in useful predicting SS.
PGE2 Generation in Myocardium from Isolated Rat Atrium under Hypoxia and Reoxygenation Conditions. Effect of Anti-β1 IgG from Patients with Chronic Severe Periodontitis  [PDF]
Sabrina Ganzinelli, Silvia Reina, Mirian Matoso, Germán González, Celina Morales, Enri Borda
Pharmacology & Pharmacy (PP) , 2014, DOI: 10.4236/pp.2014.52027
Abstract:

Background: Hypoxia is one of the most frequently encountered stresses in health and disease. Methods: We compared the effects of an anti-β1 periodontal IgG (pIgG) and an authentic β1 adrenergic agonist, xamoterol, on isolated myocardium from rat atria contractility. We used an ELISA assay to measure the generation of PGE2 in vitro after the addition of either the antibody or the adrenergic agonist. We analyzed the myocardium histopathologically in the presence of both the antibody and/or the adrenergic agonist drug during normoxia, hypoxia and reperfusion conditions. Results: PGE2 generation increased during the hypoxia and was unchanged during reoxygenation period compared with the production of this prostanoid in atria during normoxia condition. A β1 specific adrenoceptor antagonist atenolol and the β1 synthetic peptide abrogated the increment of the prostanoid in the presence of pIgG but only atenolol due to it in the presence of xamoterol. The increment of PGE2 was dependent on the activation of cox-1 and

Anti-M3 Muscarinic Acetylcholine Receptor Antibodies in Systemic Lupus Erythematosus  [PDF]
Silvia Reina, Cecilia Pisoni, Alicia Eimon, Carolina Carrizo, Roberto Arana, Enri Borda
Pharmacology & Pharmacy (PP) , 2015, DOI: 10.4236/pp.2015.61004
Abstract: Background: Evidences have shown that anti-M3 muscarinic acetylcholine receptor IgG (anti-M3 mAChR IgG) are clinically useful autoantibody that exert a cholinergic pharmacologic effect binding and interacting with M3 mAChR at the level of exocrine gland (salivary and ocular). Aims: The aim of this study was to determine the associations between serum level of anti-M3 mAChR IgG in patients with systemic lupus erythematosus (SLE) and other autoantibodies, serum prostaglandin E2 (PGE2), and clinical manifestations. Methods: Serum autoantibodies against M3 mAChR synthetic peptide were measured by enzyme-linked immuno absorbent assay (ELISA) using, as an antigen, a 25-mer peptide K-R-T-V-P-D-N-Q-C-F-I-Q-F-L-S-N-P-A-V-T-F-G-T-A-I corresponding to the amino acid sequence of the second extracellular loop of the human M3 mAChR. Serum levels of antinuclear antibodies (ANA), anti-Smith (Sm) antibodies, anti-phospholipid (APL) antibodies, and PGE2 were determined by ELISA in patients with SLE. Results: We found significantly enhanced titers of anti-M3 mAChR IgG in sera from SLE patients compared with healthy individuals (control). In addition, serum levels of PGE2 were significantly higher in SLE patients than in control patients and were significantly higher in active than in non-active SLE. No correlation was found with other autoantibodies present in SLE. By contrast, a positive correlation was found between anti-M3 mAChR IgG and PGE2 serum levels in SLE. Conclusions: As anti-M3 mAChR antibodies present in the sera of SLE patients may be another factor in the pathogenesis of this disease, and the increment of PGE2 in the sera of SLE has a modulatory action on the inflammatory process, suggesting that the presence of these autoantibodies against M3 mAChR may contribute to sustained immune deregulation and the strong inflammatory component observed in SLE.
H1-Receptor activation triggers the endogenous nitric oxide signalling system in the rat submandibular gland
Enri Borda,Graciela Stranieri,Leonor Sterin-Borda
Mediators of Inflammation , 2002, DOI: 10.1080/0962935021000051520
Abstract: Background: Histamine is released from mast cells by immunologic and non-immunologic stimuli during salivary gland inflammation, regulating salivary secretion. The receptor-secretory mechanism has not been studied in detail.
Autoantibodies to the β1-Adrenoceptor from Patients with Periodontitis as a Risk Factor for Cardiac Dysfunction
Marcela Segovia,Silvia Reina,Enri Borda,Leonor Sterin-Borda
ISRN Dentistry , 2011, DOI: 10.5402/2011/791393
Abstract:
Phosphoinositide hydrolysis mediated by H1 receptors in autoimmune myocarditis mice
Nora Goren,Claudia Perez Leiros,Leonor Sterin-Borda,Enri S. Borda
Mediators of Inflammation , 1993, DOI: 10.1155/s0962935193000444
Abstract:
Cholinoceptor Activation Subserving the Effects of Interferon Gamma on the Contractility of Rat Ileum
Enri S. Borda,Leonor Sterin-Borda,Martin Rodriguez,Maria M. E. de Bracco
Mediators of Inflammation , 1994, DOI: 10.1155/s0962935194000645
Abstract:
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