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Abstract:

Introduction: The role of apoptotic secretory epithelium as a pro-inflammatory triggering factor of exocrine dysfunction is currently explored in Sjogren's syndrome patients and in the nonobese diabetic (NOD) mouse model. Vasoactive intestinal peptide (VIP) has anti-inflammatory effects in various models of chronic inflammation. Our goal was to analyse the effect of TNF-α on apoptotic mediators in isolated acinar cells from NOD submandibular gland and their modulation by VIP. Methods: Acinar cells were isolated from submandibular glands of 16-week-old NOD females with salivary flow decline. Age-matched BALB/c females or eight-week-old NOD females were used as controls. Apoptotic mediators and TNF-α receptor expression were assessed by immunoblotting and RT-PCR, caspase 3 activity was assessed by optical density at 405 nm with Ac-DEVD-pNA as a substrate and chromatin condensation by Hoechst stain. They were evaluated in resting conditions and after a 3.5 or 6 hours of culture with TNF-α. VIP effects in acinar cells were assessed at 100 nM in TNF-α-treated cultures and VIP receptor functional assays by radio immunoassay (cAMP) or enzymatic detection (amylase). Results: NOD acinar cells at 16 weeks present an increased expression of TNF-α receptor1 together with increased Bax, tumour protein 53-induced nuclear protein1α (TP53INP1α), caspase 3 activity and chromatin condensation. Acini from NOD mice were more sensitive to TNF-α-induced increases of apoptotic mediators than control cells. VIP inhibited TNF-α-induced apoptotic events through functional VPAC1 receptors coupled to the protein kinase A (PKA) signalling pathway. Conclusions: Our results indicate that acinar cells isolated from submandibular glands of NOD mice with salivary dysfunction are more sensitive to apoptosis induced by TNF-α which could be prevented by VIP through a PKA-mediated pathway. © 2009 Calafat et al.; licensee BioMed Central Ltd.

Registro:

Documento: Artículo
Título:Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands
Autor:Calafat, M.; Larocca, L.; Roca, V.; Hauk, V.; Pregi, N.; Nesse, A.; Pérez Leirós, C.
Filiación:Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Pabellón II, 1428 Buenos Aires, Argentina
Consejo Nacional de Investigaciones Científicas y Técnicas, Avda. Rivadavia 1917, C1033AAJ Buenos Aires, Argentina
Palabras clave:amylase; caspase 3; cyclic AMP dependent protein kinase; nuclear protein; protein Bax; tumor necrosis factor alpha; tumor necrosis factor alpha receptor; tumor protein 53 induced nuclear protein 1 alpha; unclassified drug; vasoactive intestinal polypeptide; vasoactive intestinal polypeptide receptor 1; cyclic AMP dependent protein kinase; acinar cell; animal cell; animal experiment; animal model; animal tissue; apoptosis; article; controlled study; enzyme activity; enzyme substrate; female; mouse; nonhuman; nonobese diabetic mouse; protein expression; protein function; protein protein interaction; salivary gland disease; salivation; submandibular gland; animal; Bagg albino mouse; disease model; metabolism; pathology; physiology; reverse transcription polymerase chain reaction; signal transduction; Sjoegren syndrome; Western blotting; Animals; Apoptosis; Blotting, Western; Cyclic AMP-Dependent Protein Kinases; Disease Models, Animal; Female; Mice; Mice, Inbred BALB C; Mice, Inbred NOD; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction; Sjogren's Syndrome; Submandibular Gland; Tumor Necrosis Factor-alpha; Vasoactive Intestinal Peptide
Año:2009
Volumen:11
Número:2
DOI: http://dx.doi.org/10.1186/ar2671
Título revista:Arthritis Research and Therapy
Título revista abreviado:Arthritis Res. Ther.
ISSN:14786354
CODEN:ARTRC
CAS:amylase, 9000-90-2, 9000-92-4, 9001-19-8; caspase 3, 169592-56-7; vasoactive intestinal polypeptide, 37221-79-7; Cyclic AMP-Dependent Protein Kinases, 2.7.11.11; Tumor Necrosis Factor-alpha; Vasoactive Intestinal Peptide, 37221-79-7
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14786354_v11_n2_p_Calafat

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Citas:

---------- APA ----------
Calafat, M., Larocca, L., Roca, V., Hauk, V., Pregi, N., Nesse, A. & Pérez Leirós, C. (2009) . Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands. Arthritis Research and Therapy, 11(2).
http://dx.doi.org/10.1186/ar2671
---------- CHICAGO ----------
Calafat, M., Larocca, L., Roca, V., Hauk, V., Pregi, N., Nesse, A., et al. "Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands" . Arthritis Research and Therapy 11, no. 2 (2009).
http://dx.doi.org/10.1186/ar2671
---------- MLA ----------
Calafat, M., Larocca, L., Roca, V., Hauk, V., Pregi, N., Nesse, A., et al. "Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands" . Arthritis Research and Therapy, vol. 11, no. 2, 2009.
http://dx.doi.org/10.1186/ar2671
---------- VANCOUVER ----------
Calafat, M., Larocca, L., Roca, V., Hauk, V., Pregi, N., Nesse, A., et al. Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands. Arthritis Res. Ther. 2009;11(2).
http://dx.doi.org/10.1186/ar2671