title: Autoantibodies against G-protein-coupled receptors modulate heart mast cells.
abstract: Mast cells are believed to be involved in myocardial tissue remodelling under pathophysiological conditions. We examined the effects of autoantibodies against G-protein-coupled receptors in sera of patients with heart diseases on myocardial mast cells in the cultured neonatal Sprague-Dawley rat heart cells. Cells collected at day 3 and 10 of the culture were preincubated with autoantibodies against alpha1-adrenoceptor and angiotensin II AT1-receptor, agonist phenylephrine and angiotensin II, and control IgG. The pretreated cultured cells were stained for selected mast cell markers tryptase, chymase and TNF-alpha. The cultured cells were also processed for observation with electron microscopy. The autoantibodies-treatment of the 3-day cultured cells caused both increased intensity of immunofluorescence (p < 0.05) and their enlarged diameters of the mast cells when compared to age-matched ones. In contrast, the fluorescence of preincubated 10-day-old mast cells was decreased compared with controls (p < 0.01). In control samples, the fluorescence of 10-day-old mast cells was significantly higher than that of 3-day-old ones (p < 0.001). Results of electron microscopy examination demonstrated there was an increased granulation of treated 3-day-old mast cells, while a degranulation of mast cells at day 10 of application. The results suggest the modulation effect of the autoantibodies against G-protein-coupled receptors on mast cells, indicating a potential functional link between the autoantibodies against G-protein-coupled receptors and the mast cells in progression of heart disease.
authors.affiliation: Institute for Heart Research, Slovak Academy of Sciences, Dubravska cesta 9, PO Box 45, 840 05 Bratislava 45, Slovak Republic. usrdokru@savba.sk
authors.forename: Ludmila
authors.initials: L
authors.lastname: Okruhlicova
authors.forename: Rosemarie
authors.initials: R
authors.lastname: Morwinski
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Schulze
authors.forename: Sabine
authors.initials: S
authors.lastname: Bartel
authors.forename: Peter
authors.initials: P
authors.lastname: Weismann
authors.forename: Narcisa
authors.initials: N
authors.lastname: Tribulova
authors.forename: Gerd
authors.initials: G
authors.lastname: Wallukat
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000328:Adult; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D001323:Autoantibodies / Q000097:blood*; D015550:Cell Degranulation; D002454:Cell Differentiation; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D006973:Hypertension / Q000276:immunology*; D006976:Hypertension, Pulmonary / Q000276:immunology*; D008297:Male; D008407:Mast Cells / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D010656:Phenylephrine / Q000494:pharmacology; D011225:Pre-Eclampsia / Q000276:immunology*; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000276:immunology; D018340:Receptors, Adrenergic, alpha-1 / Q000276:immunology; D043562:Receptors, G-Protein-Coupled / Q000819:agonists / Q000276:immunology* / Q000378:metabolism; D013997:Time Factors
chemical_list: D000316:Adrenergic alpha-Agonists; D001323:Autoantibodies; D044140:Receptor, Angiotensin, Type 1; D018340:Receptors, Adrenergic, alpha-1; D043562:Receptors, G-Protein-Coupled; D000804:Angiotensin II; D010656:Phenylephrine