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International Journal of Physiology and Pathophysiology
SJR: 0.106

ISSN Print: 2155-014X
ISSN Online: 2155-0158

Archives: Volume 1, 2010 to Volume 9, 2018

International Journal of Physiology and Pathophysiology

DOI: 10.1615/IntJPhysPathophys.v8.i1.70
pages 65-76

Effect of Staphylococcus aureus Cell-Wall Peptidoglycan on the Rat Myometrial Contractility Regulation by Adenylate Cyclase Signaling System

Lilit S. Nasibyan
Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv, Ukraine
Igor B. Philyppov
Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv, Ukraine

ABSTRACT

Impact of Staphylococcus aureus cell-wall peptidoglycan on some links of Adenylate cyclase messenger system in the rat myometrial contractility was studied. Spontaneous and prostaglandin F2α-induced contractions of the myometrium were inhibited by non-selective adrenoceptor agonist noradrenaline and selective agonist of β2-adrenergic receptors salbutamol. Under this conditions peptidoglycan application fully restored myometrial contractility. The similar effect was observed after activating adenylate cyclase by forskolin. Simultaneously when myometrial contractions were reduced via increasing the intracellular cyclic adenosine monophosphate (cAMP) by applying either 8-bromo-cAMP or papaverin, a non-selective inhibitor of cAMP-dependent phosphodiesterases, the effect of peptidoglycan was absent. Given the activation of Gs-protein by cholera toxin, peptidoglycan restored spontaneous activity and strengthened prostaglandin-induced contractions. Downregulation of Gi/o-protein by pertussis toxin evoked loss of capacity of peptidoglycan to restore spontaneous and induced contractile activities of the myometrium, suppressed by applying β-adrenergic agonists or forskolin. Thus, the effect of peptidoglycan on the rat myometrium contractility is associated with its ability to cause rapid desensitization of adenylate cyclase due to increased functional activity of Gi-protein.


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