FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4311610686> ?p ?o ?g. }

• W4311610686 endingPage "1150" @default.
• W4311610686 startingPage "1139" @default.
• W4311610686 abstract "Formyl peptide receptors (FPRs) are an important part of innate immunity involved in antimicrobial phagocyte functions such as chemotaxis, secretory degranulation, and respiratory burst. These phagocyte responses are observed in both acute and systemic chronic inflammation. Abundant or constant release of pro-inflammatory ligands leads to the pre-activation of phagocytes when subsequent stimulation induces more intense cellular response. Binding of the formyl peptide receptor with its agonist activates production of reactive oxygen species, due to triggering phosphorylation of the cytoplasmic subunits p47phox and p67phox followed by their translocation to the plasma membrane and assembly into the NADPH oxidase complex. Rheumatoid arthritis is characterized by an imbalance of immune processes and autoimmune responses against the own joint tissues. It is known that, granulocytes produce increased amounts of oxygen radicals in various pathologies, including rheumatoid arthritis. We suggest that such enhancement may be due to increased expression of formyl peptide receptors or components of the FPR/PKC/NOX2 signaling pathway. Our aim was to study the mRNA expression of fpr1/fpr2 genes and the FPR-dependent production of reactive oxygen species by isolated peripheral blood granulocytes from the patients with rheumatoid arthritis. Materials and methods. The objects of the study were isolated peripheral blood granulocytes. We analyzed, respectively, 166 and 85 samples from the patients with rheumatoid arthritis and healthy donors. The production of reactive oxygen species was assessed using luminol-dependent chemiluminescence. For FPR1 activation we used a distinct concentration of the formyl peptide fMLF: the response to it was completely inhibited by pretreatment of the cells with FPR1 antagonist N-t-boc-MLF. FPR2 activation was performed by synthetic peptide WKYMVM, a specific receptor agonist. In the patients with rheumatoid arthritis, we have revealed an increased level of spontaneous and phorbol ester-induced production of reactive oxygen species by isolated peripheral blood granulocytes, thus reflecting a pre-activated state of the phagocytes in rheumatoid arthritis. We have found the increased FPR1-mediated production of oxygen radicals and expression of mRNA of fpr1 gene in blood granulocytes of rheumatoid arthritis patients. Furthermore, the enhancement of oxidase function may be associated with constitutive activation of the FPR1/PKC/NOX2 pathway as shown by positive correlation between the processes. The production of reactive oxygen species induced by stimulation of the FPR2 receptor is also increased, but it cannot be directly attributed to overexpression of the receptor mRNA or PKC/NOX2 activation, and requires further study. Understanding the mechanisms of regulation of the FPR1 and FPR2 signaling cascades may reveal new targets for anti-rheumatoid therapy." @default.
• W4311610686 created "2022-12-27" @default.
• W4311610686 creator A5011673021 @default.
• W4311610686 creator A5020544936 @default.
• W4311610686 creator A5022154940 @default.
• W4311610686 creator A5034060844 @default.
• W4311610686 creator A5039083030 @default.
• W4311610686 date "2022-12-08" @default.
• W4311610686 modified "2023-09-25" @default.
• W4311610686 title "Expression and function of receptors for the formylated peptides in granulocytes of the patients with rheumatoid arthritis" @default.
• W4311610686 cites W1558468202 @default.
• W4311610686 cites W1587065262 @default.
• W4311610686 cites W1592678705 @default.
• W4311610686 cites W1661985738 @default.
• W4311610686 cites W1766162468 @default.
• W4311610686 cites W1904592173 @default.
• W4311610686 cites W1977492069 @default.
• W4311610686 cites W1979751791 @default.
• W4311610686 cites W1987508105 @default.
• W4311610686 cites W1989914423 @default.
• W4311610686 cites W2001049330 @default.
• W4311610686 cites W2012034410 @default.
• W4311610686 cites W2028289020 @default.
• W4311610686 cites W2029387145 @default.
• W4311610686 cites W2030551870 @default.
• W4311610686 cites W2032019813 @default.
• W4311610686 cites W2055477913 @default.
• W4311610686 cites W2107277218 @default.
• W4311610686 cites W2127893132 @default.
• W4311610686 cites W2128361103 @default.
• W4311610686 cites W2128952811 @default.
• W4311610686 cites W2131896212 @default.
• W4311610686 cites W2134468750 @default.
• W4311610686 cites W2142633654 @default.
• W4311610686 cites W2145164843 @default.
• W4311610686 cites W2158548049 @default.
• W4311610686 cites W2578291312 @default.
• W4311610686 cites W2595655718 @default.
• W4311610686 cites W2755916089 @default.
• W4311610686 cites W2773767509 @default.
• W4311610686 cites W2783570771 @default.
• W4311610686 cites W2805428380 @default.
• W4311610686 cites W2902336604 @default.
• W4311610686 cites W2943622238 @default.
• W4311610686 cites W3002644695 @default.
• W4311610686 cites W3193527933 @default.
• W4311610686 cites W51956675 @default.
• W4311610686 doi "https://doi.org/10.15789/1563-0625-eaf-2503" @default.
• W4311610686 hasPublicationYear "2022" @default.
• W4311610686 type Work @default.
• W4311610686 citedByCount "0" @default.
• W4311610686 crossrefType "journal-article" @default.
• W4311610686 hasAuthorship W4311610686A5011673021 @default.
• W4311610686 hasAuthorship W4311610686A5020544936 @default.
• W4311610686 hasAuthorship W4311610686A5022154940 @default.
• W4311610686 hasAuthorship W4311610686A5034060844 @default.
• W4311610686 hasAuthorship W4311610686A5039083030 @default.
• W4311610686 hasBestOaLocation W43116106861 @default.
• W4311610686 hasConcept C134018914 @default.
• W4311610686 hasConcept C136449434 @default.
• W4311610686 hasConcept C170493617 @default.
• W4311610686 hasConcept C185592680 @default.
• W4311610686 hasConcept C203014093 @default.
• W4311610686 hasConcept C24998067 @default.
• W4311610686 hasConcept C2776914184 @default.
• W4311610686 hasConcept C2777575956 @default.
• W4311610686 hasConcept C2777700362 @default.
• W4311610686 hasConcept C2777983669 @default.
• W4311610686 hasConcept C2779719074 @default.
• W4311610686 hasConcept C48349386 @default.
• W4311610686 hasConcept C49802076 @default.
• W4311610686 hasConcept C54166955 @default.
• W4311610686 hasConcept C55493867 @default.
• W4311610686 hasConcept C86803240 @default.
• W4311610686 hasConcept C8891405 @default.
• W4311610686 hasConcept C99971728 @default.
• W4311610686 hasConceptScore W4311610686C134018914 @default.
• W4311610686 hasConceptScore W4311610686C136449434 @default.
• W4311610686 hasConceptScore W4311610686C170493617 @default.
• W4311610686 hasConceptScore W4311610686C185592680 @default.
• W4311610686 hasConceptScore W4311610686C203014093 @default.
• W4311610686 hasConceptScore W4311610686C24998067 @default.
• W4311610686 hasConceptScore W4311610686C2776914184 @default.
• W4311610686 hasConceptScore W4311610686C2777575956 @default.
• W4311610686 hasConceptScore W4311610686C2777700362 @default.
• W4311610686 hasConceptScore W4311610686C2777983669 @default.
• W4311610686 hasConceptScore W4311610686C2779719074 @default.
• W4311610686 hasConceptScore W4311610686C48349386 @default.
• W4311610686 hasConceptScore W4311610686C49802076 @default.
• W4311610686 hasConceptScore W4311610686C54166955 @default.
• W4311610686 hasConceptScore W4311610686C55493867 @default.
• W4311610686 hasConceptScore W4311610686C86803240 @default.
• W4311610686 hasConceptScore W4311610686C8891405 @default.
• W4311610686 hasConceptScore W4311610686C99971728 @default.
• W4311610686 hasIssue "6" @default.
• W4311610686 hasLocation W43116106861 @default.
• W4311610686 hasOpenAccess W4311610686 @default.
• W4311610686 hasPrimaryLocation W43116106861 @default.

• next