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| Item Type: | Article |
|---|---|
| Title: | An explorative approach to examining the role of ischemia and inflammation on the function of autoantibodies against G protein-coupled receptors and their corresponding agonists |
| Creators Name: | Wallukat, Gerd, Lakatos, Petra, Steinhorst, Kira, Flecks, Merle and Hohberger, Bettina |
| Abstract: | first_pagesettingsOrder Article Reprints Open AccessArticle An Explorative Approach to Examining the Role of Ischemia and Inflammation on the Function of Autoantibodies Against G Protein–Coupled Receptors and Their Corresponding Agonists by Gerd Wallukat 1,*,Petra Lakatos 2,Kira Steinhorst 2,Merle Flecks 2 andBettina Hohberger 2ORCID 1 Max Delbrück Center for Molecular Medicine, 13125 Berlin, Germany 2 Department of Ophthalmology, University of Erlangen, Friedrich-Alexander-Universität Erlangen Nürnberg, 91054 Erlangen, Germany * Author to whom correspondence should be addressed. Int. J. Mol. Sci. 2026, 27(6), 2797; https://doi.org/10.3390/ijms27062797 Submission received: 2 February 2026 / Revised: 16 March 2026 / Accepted: 17 March 2026 / Published: 19 March 2026 (This article belongs to the Special Issue Progress in Prevention and Treatment of Cardiovascular Diseases and Arrhythmias) Downloadkeyboard_arrow_down Browse Figures Versions Notes Abstract Autoantibodies (AAbs) play an important role in the development of autoimmune diseases. While many AAbs induce apoptosis of target cells, a distinct subgroup, termed functional autoantibodies (fAAbs) against G protein–coupled receptors (GPCRs), can modulate physiological receptor signaling without inducing cell death. The functional activity of GPCR-fAAbs may be influenced by various cofactors, including inflammation (e.g., inflammatory cytokine, ciliary neurotrophic factor (CNTF)) and ischemia. As ischemia triggers a substantial release of arachidonic acid (AA) from membrane phospholipids, the present study aimed to examine exploratively the influence of AA, eicosapentaenoic acid (EPA), and CNTF on the responses of spontaneously beating neonatal rat cardiomyocytes to GPCR agonists and GPCR-fAAbs. AA and EPA differentially influenced responses in cardiomyocytes induced by GPCR-fAAbs: AA altered the functional responses associated with adrenergic β2-fAAb, adrenergic α1-fAAb, angiotensin II (AT1)-fAAb, endothelin A (ETA)-fAAb and angiotensin 1–7 MAS-fAAbs. However, muscarinergic M2-fAAb responses remained largely unaffected. In contrast, EPA attenuated the responses to β2-fAAb, α1-fAAb, AT1-fAAb, and ETA-fAAb, while MAS-fAAb and M2-fAAb responses were not markedly altered. CNTF acted as a time-dependent modulator of cardiomyocyte chronotropic responses and influenced the magnitude of GPCR-mediated signaling on a cardiomyocyte bioassay. Together, these findings might suggest that lipid mediators such as AA and EPA or CNTF may modulate functional responses of cardiomyocytes associated with GPCR-fAAbs. |
| Keywords: | G Protein-Coupled Receptor, Autoantibody, Functional Autoantibody, Arachidonic Acid, Eicosapentaenoic Acid, Ciliary Neurotrophic Factor, Animals, Rats |
| Source: | International Journal of Molecular Sciences |
| ISSN: | 1422-0067 |
| Publisher: | MDPI |
| Volume: | 27 |
| Number: | 6 |
| Page Range: | 2797 |
| Date: | March 2026 |
| Official Publication: | https://doi.org/10.3390/ijms27062797 |
| PubMed: | View item in PubMed |
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