دورية أكاديمية
أعرض في EDS

Role of Formyl Peptide Receptors and β-Arrestin-1 in suPAR Signal Transduction in Mouse Podocytes: Interactions with αVβ3-Integrin.

التفاصيل البيبلوغرافية
العنوان: Role of Formyl Peptide Receptors and β-Arrestin-1 in suPAR Signal Transduction in Mouse Podocytes: Interactions with αVβ3-Integrin.
المؤلفون: Kim EY; Department of Biology and Biochemistry, University of Houston, Houston, TX 77204, USA., Dryer SE; Department of Biology and Biochemistry, University of Houston, Houston, TX 77204, USA.; Department of Biomedical Sciences, Tilman J. Fertitta Family College of Medicine, University of Houston, Houston, TX 77204, USA.
المصدر: Cells [Cells] 2024 Jan 17; Vol. 13 (2). Date of Electronic Publication: 2024 Jan 17.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101600052 Publication Model: Electronic Cited Medium: Internet ISSN: 2073-4409 (Electronic) Linking ISSN: 20734409 NLM ISO Abbreviation: Cells Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI
مواضيع طبية MeSH: beta-Arrestin 1* , Receptors, Formyl Peptide* , Receptors, Urokinase Plasminogen Activator*, Animals ; Mice ; Integrin beta3 ; Podocytes ; Reactive Oxygen Species ; Receptor for Advanced Glycation End Products ; Signal Transduction ; Integrin alpha5
مستخلص: The soluble urokinase plasminogen activator receptor (suPAR) has been implicated in a wide range of pathological conditions including primary nephrotic syndromes and acute kidney injuries. suPAR can trigger transduction cascades in podocytes by outside-in activation of αVβ3-integrin, but there is evidence that the functional cell surface response element is actually a complex of different types of receptors, which may also include the receptor for advanced glycation end-products (RAGE) and formyl peptide receptors (FPRs). Here we observed that ROS accumulation and Src activation could be evoked by continuous 24 h exposure to either suPAR or the FPR agonist fMLF. Responses to suPAR and fMLF were completely blocked by either the FPR antagonist WRW4 or by the αV-integrin inhibitor cilengitide. Moreover, endogenous podocyte mouse Fpr1 co-immunoprecipitates with β3-integrin, suggesting that these receptors occur as a complex on the cell surface. suPAR- and fMLF-evoked activation of Src and ROS differed in time course. Thus, robust pertussis toxin (PTX)-sensitive responses were evoked by 60 min exposures to fMLF but not to suPAR. By contrast, responses to 24 h exposures to either suPAR or fMLF were PTX-resistant and were instead abolished by knockdown of β-arrestin-1 (BAR1). FPRs, integrins, and RAGE (along with various Toll-like receptors) can all function as pattern-recognition receptors that respond to "danger signals" associated with infections and tissue injury. The fact that podocytes express such a wide array of pattern-recognition receptors suggests that the glomerular filter is designed to change its function under certain conditions, possibly to facilitate clearance of toxic macromolecules.
References: J Biol Chem. 2003 Aug 15;278(33):31251-60. (PMID: 12759359)
Nat Commun. 2022 Sep 5;13(1):5232. (PMID: 36064945)
Transplantation. 2015 Dec;99(12):2593-7. (PMID: 26371597)
Biochim Biophys Acta Mol Basis Dis. 2021 Oct 1;1867(10):166186. (PMID: 34166766)
Curr Opin Cell Biol. 2008 Oct;20(5):514-9. (PMID: 18638550)
Mol Cell Biochem. 2009 Jan;321(1-2):111-22. (PMID: 18830568)
Pharmacol Rev. 2009 Jun;61(2):119-61. (PMID: 19498085)
Front Biosci (Landmark Ed). 2009 Jan 01;14(7):2494-503. (PMID: 19273214)
Crit Rev Clin Lab Sci. 2017 Mar;54(2):117-133. (PMID: 28084848)
Signal Transduct Target Ther. 2021 Aug 4;6(1):291. (PMID: 34344870)
J Clin Invest. 2004 May;113(10):1390-7. (PMID: 15146236)
Exp Cell Res. 2014 Apr 15;323(1):209-217. (PMID: 24491917)
Am Fam Physician. 2010 Sep 15;82(6):645-51. (PMID: 20842993)
Exp Cell Res. 1997 Oct 10;236(1):248-58. (PMID: 9344605)
Annu Rev Physiol. 2022 Feb 10;84:17-40. (PMID: 34705480)
Biochim Biophys Acta Mol Basis Dis. 2017 Sep;1863(9):2342-2354. (PMID: 28629718)
N Engl J Med. 2020 Jan 30;382(5):416-426. (PMID: 31995687)
Crit Care Med. 2018 Dec;46(12):1961-1968. (PMID: 30247244)
Annu Rev Med. 2018 Jan 29;69:349-364. (PMID: 29106804)
JCI Insight. 2023 Apr 10;8(7):. (PMID: 37036003)
J Pediatr. 1982 Nov;101(5):661-8. (PMID: 7131137)
Nat Rev Mol Cell Biol. 2010 Jan;11(1):23-36. (PMID: 20027185)
J Biol Chem. 1991 Jan 25;266(3):1926-33. (PMID: 1846368)
Proc Natl Acad Sci U S A. 2006 Sep 19;103(38):14110-5. (PMID: 16968782)
Eur J Med Chem. 2021 Dec 15;226:113805. (PMID: 34536667)
Biochim Biophys Acta Mol Basis Dis. 2018 Oct;1864(10):3527-3536. (PMID: 30293571)
Mol Neurodegener. 2012 Nov 20;7:55. (PMID: 23164356)
Int J Mol Sci. 2019 Jul 12;20(14):. (PMID: 31336833)
Front Pediatr. 2018 Aug 17;6:202. (PMID: 30175088)
Nat Med. 2008 Jan;14(1):55-63. (PMID: 18084301)
J Virol. 2013 Dec;87(24):13911-6. (PMID: 24109241)
Science. 2003 Sep 5;301(5638):1394-7. (PMID: 12958365)
Kidney Dis (Basel). 2022 Jun 8;8(4):265-274. (PMID: 35949208)
J Immunol. 2004 Jul 1;173(1):607-14. (PMID: 15210823)
Acc Chem Res. 2009 Jul 21;42(7):969-80. (PMID: 19489579)
Nat Med. 2017 Jan;23(1):100-106. (PMID: 27941791)
J Sports Med Phys Fitness. 2016 Sep;56(9):1060-76. (PMID: 25854772)
Am J Physiol Renal Physiol. 2008 Jul;295(1):F235-46. (PMID: 18480178)
Inflammation. 2007 Dec;30(6):224-9. (PMID: 17687636)
ACS Pharmacol Transl Sci. 2020 Mar 11;3(2):203-220. (PMID: 32296763)
Cold Spring Harb Perspect Biol. 2011 Mar 01;3(3):. (PMID: 21421922)
Am J Physiol Renal Physiol. 2018 Nov 1;315(5):F1283-F1294. (PMID: 29923769)
J Am Soc Nephrol. 2004 Sep;15(9):2246-8. (PMID: 15339973)
J Am Soc Nephrol. 2020 Nov;31(11):2725-2735. (PMID: 32963090)
Anticancer Agents Med Chem. 2010 Dec;10(10):753-68. (PMID: 21269250)
Intensive Care Med. 2000 Sep;26(9):1364-8. (PMID: 11089766)
Genomics. 1998 Jul 15;51(2):270-6. (PMID: 9722950)
Dis Markers. 2009;27(3):157-72. (PMID: 19893210)
Int J Mol Sci. 2017 Jul 31;18(8):. (PMID: 28758975)
Cytokine Growth Factor Rev. 2006 Dec;17(6):501-19. (PMID: 17084101)
Sci Rep. 2016 Dec 22;6:39513. (PMID: 28004760)
Front Immunol. 2023 Jul 26;14:1201619. (PMID: 37564655)
Pflugers Arch. 2017 Aug;469(7-8):1017-1020. (PMID: 28689240)
J Surg Res. 2015 May 15;195(2):396-405. (PMID: 25758338)
Nat Rev Immunol. 2019 Oct;19(10):599-613. (PMID: 31350531)
Front Immunol. 2017 Feb 08;8:122. (PMID: 28228761)
J Biol Chem. 2023 Mar;299(3):102922. (PMID: 36669646)
Cell. 2020 Sep 3;182(5):1362-1362.e1. (PMID: 32888497)
Nat Med. 2011 Jul 31;17(8):952-60. (PMID: 21804539)
Front Immunol. 2021 Dec 02;12:780641. (PMID: 34925360)
Am Fam Physician. 2017 Feb 15;95(4):248-254. (PMID: 28290633)
Proc Natl Acad Sci U S A. 2002 Feb 5;99(3):1359-64. (PMID: 11818541)
معلومات مُعتمدة: R01 DK104708 United States DK NIDDK NIH HHS; R01-DK104708 United States NH NIH HHS
فهرسة مساهمة: Keywords: acute kidney injury; formyl peptide receptors; nephrotic syndrome; pattern-recognition receptor; podocytes; suPAR; β-arrestin
المشرفين على المادة: 0 (beta-Arrestin 1)
0 (Integrin beta3)
0 (Reactive Oxygen Species)
0 (Receptor for Advanced Glycation End Products)
0 (Receptors, Formyl Peptide)
0 (Receptors, Urokinase Plasminogen Activator)
0 (Integrin alpha5)
تواريخ الأحداث: Date Created: 20240122 Date Completed: 20240209 Latest Revision: 20240209
رمز التحديث: 20240210
مُعرف محوري في PubMed: PMC10814688
DOI: 10.3390/cells13020172
PMID: 38247863
قاعدة البيانات: MEDLINE
الوصف
تدمد:2073-4409
DOI:10.3390/cells13020172