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ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2024

Gastrin-releasing peptide receptor antagonist RC-3095 inhibits Porphyromonas gingivalis lipopolysaccharide-accelerated atherosclerosis by suppressing inflammatory responses in endothelial cells and macrophages.

Hyun-Joo Park, Mi-Kyoung Kim, Yeon Kim, Hyung Joon Kim, Hae Ryoun Park, Soo-Kyung Bae, Moon-Kyoung Bae

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

7 authors.

Hyun-Joo ParkDepartment of Oral Physiology, School of Dentistry, Pusan National University, Yangsan, 50612, South Korea.
Mi-Kyoung KimDepartment of Oral Physiology, School of Dentistry, Pusan National University, Yangsan, 50612, South Korea.
Yeon KimDepartment of Oral Physiology, School of Dentistry, Pusan National University, Yangsan, 50612, South Korea.
Hyung Joon KimDepartment of Oral Physiology, School of Dentistry, Pusan National University, Yangsan, 50612, South Korea.
Hae Ryoun ParkPeriodontal Disease Signaling Network Research Center (MRC), School of Dentistry, Pusan National University, Yangsan, 50612, South Korea.
Soo-Kyung BaePeriodontal Disease Signaling Network Research Center (MRC), School of Dentistry, Pusan National University, Yangsan, 50612, South Korea.
Moon-Kyoung BaeDepartment of Oral Physiology, School of Dentistry, Pusan National University, Yangsan, 50612, South Korea. mkbae@pusan.ac.kr.

Funding

National Research Foundation of Korea, funded by the Korean government MSIT, NRF-2018R1A5A2023879
6 · The paper itself

Abstract

objectivePorphyromonas gingivalis (P. gingivalis), one of the major periodontopathogens, is associated with the progression and exacerbation of atherosclerosis. In this study, we aimed to investigate whether the gastrin-releasing peptide receptor antagonist, RC-3095, could attenuate P. gingivalis LPS-induced inflammatory responses in endothelial cells and macrophages, as well as atherosclerosis in an ApoE

methodsThe effect of RC-3095 on P. gingivalis LPS-induced endothelial inflammation was examined using HUVECs and rat aortic endothelium. THP-1 cells were polarized into M1 macrophages by exposure to P. gingivalis LPS, with or without RC-3095. The effect of RC-3095 on atherosclerosis progression was assessed in high-fat-fed male ApoE

resultsRC-3095 significantly reduced P. gingivalis LPS-induced leukocyte adhesion to endothelial cells and aortic endothelium by suppressing NF-κB-dependent expressions of ICAM-1 and VCAM-1. In addition, RC-3095 inhibited the P. gingivalis LPS-induced polarization of M1 macrophages by blocking the MAPK and NF-κB signaling pathways. Moreover, RC-3095 decreased the area of atherosclerotic lesions in ApoE

conclusionsRC-3095 can alleviate P. gingivalis LPS-induced endothelial inflammation, macrophage polarization, and atherosclerosis progression, suggesting its potential as a therapeutic approach for periodontal pathogen-associated atherosclerosis.

Indexed as

AtherosclerosisHuman Umbilical Vein Endothelial CellsLipopolysaccharidesMacrophagesPeptide FragmentsPorphyromonas gingivalisAnimalsAortaApolipoproteins EBombesinEndothelial CellsHumansInflammationMaleMiceMice, Inbred C57BLApolipoproteins EBombesinbombesin (6-14), Tpi(6)-Leu(13)-psi(CH2NH)-Leu(14)-LipopolysaccharidesNF-kappa BPeptide FragmentsReceptors, BombesinAtherosclerosisGastrin-releasing peptide receptorLipopolysaccharidePorphyromonas gingivalisRC-3095

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.