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      • Record: found
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      E prostanoid receptor‐3 promotes oxidized low‐density lipoprotein‐induced human aortic smooth muscle cells inflammation

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          Abstract

          Aim

          The progression of atherosclerosis can lead to the occurrence of multiple cardiovascular diseases (coronary heart disease, etc.). E prostanoid receptor‐3 (EP3) is known to participate in the progression of atherosclerosis. This study aimed to investigate the mechanism by which EP3 modulates the development of atherosclerosis.

          Methods and results

          ApoE −/− mice were used to construct in vivo model of atherosclerosis. Human aortic smooth muscle cells (HASMCs) were stimulated with oxidized low‐density lipoprotein (ox‐LDL) to construct in vitro model of atherosclerosis. mRNA expressions were assessed by qRT‐PCR, and western blot was applied to assess the protein levels. CCK‐8 assay was applied to assess the cell viability. The inflammatory cytokines levels were assessed by enzyme‐linked immunosorbent assay, and flow cytometry was applied to assess cell apoptosis. In vivo experiment was constructed to investigate the impact of EP3 in atherosclerosis development. L‐798106 (EP3 inhibitor) significantly inhibited the levels of pro‐inflammatory cytokines in atherosclerosis in vivo. EP3 inhibitor (L‐798106) significantly reversed ox‐LDL‐caused HASMCs injury via inhibiting the apoptosis and inflammatory responses ( P < 0.05). The levels of interleukin‐17 (IL‐17) and intercellular adhesion molecule‐1 (ICAM‐1) in HASMCs were elevated by ox‐LDL, whereas L‐798106 or knockdown of cyclic AMP (cAMP) response element‐binding protein (CREB) notably restored this phenomenon ( P < 0.05). EP3 overexpression further aggravated ox‐LDL‐induced inflammation in HASMCs, and EP3 up‐regulated the levels of IL‐17 and ICAM‐1 in ox‐LDL‐treated HASMCs ( P < 0.05). EP3 up‐regulation promoted the inflammatory responses in ox‐LDL‐treated HASMCs through mediation of cAMP/protein kinase A (PKA)/CREB/IL‐17/ICAM‐1 axis ( P < 0.05).

          Conclusions

          EP3 inhibitor alleviates ox‐LDL‐induced HASMC inflammation via mediation of cAMP/PKA/CREB/IL‐17/ICAM‐1 axis. Our study might shed new lights on discovering novel strategies against atherosclerosis.

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          Most cited references46

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          Proinflammatory activation pattern of human umbilical vein endothelial cells induced by IL-1β, TNF-α, and LPS.

          Z Weiszhár, László Cervenak, Zoltán Prohászka … (2010)
          Endothelial cells play a critical role in inflammation by responding to several endogenous and exogenous proinflammatory stimuli. The three most studied factors that provide inflammatory signals to endothelial cells are lipopolysaccharide (LPS), tumor necrosis factor (TNF)-α, and interleukin (IL)-1β; however, their effects on endothelial cells were thoroughly compared at the level of gene expression only. Therefore, our aim was to assess the differences in the signaling pathways, adhesion molecules, and cytokines induced by proinflammatory factors in human umbilical vein endothelial cells (HUVEC). In this study, we demonstrated that signaling of LPS was less effective than that of IL-1β, and was significantly slower than that ofTNF-α and IL-1β, which can be partially explained by the special localization of Toll-like receptor 4 (TLR4). We showed that TLR4 is mainly localized in Golgi apparatus in HUVEC. The proinflammatory capacity of TNF-α was similar to that of IL-1β in inducing NF-κB nuclear translocation, while IL-1β was the strongest activator of MAPK pathways. Moreover, expression of E-selectin, IL-6, and IL-8 was induced most efficiently by IL-1β, while LPS and TNF-α had less effect, whereas we did not find such a difference in ICAM-1 and MCP-1 expression. Due to the higher induction of E-selectin and IL-8, IL-1β might have more important role in neutrophil recruitment than LPS and TNF-α. By above-mentioned parameters we identified a signaling and expression pattern for the three proinflammatory molecules. This pattern illustrates how complex a proinflammatory process can be, and may enable us to predict and compare the pathomechanism of various inflammatory diseases. Copyright © 2010 International Society for Advancement of Cytometry.
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            Antioxidant properties of anthocyanins and their mechanism of action in atherosclerosis

            Chelsea Garcia, Christopher Blesso (2021)
            Article 0 comments Cited 34 times – based on 0 reviews     Review now
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              GLP-1 improves the neuronal supportive ability of astrocytes in Alzheimer's disease by regulating mitochondrial dysfunction via the cAMP/PKA pathway.

              Yunzhen Xie, Jiaping Zheng, Shiqi Li … (2021)
              The glucagon-like peptide-1 (GLP-1) was shown to have neuroprotective effects in Alzheimer's disease (AD). However, the underlying mechanism remains elusive. Astrocytic mitochondrial abnormalities have been revealed to constitute important pathologies. In the present study, we investigated the role of astrocytic mitochondria in the neuroprotective effect of GLP-1 in AD. To this end, 6-month-old 5 × FAD mice were subcutaneously treated with liraglutide, a GLP-1 analogue (25 nmol/kg/qd) for 8 weeks. Liraglutide ameliorated mitochondrial dysfunction and prevented neuronal loss with activation of the cyclic adenosine 3',5'-monophosphate (cAMP)/phosphorylate protein kinase A (PKA) pathway in the brain of 5 × FAD mice. Next, we exposed astrocytes to β-amyloid (Aβ) in vitro and treated them with GLP-1. By activating the cAMP/PKA pathway, GLP-1 increased the phosphorylation of DRP-1 at the s637 site and mitigated mitochondrial fragmentation in Aβ-treated astrocytes. GLP-1 further improved the Aβ-induced energy failure, mitochondrial reactive oxygen species (ROS) overproduction, mitochondrial membrane potential (MMP) collapse, and cell toxicity in astrocytes. Moreover, GLP-1 also promoted the neuronal supportive ability of Aβ-treated astrocytes via the cAMP/PKA pathway. This study revealed a new mechanism behind the neuroprotective effect of GLP-1 in AD.
              Article 0 comments Cited 22 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Yu‐Bin Xia:
                ORCID: https://orcid.org/0000-0002-7425-8026
                xiayubin1979@163.com
                Journal
                Journal ID (nlm-ta): ESC Heart Fail
                Journal ID (iso-abbrev): ESC Heart Fail
                Journal ID (doi): 10.1002/(ISSN)2055-5822
                Journal ID (publisher-id): EHF2
                Title: ESC Heart Failure
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2055-5822
                Publication date (Electronic): 28 December 2022
                Publication date Collection: April 2023
                Volume: 10
                Issue: 2 ( doiID: 10.1002/ehf2.v10.2 )
                Pages: 1077-1089
                Affiliations
                [ 1 ] Department of Cardiology First Affiliated Hospital of Shantou University Medical College Shantou Guangdong Province China
                [ 2 ] Laboratory of Molecular Cardiology First Affiliated Hospital of Shantou University Medical College Shantou Guangdong Province China
                [ 3 ] Laboratory of Medical Molecular Imaging First Affiliated Hospital of Shantou University Medical College Shantou Guangdong Province China
                [ 4 ] Department of Cardiac Surgery First Affiliated Hospital of Shantou University Medical College Shantou Guangdong Province China
                [ 5 ] Department of Nephrology First Affiliated Hospital of Shantou University Medical College No. 57, Changping Rd Shantou 515000 Guangdong Province China
                Author notes
                [*] [* ]Correspondence to: Dr Yu‐Bin Xia, Department of Nephrology, First Affiliated Hospital of Shantou University Medical College, No. 57, Changping Rd, Shantou 515000, Guangdong Province, China. Email: xiayubin1979@ 123456163.com
                Author information
                https://orcid.org/0000-0002-7425-8026
                Article
                Publisher ID: EHF214264 Other ID: ESCHF-22-00664
                DOI: 10.1002/ehf2.14264
                PMC ID: 10053191
                PubMed ID: 36578105
                SO-VID: 5f4c3aa2-e39e-4aca-865e-bfb37efe88a4
                Copyright © © 2022 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                Date revision received : 24 October 2022
                Date received : 24 August 2022
                Date accepted : 27 November 2022
                Page count
                Figures: 7, Tables: 1, Pages: 1089, Words: 4854
                Funding
                Funded by: Guangdong Medical Science and Technology Research Project
                Award ID: A2020190
                Award ID: A2022288
                Funded by: Shantou Science and Technology Plan Project
                Award ID: 200623085260122
                Categories
                Subject: Original Article
                Subject: Original Articles
                Custom metadata
                source-schema-version-number 2.0
                cover-date April 2023
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.2.7 mode:remove_FC converted:29.03.2023

                Keywords: atherosclerosis,ep3,camp/pka,creb,il‐17,icam‐1
                Data availability:
                Keywords: atherosclerosis, ep3, camp/pka, creb, il‐17, icam‐1

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