Loading…
Resveratrol Downregulates Granulocyte-Macrophage Colony-Stimulating Factor-Induced Oncostatin M Production through Blocking of PI3K/Akt/NF-κB Signal Cascade in Neutrophil-like Differentiated HL-60 Cells
Oncostatin M (OSM) is essential in a wide range of inflammatory responses, and most OSM is produced by neutrophils in respiratory diseases. While resveratrol (RES) is regarded as an anti-inflammatory agent in a variety of conditions, the mechanism of OSM inhibition by RES in neutrophils remains to b...
Saved in:
Published in: | Current issues in molecular biology 2022-01, Vol.44 (2), p.541-549 |
---|---|
Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | cdi_FETCH-LOGICAL-c427t-d8a02b49db32dfda760b1ed5326b241d4822489c6e95e977267754bc4dbc3cef3 |
---|---|
cites | cdi_FETCH-LOGICAL-c427t-d8a02b49db32dfda760b1ed5326b241d4822489c6e95e977267754bc4dbc3cef3 |
container_end_page | 549 |
container_issue | 2 |
container_start_page | 541 |
container_title | Current issues in molecular biology |
container_volume | 44 |
creator | Han, Na-Ra Park, Hi-Joon Moon, Phil-Dong |
description | Oncostatin M (OSM) is essential in a wide range of inflammatory responses, and most OSM is produced by neutrophils in respiratory diseases. While resveratrol (RES) is regarded as an anti-inflammatory agent in a variety of conditions, the mechanism of OSM inhibition by RES in neutrophils remains to be elucidated. In this study, we investigated whether RES could inhibit OSM production in neutrophil-like differentiated (d)HL-60 cells. The effects of RES were measured by means of an enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and Western blotting. Increases in production and mRNA expression of OSM resulted from the addition of granulocyte-macrophage colony-stimulating factor (GM-CSF) in neutrophil-like dHL-60 cells; however, these increases were downregulated by RES treatment. Exposure to GM-CSF led to elevations of phosphorylation of phosphatidylinositol 3-kinase (PI3K), Akt, and nuclear factor (NF)-kB. Treatment with RES induced downregulation of the phosphorylated levels of PI3K, Akt, and NF-κB in neutrophil-like dHL-60 cells. These results suggest that RES could be applicable to prevent and/or treat inflammatory disorders through blockade of OSM. |
doi_str_mv | 10.3390/cimb44020037 |
format | article |
fullrecord | <record><control><sourceid>proquest_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_01c2e025d6da48c18e4664bea10f3b0b</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_01c2e025d6da48c18e4664bea10f3b0b</doaj_id><sourcerecordid>2678739925</sourcerecordid><originalsourceid>FETCH-LOGICAL-c427t-d8a02b49db32dfda760b1ed5326b241d4822489c6e95e977267754bc4dbc3cef3</originalsourceid><addsrcrecordid>eNpVkt1u0zAUxyMEYmNwxwP4kgtCHduJkxukraNbRfchBteRP05Sr67d2c5QX22vMIlnIqUT2q58dM7fv_OZZR8L_IXSBk-UWUvGMMGY8lfZYcEqnlPMytfP7IPsXYy3GJe85sXb7ICWnFBK6GH2-APiPQSRgrfo1P92AfrBigQRnQXhBuvVNkF-IVTwm6XoAU299W6b3ySz3gmN69FMqORDPnd6UKDRlVM-pl0IXaDr4EdvMt6htAx-6JfoZISudv98h67n9PvkeJUml7P8z8MJujG9ExZNRVRCAxoRlzCkXW5jc2tWgE5N10EAl8xYpUbni7zCaArWxvfZm07YCB-e3qPs1-zbz-l5vrg6m0-PF7lihKdc1wITyRotKdGdFrzCsgBdUlJJwgrNakJY3agKmhIazknFecmkYloqqqCjR9l8z9Ve3LabYNYibFsvTPvP4UPfipCMstDiQhHApNSVFqxWRQ2sqpgEUeCOSixH1tc9azPINWg19hWEfQF9GXFm2fb-vq0bUjdVMQI-PQGCvxsgpnZtohrHIRz4IbZj9TWnTUPKUfp5Lx13GWOA7n-aAre7W2qf3xL9CzrXwKM</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2678739925</pqid></control><display><type>article</type><title>Resveratrol Downregulates Granulocyte-Macrophage Colony-Stimulating Factor-Induced Oncostatin M Production through Blocking of PI3K/Akt/NF-κB Signal Cascade in Neutrophil-like Differentiated HL-60 Cells</title><source>PubMed (Medline)</source><creator>Han, Na-Ra ; Park, Hi-Joon ; Moon, Phil-Dong</creator><creatorcontrib>Han, Na-Ra ; Park, Hi-Joon ; Moon, Phil-Dong</creatorcontrib><description>Oncostatin M (OSM) is essential in a wide range of inflammatory responses, and most OSM is produced by neutrophils in respiratory diseases. While resveratrol (RES) is regarded as an anti-inflammatory agent in a variety of conditions, the mechanism of OSM inhibition by RES in neutrophils remains to be elucidated. In this study, we investigated whether RES could inhibit OSM production in neutrophil-like differentiated (d)HL-60 cells. The effects of RES were measured by means of an enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and Western blotting. Increases in production and mRNA expression of OSM resulted from the addition of granulocyte-macrophage colony-stimulating factor (GM-CSF) in neutrophil-like dHL-60 cells; however, these increases were downregulated by RES treatment. Exposure to GM-CSF led to elevations of phosphorylation of phosphatidylinositol 3-kinase (PI3K), Akt, and nuclear factor (NF)-kB. Treatment with RES induced downregulation of the phosphorylated levels of PI3K, Akt, and NF-κB in neutrophil-like dHL-60 cells. These results suggest that RES could be applicable to prevent and/or treat inflammatory disorders through blockade of OSM.</description><identifier>ISSN: 1467-3045</identifier><identifier>ISSN: 1467-3037</identifier><identifier>EISSN: 1467-3045</identifier><identifier>DOI: 10.3390/cimb44020037</identifier><identifier>PMID: 35723323</identifier><language>eng</language><publisher>MDPI</publisher><subject>Akt ; neutrophil-like differentiated HL-60 cells ; NF-κB ; oncostatin M ; PI3K ; resveratrol</subject><ispartof>Current issues in molecular biology, 2022-01, Vol.44 (2), p.541-549</ispartof><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c427t-d8a02b49db32dfda760b1ed5326b241d4822489c6e95e977267754bc4dbc3cef3</citedby><cites>FETCH-LOGICAL-c427t-d8a02b49db32dfda760b1ed5326b241d4822489c6e95e977267754bc4dbc3cef3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8928961/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8928961/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids></links><search><creatorcontrib>Han, Na-Ra</creatorcontrib><creatorcontrib>Park, Hi-Joon</creatorcontrib><creatorcontrib>Moon, Phil-Dong</creatorcontrib><title>Resveratrol Downregulates Granulocyte-Macrophage Colony-Stimulating Factor-Induced Oncostatin M Production through Blocking of PI3K/Akt/NF-κB Signal Cascade in Neutrophil-like Differentiated HL-60 Cells</title><title>Current issues in molecular biology</title><description>Oncostatin M (OSM) is essential in a wide range of inflammatory responses, and most OSM is produced by neutrophils in respiratory diseases. While resveratrol (RES) is regarded as an anti-inflammatory agent in a variety of conditions, the mechanism of OSM inhibition by RES in neutrophils remains to be elucidated. In this study, we investigated whether RES could inhibit OSM production in neutrophil-like differentiated (d)HL-60 cells. The effects of RES were measured by means of an enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and Western blotting. Increases in production and mRNA expression of OSM resulted from the addition of granulocyte-macrophage colony-stimulating factor (GM-CSF) in neutrophil-like dHL-60 cells; however, these increases were downregulated by RES treatment. Exposure to GM-CSF led to elevations of phosphorylation of phosphatidylinositol 3-kinase (PI3K), Akt, and nuclear factor (NF)-kB. Treatment with RES induced downregulation of the phosphorylated levels of PI3K, Akt, and NF-κB in neutrophil-like dHL-60 cells. These results suggest that RES could be applicable to prevent and/or treat inflammatory disorders through blockade of OSM.</description><subject>Akt</subject><subject>neutrophil-like differentiated HL-60 cells</subject><subject>NF-κB</subject><subject>oncostatin M</subject><subject>PI3K</subject><subject>resveratrol</subject><issn>1467-3045</issn><issn>1467-3037</issn><issn>1467-3045</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpVkt1u0zAUxyMEYmNwxwP4kgtCHduJkxukraNbRfchBteRP05Sr67d2c5QX22vMIlnIqUT2q58dM7fv_OZZR8L_IXSBk-UWUvGMMGY8lfZYcEqnlPMytfP7IPsXYy3GJe85sXb7ICWnFBK6GH2-APiPQSRgrfo1P92AfrBigQRnQXhBuvVNkF-IVTwm6XoAU299W6b3ySz3gmN69FMqORDPnd6UKDRlVM-pl0IXaDr4EdvMt6htAx-6JfoZISudv98h67n9PvkeJUml7P8z8MJujG9ExZNRVRCAxoRlzCkXW5jc2tWgE5N10EAl8xYpUbni7zCaArWxvfZm07YCB-e3qPs1-zbz-l5vrg6m0-PF7lihKdc1wITyRotKdGdFrzCsgBdUlJJwgrNakJY3agKmhIazknFecmkYloqqqCjR9l8z9Ve3LabYNYibFsvTPvP4UPfipCMstDiQhHApNSVFqxWRQ2sqpgEUeCOSixH1tc9azPINWg19hWEfQF9GXFm2fb-vq0bUjdVMQI-PQGCvxsgpnZtohrHIRz4IbZj9TWnTUPKUfp5Lx13GWOA7n-aAre7W2qf3xL9CzrXwKM</recordid><startdate>20220122</startdate><enddate>20220122</enddate><creator>Han, Na-Ra</creator><creator>Park, Hi-Joon</creator><creator>Moon, Phil-Dong</creator><general>MDPI</general><general>MDPI AG</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20220122</creationdate><title>Resveratrol Downregulates Granulocyte-Macrophage Colony-Stimulating Factor-Induced Oncostatin M Production through Blocking of PI3K/Akt/NF-κB Signal Cascade in Neutrophil-like Differentiated HL-60 Cells</title><author>Han, Na-Ra ; Park, Hi-Joon ; Moon, Phil-Dong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-d8a02b49db32dfda760b1ed5326b241d4822489c6e95e977267754bc4dbc3cef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Akt</topic><topic>neutrophil-like differentiated HL-60 cells</topic><topic>NF-κB</topic><topic>oncostatin M</topic><topic>PI3K</topic><topic>resveratrol</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Han, Na-Ra</creatorcontrib><creatorcontrib>Park, Hi-Joon</creatorcontrib><creatorcontrib>Moon, Phil-Dong</creatorcontrib><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>Current issues in molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Han, Na-Ra</au><au>Park, Hi-Joon</au><au>Moon, Phil-Dong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Resveratrol Downregulates Granulocyte-Macrophage Colony-Stimulating Factor-Induced Oncostatin M Production through Blocking of PI3K/Akt/NF-κB Signal Cascade in Neutrophil-like Differentiated HL-60 Cells</atitle><jtitle>Current issues in molecular biology</jtitle><date>2022-01-22</date><risdate>2022</risdate><volume>44</volume><issue>2</issue><spage>541</spage><epage>549</epage><pages>541-549</pages><issn>1467-3045</issn><issn>1467-3037</issn><eissn>1467-3045</eissn><abstract>Oncostatin M (OSM) is essential in a wide range of inflammatory responses, and most OSM is produced by neutrophils in respiratory diseases. While resveratrol (RES) is regarded as an anti-inflammatory agent in a variety of conditions, the mechanism of OSM inhibition by RES in neutrophils remains to be elucidated. In this study, we investigated whether RES could inhibit OSM production in neutrophil-like differentiated (d)HL-60 cells. The effects of RES were measured by means of an enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and Western blotting. Increases in production and mRNA expression of OSM resulted from the addition of granulocyte-macrophage colony-stimulating factor (GM-CSF) in neutrophil-like dHL-60 cells; however, these increases were downregulated by RES treatment. Exposure to GM-CSF led to elevations of phosphorylation of phosphatidylinositol 3-kinase (PI3K), Akt, and nuclear factor (NF)-kB. Treatment with RES induced downregulation of the phosphorylated levels of PI3K, Akt, and NF-κB in neutrophil-like dHL-60 cells. These results suggest that RES could be applicable to prevent and/or treat inflammatory disorders through blockade of OSM.</abstract><pub>MDPI</pub><pmid>35723323</pmid><doi>10.3390/cimb44020037</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1467-3045 |
ispartof | Current issues in molecular biology, 2022-01, Vol.44 (2), p.541-549 |
issn | 1467-3045 1467-3037 1467-3045 |
language | eng |
recordid | cdi_doaj_primary_oai_doaj_org_article_01c2e025d6da48c18e4664bea10f3b0b |
source | PubMed (Medline) |
subjects | Akt neutrophil-like differentiated HL-60 cells NF-κB oncostatin M PI3K resveratrol |
title | Resveratrol Downregulates Granulocyte-Macrophage Colony-Stimulating Factor-Induced Oncostatin M Production through Blocking of PI3K/Akt/NF-κB Signal Cascade in Neutrophil-like Differentiated HL-60 Cells |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-04T19%3A26%3A14IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_doaj_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Resveratrol%20Downregulates%20Granulocyte-Macrophage%20Colony-Stimulating%20Factor-Induced%20Oncostatin%20M%20Production%20through%20Blocking%20of%20PI3K/Akt/NF-%CE%BAB%20Signal%20Cascade%20in%20Neutrophil-like%20Differentiated%20HL-60%20Cells&rft.jtitle=Current%20issues%20in%20molecular%20biology&rft.au=Han,%20Na-Ra&rft.date=2022-01-22&rft.volume=44&rft.issue=2&rft.spage=541&rft.epage=549&rft.pages=541-549&rft.issn=1467-3045&rft.eissn=1467-3045&rft_id=info:doi/10.3390/cimb44020037&rft_dat=%3Cproquest_doaj_%3E2678739925%3C/proquest_doaj_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c427t-d8a02b49db32dfda760b1ed5326b241d4822489c6e95e977267754bc4dbc3cef3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2678739925&rft_id=info:pmid/35723323&rfr_iscdi=true |