Changes in the expression of the Toll-like receptor system in the aging rat kidneys
The mechanisms of kidney aging are not yet clear. Studies have shown that immunological inflammation is related to kidney aging. Toll-like receptors (TLRs) are one of the receptor types of the body's innate immune system. The function of the TLR system and the mechanisms by which it functions i...
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| description | The mechanisms of kidney aging are not yet clear. Studies have shown that immunological inflammation is related to kidney aging. Toll-like receptors (TLRs) are one of the receptor types of the body's innate immune system. The function of the TLR system and the mechanisms by which it functions in renal aging remain unclear. In the present study, we, for the first time, systematically investigated the role of the TLR system and the inflammation responses activated by TLRs during kidney aging.
We used western blot and immunohistochemistry to systematically analyze the changes in the expression and activation of the endogenous TLR ligands HSP70 and HMGB1, the TLRs (TLR1-TLR11), their downstream signaling pathway molecules MyD88 and Phospho-IRF-3, and the NF-κB signaling pathway molecules Phospho-IKKβ, Phospho-IκBα (NF-κB inhibition factor α), NF-κBp65, and Phospho-NF-κBp65 (activated NF-κB p65) in the kidneys of 3 months old (youth group), 12 months old (middle age group), and 24 months old (elderly group) rats. We used RT-qPCR to detect the mRNA expression changes of the proinflammatory cytokines CCL3, CCL4, CCL5, CD80, TNF-α, and IL-12b in the rat renal tissues of the various age groups.
We found that during kidney aging, the HSP70 and HMGB1 expression levels were significantly increased, and the expression levels of TLR1, 2, 3, 4, 5, and 11 and their downstream signaling pathway molecules MyD88 and Phospho-IRF-3 were markedly elevated. Further studies have shown that in the aging kidneys, the expression levels of the NF-κB signaling pathway molecules Phospho-IKKβ, Phospho-IκBα, NF-κBp65, and Phospho-NF-κBp65 were obviously increased, and those of the proinflammatory cytokines CCL3, CCL4, CCL5, CD80, TNF-α, and IL-12b were significantly upregulated.
These results showed that the TLR system might play an important role during the kidney aging process maybe by activating the NF-κB signaling pathway and promoting the high expression of inflammation factors. |
| doi_str_mv | 10.1371/journal.pone.0096351 |
| format | Article |
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We used western blot and immunohistochemistry to systematically analyze the changes in the expression and activation of the endogenous TLR ligands HSP70 and HMGB1, the TLRs (TLR1-TLR11), their downstream signaling pathway molecules MyD88 and Phospho-IRF-3, and the NF-κB signaling pathway molecules Phospho-IKKβ, Phospho-IκBα (NF-κB inhibition factor α), NF-κBp65, and Phospho-NF-κBp65 (activated NF-κB p65) in the kidneys of 3 months old (youth group), 12 months old (middle age group), and 24 months old (elderly group) rats. We used RT-qPCR to detect the mRNA expression changes of the proinflammatory cytokines CCL3, CCL4, CCL5, CD80, TNF-α, and IL-12b in the rat renal tissues of the various age groups.
We found that during kidney aging, the HSP70 and HMGB1 expression levels were significantly increased, and the expression levels of TLR1, 2, 3, 4, 5, and 11 and their downstream signaling pathway molecules MyD88 and Phospho-IRF-3 were markedly elevated. Further studies have shown that in the aging kidneys, the expression levels of the NF-κB signaling pathway molecules Phospho-IKKβ, Phospho-IκBα, NF-κBp65, and Phospho-NF-κBp65 were obviously increased, and those of the proinflammatory cytokines CCL3, CCL4, CCL5, CD80, TNF-α, and IL-12b were significantly upregulated.
These results showed that the TLR system might play an important role during the kidney aging process maybe by activating the NF-κB signaling pathway and promoting the high expression of inflammation factors.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0096351</identifier><identifier>PMID: 24810370</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Age ; Aging ; Aging - metabolism ; Animal tissues ; Animals ; Carbon tetrachloride ; CCL3 protein ; CCL4 protein ; CD80 antigen ; Change detection ; Cytokines ; Diabetes ; Gene expression ; Geriatrics ; Heat shock proteins ; HMGB1 protein ; Hsp70 protein ; Immune system ; Immunohistochemistry ; Immunology ; Inflammation ; Innate immunity ; Interferon regulatory factor 3 ; Kidney - growth & development ; Kidney - metabolism ; Kidney diseases ; Kidneys ; Laboratory animals ; Ligands ; Male ; Medicine and Health Sciences ; Methods ; MyD88 protein ; Nephrology ; NF-kappa B - metabolism ; NF-κB protein ; Older people ; Oxidative stress ; Pattern recognition ; Phosphorylation ; Proteins ; Rats ; Rats, Inbred F344 ; Receptors ; RNA ; Rodents ; Senescence ; Signal transduction ; Signal Transduction - physiology ; Signaling ; TLR1 protein ; Toll-like receptors ; Toll-Like Receptors - metabolism ; Tumor necrosis factor-α ; Urine ; Youth</subject><ispartof>PloS one, 2014-05, Vol.9 (5), p.e96351-e96351</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Xi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Xi et al 2014 Xi et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-12ec30ff7bf04fba9416ef4ce611692c6c54e8ccfdcefdbd7cfce389020da48f3</citedby><cites>FETCH-LOGICAL-c692t-12ec30ff7bf04fba9416ef4ce611692c6c54e8ccfdcefdbd7cfce389020da48f3</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/PMC4014502/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4014502/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23871,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24810370$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Ma, Daqing</contributor><creatorcontrib>Xi, Yue</creatorcontrib><creatorcontrib>Shao, Feng</creatorcontrib><creatorcontrib>Bai, Xue-Yuan</creatorcontrib><creatorcontrib>Cai, Guangyan</creatorcontrib><creatorcontrib>Lv, Yang</creatorcontrib><creatorcontrib>Chen, Xiangmei</creatorcontrib><title>Changes in the expression of the Toll-like receptor system in the aging rat kidneys</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The mechanisms of kidney aging are not yet clear. Studies have shown that immunological inflammation is related to kidney aging. Toll-like receptors (TLRs) are one of the receptor types of the body's innate immune system. The function of the TLR system and the mechanisms by which it functions in renal aging remain unclear. In the present study, we, for the first time, systematically investigated the role of the TLR system and the inflammation responses activated by TLRs during kidney aging.
We used western blot and immunohistochemistry to systematically analyze the changes in the expression and activation of the endogenous TLR ligands HSP70 and HMGB1, the TLRs (TLR1-TLR11), their downstream signaling pathway molecules MyD88 and Phospho-IRF-3, and the NF-κB signaling pathway molecules Phospho-IKKβ, Phospho-IκBα (NF-κB inhibition factor α), NF-κBp65, and Phospho-NF-κBp65 (activated NF-κB p65) in the kidneys of 3 months old (youth group), 12 months old (middle age group), and 24 months old (elderly group) rats. We used RT-qPCR to detect the mRNA expression changes of the proinflammatory cytokines CCL3, CCL4, CCL5, CD80, TNF-α, and IL-12b in the rat renal tissues of the various age groups.
We found that during kidney aging, the HSP70 and HMGB1 expression levels were significantly increased, and the expression levels of TLR1, 2, 3, 4, 5, and 11 and their downstream signaling pathway molecules MyD88 and Phospho-IRF-3 were markedly elevated. Further studies have shown that in the aging kidneys, the expression levels of the NF-κB signaling pathway molecules Phospho-IKKβ, Phospho-IκBα, NF-κBp65, and Phospho-NF-κBp65 were obviously increased, and those of the proinflammatory cytokines CCL3, CCL4, CCL5, CD80, TNF-α, and IL-12b were significantly upregulated.
These results showed that the TLR system might play an important role during the kidney aging process maybe by activating the NF-κB signaling pathway and promoting the high expression of inflammation factors.</description><subject>Age</subject><subject>Aging</subject><subject>Aging - metabolism</subject><subject>Animal tissues</subject><subject>Animals</subject><subject>Carbon tetrachloride</subject><subject>CCL3 protein</subject><subject>CCL4 protein</subject><subject>CD80 antigen</subject><subject>Change detection</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Gene expression</subject><subject>Geriatrics</subject><subject>Heat shock proteins</subject><subject>HMGB1 protein</subject><subject>Hsp70 protein</subject><subject>Immune system</subject><subject>Immunohistochemistry</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Innate immunity</subject><subject>Interferon regulatory factor 3</subject><subject>Kidney - growth & development</subject><subject>Kidney - metabolism</subject><subject>Kidney diseases</subject><subject>Kidneys</subject><subject>Laboratory animals</subject><subject>Ligands</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Methods</subject><subject>MyD88 protein</subject><subject>Nephrology</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Older people</subject><subject>Oxidative stress</subject><subject>Pattern recognition</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Inbred F344</subject><subject>Receptors</subject><subject>RNA</subject><subject>Rodents</subject><subject>Senescence</subject><subject>Signal transduction</subject><subject>Signal Transduction - physiology</subject><subject>Signaling</subject><subject>TLR1 protein</subject><subject>Toll-like receptors</subject><subject>Toll-Like Receptors - metabolism</subject><subject>Tumor necrosis factor-α</subject><subject>Urine</subject><subject>Youth</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAUhoso7rr6D0QLgujFjPlq2t4Iy-DHwMKCu3ob0vSkk9lMMyap7Px7M1_LVPZCepFy8rxvTk7eLHuN0RTTEn9ausH30k7XrocpQjWnBX6SneOakgkniD49-T_LXoSwRKigFefPszPCKoxoic6zm9lC9h2E3PR5XEAO92sPIRjX507vKrfO2ok1d5B7ULCOzudhEyKsjhLZmb7LvYz5nWl72ISX2TMtbYBXh_Ui-_n1y-3s--Tq-tt8dnk1UbwmcYIJKIq0LhuNmG5kzTAHzRRwjBOguCoYVErpVoFum7ZUWgGtakRQK1ml6UX2du-7ti6IwzyCwAUhJeEFJomY74nWyaVYe7OSfiOcNGJXcL4T0kejLAjOCEGlVrVijKm6rRjX0DR1KSVHuMbJ6_PhtKFZQeqpj17akel4pzcL0bk_giHMCrRt5sPBwLvfA4QoViYosFb24IZd35ShinCU0Hf_oI_f7kB1Ml3A9Nqlc9XWVFwyXHHKOKoTNX2ESl8LK6NSeLRJ9ZHg40iQmAj3sZNDCGJ-8-P_2etfY_b9CbsAaeMiODvEFLYwBtkeVN6F4EE_DBkjsc3-cRpim31xyH6SvTl9oAfRMez0L-Ww_vM</recordid><startdate>20140508</startdate><enddate>20140508</enddate><creator>Xi, Yue</creator><creator>Shao, Feng</creator><creator>Bai, Xue-Yuan</creator><creator>Cai, Guangyan</creator><creator>Lv, Yang</creator><creator>Chen, Xiangmei</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140508</creationdate><title>Changes in the expression of the Toll-like receptor system in the aging rat kidneys</title><author>Xi, Yue ; Shao, Feng ; Bai, Xue-Yuan ; Cai, Guangyan ; Lv, Yang ; Chen, Xiangmei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-12ec30ff7bf04fba9416ef4ce611692c6c54e8ccfdcefdbd7cfce389020da48f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Age</topic><topic>Aging</topic><topic>Aging - metabolism</topic><topic>Animal tissues</topic><topic>Animals</topic><topic>Carbon tetrachloride</topic><topic>CCL3 protein</topic><topic>CCL4 protein</topic><topic>CD80 antigen</topic><topic>Change detection</topic><topic>Cytokines</topic><topic>Diabetes</topic><topic>Gene expression</topic><topic>Geriatrics</topic><topic>Heat shock proteins</topic><topic>HMGB1 protein</topic><topic>Hsp70 protein</topic><topic>Immune system</topic><topic>Immunohistochemistry</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Innate immunity</topic><topic>Interferon regulatory factor 3</topic><topic>Kidney - growth & development</topic><topic>Kidney - metabolism</topic><topic>Kidney diseases</topic><topic>Kidneys</topic><topic>Laboratory animals</topic><topic>Ligands</topic><topic>Male</topic><topic>Medicine and Health Sciences</topic><topic>Methods</topic><topic>MyD88 protein</topic><topic>Nephrology</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Older people</topic><topic>Oxidative stress</topic><topic>Pattern recognition</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Inbred F344</topic><topic>Receptors</topic><topic>RNA</topic><topic>Rodents</topic><topic>Senescence</topic><topic>Signal transduction</topic><topic>Signal Transduction - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xi, Yue</au><au>Shao, Feng</au><au>Bai, Xue-Yuan</au><au>Cai, Guangyan</au><au>Lv, Yang</au><au>Chen, Xiangmei</au><au>Ma, Daqing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Changes in the expression of the Toll-like receptor system in the aging rat kidneys</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-05-08</date><risdate>2014</risdate><volume>9</volume><issue>5</issue><spage>e96351</spage><epage>e96351</epage><pages>e96351-e96351</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The mechanisms of kidney aging are not yet clear. Studies have shown that immunological inflammation is related to kidney aging. Toll-like receptors (TLRs) are one of the receptor types of the body's innate immune system. The function of the TLR system and the mechanisms by which it functions in renal aging remain unclear. In the present study, we, for the first time, systematically investigated the role of the TLR system and the inflammation responses activated by TLRs during kidney aging.
We used western blot and immunohistochemistry to systematically analyze the changes in the expression and activation of the endogenous TLR ligands HSP70 and HMGB1, the TLRs (TLR1-TLR11), their downstream signaling pathway molecules MyD88 and Phospho-IRF-3, and the NF-κB signaling pathway molecules Phospho-IKKβ, Phospho-IκBα (NF-κB inhibition factor α), NF-κBp65, and Phospho-NF-κBp65 (activated NF-κB p65) in the kidneys of 3 months old (youth group), 12 months old (middle age group), and 24 months old (elderly group) rats. We used RT-qPCR to detect the mRNA expression changes of the proinflammatory cytokines CCL3, CCL4, CCL5, CD80, TNF-α, and IL-12b in the rat renal tissues of the various age groups.
We found that during kidney aging, the HSP70 and HMGB1 expression levels were significantly increased, and the expression levels of TLR1, 2, 3, 4, 5, and 11 and their downstream signaling pathway molecules MyD88 and Phospho-IRF-3 were markedly elevated. Further studies have shown that in the aging kidneys, the expression levels of the NF-κB signaling pathway molecules Phospho-IKKβ, Phospho-IκBα, NF-κBp65, and Phospho-NF-κBp65 were obviously increased, and those of the proinflammatory cytokines CCL3, CCL4, CCL5, CD80, TNF-α, and IL-12b were significantly upregulated.
These results showed that the TLR system might play an important role during the kidney aging process maybe by activating the NF-κB signaling pathway and promoting the high expression of inflammation factors.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24810370</pmid><doi>10.1371/journal.pone.0096351</doi><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1522726512 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Age Aging Aging - metabolism Animal tissues Animals Carbon tetrachloride CCL3 protein CCL4 protein CD80 antigen Change detection Cytokines Diabetes Gene expression Geriatrics Heat shock proteins HMGB1 protein Hsp70 protein Immune system Immunohistochemistry Immunology Inflammation Innate immunity Interferon regulatory factor 3 Kidney - growth & development Kidney - metabolism Kidney diseases Kidneys Laboratory animals Ligands Male Medicine and Health Sciences Methods MyD88 protein Nephrology NF-kappa B - metabolism NF-κB protein Older people Oxidative stress Pattern recognition Phosphorylation Proteins Rats Rats, Inbred F344 Receptors RNA Rodents Senescence Signal transduction Signal Transduction - physiology Signaling TLR1 protein Toll-like receptors Toll-Like Receptors - metabolism Tumor necrosis factor-α Urine Youth |
| title | Changes in the expression of the Toll-like receptor system in the aging rat kidneys |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-16T10%3A40%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Changes%20in%20the%20expression%20of%20the%20Toll-like%20receptor%20system%20in%20the%20aging%20rat%20kidneys&rft.jtitle=PloS%20one&rft.au=Xi,%20Yue&rft.date=2014-05-08&rft.volume=9&rft.issue=5&rft.spage=e96351&rft.epage=e96351&rft.pages=e96351-e96351&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0096351&rft_dat=%3Cgale_plos_%3EA418634609%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1522726512&rft_id=info:pmid/24810370&rft_galeid=A418634609&rft_doaj_id=oai_doaj_org_article_642207fc9c444c9d846febb97aa60191&rfr_iscdi=true |