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Histamine H3 Receptor Signaling Regulates the NLRP3 Inflammasome Activation in C2C12 Myocyte During Myogenic Differentiation
NLRP3 inflammasome has been implicated in impaired post-injury muscle healing and in muscle atrophy. Histamine receptors play an important role in inflammation, but the role of histamine H 3 receptor (H 3 R) in myocyte regeneration and in the regulation of NLRP3 inflammasome is not known. We studied...
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Published in: | Frontiers in pharmacology 2021-05, Vol.12, p.599393-599393 |
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description | NLRP3 inflammasome has been implicated in impaired post-injury muscle healing and in muscle atrophy. Histamine receptors play an important role in inflammation, but the role of histamine H
3
receptor (H
3
R) in myocyte regeneration and in the regulation of NLRP3 inflammasome is not known. We studied the effects of H
3
R signaling on C2C12 myocyte viability, apoptosis, and tumor necrosis factor alpha (TNFα)-induced NLRP3 inflammasome activation during striated myogenic differentiation at three time points (days 0, 3, and 6). Expression of
Nlrp3
, interleukin-1β (IL-1β), and myogenesis markers were determined. TNFα reduced overall viability of C2C12 cells, and exposure to TNFα induced apoptosis of cells at D6. Activation of H
3
R had no effect on viability or apoptosis, whereas inhibition of H
3
R increased TNFα-induced apoptosis. Stimulation of C2C12 cells with TNFα increased
Nlrp3
mRNA expression at D3 and D6. Moreover, TNFα reduced the expression of myogenesis markers MyoD1, Myogenin, and Myosin-2 at D3 and D6. H
3
R attenuated TNFα-induced expression of
Nlrp3
and further inhibited the myogenesis marker expression; while H
3
R -blockage enhanced the proinflammatory effects of TNFα and increased the myogenesis marker expression. TNFα-induced secretion of mature IL-1β was dependent on the activation of the NLRP3 inflammasome, as shown by the reduced secretion of mature IL-1β upon treatment of the cells with the small molecule inhibitor of the NLRP3 inflammasome (MCC950). The activation of H
3
R reduced TNFα-induced IL-1β secretion, while the H
3
R blockage had an opposite effect. In conclusion, the modulation of H
3
R activity regulates the effects of TNFα on C2C12 myocyte differentiation and TNFα-induced activation of NLRP3 inflammasome. Thus, H
3
R signaling may represent a novel target for limiting postinjury muscle inflammation and muscle atrophy. |
doi_str_mv | 10.3389/fphar.2021.599393 |
format | article |
fullrecord | <record><control><sourceid>proquest_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_3686a25d095045b28156101e3dbb19d6</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_3686a25d095045b28156101e3dbb19d6</doaj_id><sourcerecordid>2542363467</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3573-6f82bc1f8e4c71daafc6332779ddb38d0e680cf1c6275d9c921034a7241de6023</originalsourceid><addsrcrecordid>eNpVkk1v3CAQhq2qVROl-QG9cexlt8DY2FwqRZu2u9L2Q2l7RhgGL5FttoAjrdQfH-9uFDVzmWF4eWDEWxTvGV0CNPKj2-90XHLK2bKSEiS8Ki6ZELCQDeOv_6sviuuU7ukcMOtE-ba4gJJBVVf0svi39inrwY9I1kDu0OA-h0h--W7UvR-7udVNvc6YSN4h-b69-wlkM7peD4NOYUByY7J_0NmHkfiRrPiKcfLtEMwhI7md4pExLzscvSG33jmMOGZ_OvCueON0n_D6KV8Vf758_r1aL7Y_vm5WN9uFmV8JC-Ea3hrmGixNzazWzggAXtfS2hYaS1E01DhmBK8rK43kjEKpa14yi4JyuCo2Z64N-l7tox90PKigvTo1QuyUjtmbHhWIRmheWSorWlYtb1glGGUItm2ZtGJmfTqz9lM7oDXzMFH3L6Avd0a_U114UM38VbSuZ8CHJ0AMfydMWQ0-Gex7PWKYkuJVyUFAKY5SdpaaGFKK6J6vYVQdTaBOJlBHE6izCeARqdqkgQ</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2542363467</pqid></control><display><type>article</type><title>Histamine H3 Receptor Signaling Regulates the NLRP3 Inflammasome Activation in C2C12 Myocyte During Myogenic Differentiation</title><source>PubMed Central</source><creator>Chen, Yan ; Ma, Yuan ; Feng, Jin Jin ; Wang, Yi He ; Li, Tian Fang ; Nurmi, Katariina ; Eklund, Kari K. ; Wen, Jian Guo</creator><creatorcontrib>Chen, Yan ; Ma, Yuan ; Feng, Jin Jin ; Wang, Yi He ; Li, Tian Fang ; Nurmi, Katariina ; Eklund, Kari K. ; Wen, Jian Guo</creatorcontrib><description>NLRP3 inflammasome has been implicated in impaired post-injury muscle healing and in muscle atrophy. Histamine receptors play an important role in inflammation, but the role of histamine H
3
receptor (H
3
R) in myocyte regeneration and in the regulation of NLRP3 inflammasome is not known. We studied the effects of H
3
R signaling on C2C12 myocyte viability, apoptosis, and tumor necrosis factor alpha (TNFα)-induced NLRP3 inflammasome activation during striated myogenic differentiation at three time points (days 0, 3, and 6). Expression of
Nlrp3
, interleukin-1β (IL-1β), and myogenesis markers were determined. TNFα reduced overall viability of C2C12 cells, and exposure to TNFα induced apoptosis of cells at D6. Activation of H
3
R had no effect on viability or apoptosis, whereas inhibition of H
3
R increased TNFα-induced apoptosis. Stimulation of C2C12 cells with TNFα increased
Nlrp3
mRNA expression at D3 and D6. Moreover, TNFα reduced the expression of myogenesis markers MyoD1, Myogenin, and Myosin-2 at D3 and D6. H
3
R attenuated TNFα-induced expression of
Nlrp3
and further inhibited the myogenesis marker expression; while H
3
R -blockage enhanced the proinflammatory effects of TNFα and increased the myogenesis marker expression. TNFα-induced secretion of mature IL-1β was dependent on the activation of the NLRP3 inflammasome, as shown by the reduced secretion of mature IL-1β upon treatment of the cells with the small molecule inhibitor of the NLRP3 inflammasome (MCC950). The activation of H
3
R reduced TNFα-induced IL-1β secretion, while the H
3
R blockage had an opposite effect. In conclusion, the modulation of H
3
R activity regulates the effects of TNFα on C2C12 myocyte differentiation and TNFα-induced activation of NLRP3 inflammasome. Thus, H
3
R signaling may represent a novel target for limiting postinjury muscle inflammation and muscle atrophy.</description><identifier>ISSN: 1663-9812</identifier><identifier>EISSN: 1663-9812</identifier><identifier>DOI: 10.3389/fphar.2021.599393</identifier><identifier>PMID: 34135750</identifier><language>eng</language><publisher>Frontiers Media S.A</publisher><subject>histamine H3 receptor ; IL-1β ; inflammation ; myogenesis ; NLRP3 inflammasome ; Pharmacology ; TNFα</subject><ispartof>Frontiers in pharmacology, 2021-05, Vol.12, p.599393-599393</ispartof><rights>Copyright © 2021 Chen, Ma, Feng, Wang, Li, Nurmi, Eklund and Wen. 2021 Chen, Ma, Feng, Wang, Li, Nurmi, Eklund and Wen</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3573-6f82bc1f8e4c71daafc6332779ddb38d0e680cf1c6275d9c921034a7241de6023</citedby><cites>FETCH-LOGICAL-c3573-6f82bc1f8e4c71daafc6332779ddb38d0e680cf1c6275d9c921034a7241de6023</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/PMC8202077/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8202077/$$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>Chen, Yan</creatorcontrib><creatorcontrib>Ma, Yuan</creatorcontrib><creatorcontrib>Feng, Jin Jin</creatorcontrib><creatorcontrib>Wang, Yi He</creatorcontrib><creatorcontrib>Li, Tian Fang</creatorcontrib><creatorcontrib>Nurmi, Katariina</creatorcontrib><creatorcontrib>Eklund, Kari K.</creatorcontrib><creatorcontrib>Wen, Jian Guo</creatorcontrib><title>Histamine H3 Receptor Signaling Regulates the NLRP3 Inflammasome Activation in C2C12 Myocyte During Myogenic Differentiation</title><title>Frontiers in pharmacology</title><description>NLRP3 inflammasome has been implicated in impaired post-injury muscle healing and in muscle atrophy. Histamine receptors play an important role in inflammation, but the role of histamine H
3
receptor (H
3
R) in myocyte regeneration and in the regulation of NLRP3 inflammasome is not known. We studied the effects of H
3
R signaling on C2C12 myocyte viability, apoptosis, and tumor necrosis factor alpha (TNFα)-induced NLRP3 inflammasome activation during striated myogenic differentiation at three time points (days 0, 3, and 6). Expression of
Nlrp3
, interleukin-1β (IL-1β), and myogenesis markers were determined. TNFα reduced overall viability of C2C12 cells, and exposure to TNFα induced apoptosis of cells at D6. Activation of H
3
R had no effect on viability or apoptosis, whereas inhibition of H
3
R increased TNFα-induced apoptosis. Stimulation of C2C12 cells with TNFα increased
Nlrp3
mRNA expression at D3 and D6. Moreover, TNFα reduced the expression of myogenesis markers MyoD1, Myogenin, and Myosin-2 at D3 and D6. H
3
R attenuated TNFα-induced expression of
Nlrp3
and further inhibited the myogenesis marker expression; while H
3
R -blockage enhanced the proinflammatory effects of TNFα and increased the myogenesis marker expression. TNFα-induced secretion of mature IL-1β was dependent on the activation of the NLRP3 inflammasome, as shown by the reduced secretion of mature IL-1β upon treatment of the cells with the small molecule inhibitor of the NLRP3 inflammasome (MCC950). The activation of H
3
R reduced TNFα-induced IL-1β secretion, while the H
3
R blockage had an opposite effect. In conclusion, the modulation of H
3
R activity regulates the effects of TNFα on C2C12 myocyte differentiation and TNFα-induced activation of NLRP3 inflammasome. Thus, H
3
R signaling may represent a novel target for limiting postinjury muscle inflammation and muscle atrophy.</description><subject>histamine H3 receptor</subject><subject>IL-1β</subject><subject>inflammation</subject><subject>myogenesis</subject><subject>NLRP3 inflammasome</subject><subject>Pharmacology</subject><subject>TNFα</subject><issn>1663-9812</issn><issn>1663-9812</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpVkk1v3CAQhq2qVROl-QG9cexlt8DY2FwqRZu2u9L2Q2l7RhgGL5FttoAjrdQfH-9uFDVzmWF4eWDEWxTvGV0CNPKj2-90XHLK2bKSEiS8Ki6ZELCQDeOv_6sviuuU7ukcMOtE-ba4gJJBVVf0svi39inrwY9I1kDu0OA-h0h--W7UvR-7udVNvc6YSN4h-b69-wlkM7peD4NOYUByY7J_0NmHkfiRrPiKcfLtEMwhI7md4pExLzscvSG33jmMOGZ_OvCueON0n_D6KV8Vf758_r1aL7Y_vm5WN9uFmV8JC-Ea3hrmGixNzazWzggAXtfS2hYaS1E01DhmBK8rK43kjEKpa14yi4JyuCo2Z64N-l7tox90PKigvTo1QuyUjtmbHhWIRmheWSorWlYtb1glGGUItm2ZtGJmfTqz9lM7oDXzMFH3L6Avd0a_U114UM38VbSuZ8CHJ0AMfydMWQ0-Gex7PWKYkuJVyUFAKY5SdpaaGFKK6J6vYVQdTaBOJlBHE6izCeARqdqkgQ</recordid><startdate>20210531</startdate><enddate>20210531</enddate><creator>Chen, Yan</creator><creator>Ma, Yuan</creator><creator>Feng, Jin Jin</creator><creator>Wang, Yi He</creator><creator>Li, Tian Fang</creator><creator>Nurmi, Katariina</creator><creator>Eklund, Kari K.</creator><creator>Wen, Jian Guo</creator><general>Frontiers Media S.A</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20210531</creationdate><title>Histamine H3 Receptor Signaling Regulates the NLRP3 Inflammasome Activation in C2C12 Myocyte During Myogenic Differentiation</title><author>Chen, Yan ; Ma, Yuan ; Feng, Jin Jin ; Wang, Yi He ; Li, Tian Fang ; Nurmi, Katariina ; Eklund, Kari K. ; Wen, Jian Guo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3573-6f82bc1f8e4c71daafc6332779ddb38d0e680cf1c6275d9c921034a7241de6023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>histamine H3 receptor</topic><topic>IL-1β</topic><topic>inflammation</topic><topic>myogenesis</topic><topic>NLRP3 inflammasome</topic><topic>Pharmacology</topic><topic>TNFα</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Yan</creatorcontrib><creatorcontrib>Ma, Yuan</creatorcontrib><creatorcontrib>Feng, Jin Jin</creatorcontrib><creatorcontrib>Wang, Yi He</creatorcontrib><creatorcontrib>Li, Tian Fang</creatorcontrib><creatorcontrib>Nurmi, Katariina</creatorcontrib><creatorcontrib>Eklund, Kari K.</creatorcontrib><creatorcontrib>Wen, Jian Guo</creatorcontrib><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Frontiers in pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Yan</au><au>Ma, Yuan</au><au>Feng, Jin Jin</au><au>Wang, Yi He</au><au>Li, Tian Fang</au><au>Nurmi, Katariina</au><au>Eklund, Kari K.</au><au>Wen, Jian Guo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Histamine H3 Receptor Signaling Regulates the NLRP3 Inflammasome Activation in C2C12 Myocyte During Myogenic Differentiation</atitle><jtitle>Frontiers in pharmacology</jtitle><date>2021-05-31</date><risdate>2021</risdate><volume>12</volume><spage>599393</spage><epage>599393</epage><pages>599393-599393</pages><issn>1663-9812</issn><eissn>1663-9812</eissn><abstract>NLRP3 inflammasome has been implicated in impaired post-injury muscle healing and in muscle atrophy. Histamine receptors play an important role in inflammation, but the role of histamine H
3
receptor (H
3
R) in myocyte regeneration and in the regulation of NLRP3 inflammasome is not known. We studied the effects of H
3
R signaling on C2C12 myocyte viability, apoptosis, and tumor necrosis factor alpha (TNFα)-induced NLRP3 inflammasome activation during striated myogenic differentiation at three time points (days 0, 3, and 6). Expression of
Nlrp3
, interleukin-1β (IL-1β), and myogenesis markers were determined. TNFα reduced overall viability of C2C12 cells, and exposure to TNFα induced apoptosis of cells at D6. Activation of H
3
R had no effect on viability or apoptosis, whereas inhibition of H
3
R increased TNFα-induced apoptosis. Stimulation of C2C12 cells with TNFα increased
Nlrp3
mRNA expression at D3 and D6. Moreover, TNFα reduced the expression of myogenesis markers MyoD1, Myogenin, and Myosin-2 at D3 and D6. H
3
R attenuated TNFα-induced expression of
Nlrp3
and further inhibited the myogenesis marker expression; while H
3
R -blockage enhanced the proinflammatory effects of TNFα and increased the myogenesis marker expression. TNFα-induced secretion of mature IL-1β was dependent on the activation of the NLRP3 inflammasome, as shown by the reduced secretion of mature IL-1β upon treatment of the cells with the small molecule inhibitor of the NLRP3 inflammasome (MCC950). The activation of H
3
R reduced TNFα-induced IL-1β secretion, while the H
3
R blockage had an opposite effect. In conclusion, the modulation of H
3
R activity regulates the effects of TNFα on C2C12 myocyte differentiation and TNFα-induced activation of NLRP3 inflammasome. Thus, H
3
R signaling may represent a novel target for limiting postinjury muscle inflammation and muscle atrophy.</abstract><pub>Frontiers Media S.A</pub><pmid>34135750</pmid><doi>10.3389/fphar.2021.599393</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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source | PubMed Central |
subjects | histamine H3 receptor IL-1β inflammation myogenesis NLRP3 inflammasome Pharmacology TNFα |
title | Histamine H3 Receptor Signaling Regulates the NLRP3 Inflammasome Activation in C2C12 Myocyte During Myogenic Differentiation |
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