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Ghrelin mediated cardioprotection using in vitro models of oxidative stress
Ghrelin is commonly known as the ‘hunger hormone’ due to its role in stimulating food intake in humans. However, the roles of ghrelin extend beyond regulating hunger. Our aim was to investigate the ability of ghrelin to protect against hydrogen peroxide (H 2 O 2 ), a reactive oxygen species commonly...
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| Published in: | Gene therapy 2024-03, Vol.31 (3-4), p.165-174 |
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| Main Authors: | , , , , , , , |
| Format: | Article |
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| cites | cdi_FETCH-LOGICAL-c419t-f71f89195b29a74a9ba65b09952716a435ea6bcfab3c19e84dd3950c8d82360a3 |
| container_end_page | 174 |
| container_issue | 3-4 |
| container_start_page | 165 |
| container_title | Gene therapy |
| container_volume | 31 |
| creator | Kok, Cindy Y. Ghossein, George Igoor, Sindhu Rao, Renuka Titus, Tracy Tsurusaki, Shinya Chong, James JH Kizana, Eddy |
| description | Ghrelin is commonly known as the ‘hunger hormone’ due to its role in stimulating food intake in humans. However, the roles of ghrelin extend beyond regulating hunger. Our aim was to investigate the ability of ghrelin to protect against hydrogen peroxide (H
2
O
2
), a reactive oxygen species commonly associated with cardiac injury. An in vitro model of oxidative stress was developed using H
2
O
2
injured H9c2 cells. Despite lentiviral ghrelin overexpression, H9c2 cell viability and mitochondrial function were not protected following H
2
O
2
injury. We found that H9c2 cells lack expression of the preproghrelin cleavage enzyme prohormone convertase 1 (encoded by
PCSK1
), required to convert ghrelin to its active form. In contrast, we found that primary rat cardiomyocytes do express
PCSK1
and were protected from H
2
O
2
injury by lentiviral ghrelin overexpression. In conclusion, we have shown that ghrelin expression can protect primary rat cardiomyocytes against H
2
O
2
, though this effect was not observed in other cell types tested. |
| doi_str_mv | 10.1038/s41434-023-00435-9 |
| format | article |
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2
O
2
), a reactive oxygen species commonly associated with cardiac injury. An in vitro model of oxidative stress was developed using H
2
O
2
injured H9c2 cells. Despite lentiviral ghrelin overexpression, H9c2 cell viability and mitochondrial function were not protected following H
2
O
2
injury. We found that H9c2 cells lack expression of the preproghrelin cleavage enzyme prohormone convertase 1 (encoded by
PCSK1
), required to convert ghrelin to its active form. In contrast, we found that primary rat cardiomyocytes do express
PCSK1
and were protected from H
2
O
2
injury by lentiviral ghrelin overexpression. In conclusion, we have shown that ghrelin expression can protect primary rat cardiomyocytes against H
2
O
2
, though this effect was not observed in other cell types tested.</description><identifier>ISSN: 0969-7128</identifier><identifier>EISSN: 1476-5462</identifier><identifier>DOI: 10.1038/s41434-023-00435-9</identifier><identifier>PMID: 38177343</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/100 ; 13/106 ; 13/2 ; 13/44 ; 14/34 ; 38/35 ; 631/61/201 ; 692/699/75 ; Animal models ; Animals ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Cardiomyocytes ; Cell Biology ; Cell viability ; Food intake ; Gene Expression ; Gene Therapy ; Ghrelin ; Ghrelin - genetics ; Ghrelin - metabolism ; Ghrelin - pharmacology ; Hormones ; Human Genetics ; Humans ; Hunger ; Hydrogen peroxide ; Hydrogen Peroxide - pharmacology ; In vitro ; Myocytes, Cardiac - metabolism ; Nanotechnology ; Oxidative Stress ; Proprotein convertases ; Rats ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Reactive Oxygen Species - pharmacology ; Signal Transduction</subject><ispartof>Gene therapy, 2024-03, Vol.31 (3-4), p.165-174</ispartof><rights>Crown 2024</rights><rights>2024. Crown.</rights><rights>Crown 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-f71f89195b29a74a9ba65b09952716a435ea6bcfab3c19e84dd3950c8d82360a3</citedby><cites>FETCH-LOGICAL-c419t-f71f89195b29a74a9ba65b09952716a435ea6bcfab3c19e84dd3950c8d82360a3</cites><orcidid>0000-0002-7266-6720 ; 0000-0002-2592-4555 ; 0000-0002-4161-0820 ; 0000-0002-9536-1989 ; 0000-0002-5201-4856 ; 0000-0003-3086-7097</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38177343$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kok, Cindy Y.</creatorcontrib><creatorcontrib>Ghossein, George</creatorcontrib><creatorcontrib>Igoor, Sindhu</creatorcontrib><creatorcontrib>Rao, Renuka</creatorcontrib><creatorcontrib>Titus, Tracy</creatorcontrib><creatorcontrib>Tsurusaki, Shinya</creatorcontrib><creatorcontrib>Chong, James JH</creatorcontrib><creatorcontrib>Kizana, Eddy</creatorcontrib><title>Ghrelin mediated cardioprotection using in vitro models of oxidative stress</title><title>Gene therapy</title><addtitle>Gene Ther</addtitle><addtitle>Gene Ther</addtitle><description>Ghrelin is commonly known as the ‘hunger hormone’ due to its role in stimulating food intake in humans. However, the roles of ghrelin extend beyond regulating hunger. Our aim was to investigate the ability of ghrelin to protect against hydrogen peroxide (H
2
O
2
), a reactive oxygen species commonly associated with cardiac injury. An in vitro model of oxidative stress was developed using H
2
O
2
injured H9c2 cells. Despite lentiviral ghrelin overexpression, H9c2 cell viability and mitochondrial function were not protected following H
2
O
2
injury. We found that H9c2 cells lack expression of the preproghrelin cleavage enzyme prohormone convertase 1 (encoded by
PCSK1
), required to convert ghrelin to its active form. In contrast, we found that primary rat cardiomyocytes do express
PCSK1
and were protected from H
2
O
2
injury by lentiviral ghrelin overexpression. In conclusion, we have shown that ghrelin expression can protect primary rat cardiomyocytes against H
2
O
2
, though this effect was not observed in other cell types tested.</description><subject>13/100</subject><subject>13/106</subject><subject>13/2</subject><subject>13/44</subject><subject>14/34</subject><subject>38/35</subject><subject>631/61/201</subject><subject>692/699/75</subject><subject>Animal models</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cardiomyocytes</subject><subject>Cell Biology</subject><subject>Cell viability</subject><subject>Food intake</subject><subject>Gene Expression</subject><subject>Gene Therapy</subject><subject>Ghrelin</subject><subject>Ghrelin - genetics</subject><subject>Ghrelin - metabolism</subject><subject>Ghrelin - pharmacology</subject><subject>Hormones</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Hunger</subject><subject>Hydrogen peroxide</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>In vitro</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Nanotechnology</subject><subject>Oxidative Stress</subject><subject>Proprotein convertases</subject><subject>Rats</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Reactive Oxygen Species - pharmacology</subject><subject>Signal Transduction</subject><issn>0969-7128</issn><issn>1476-5462</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kD1PwzAQhi0EoqXwBxhQJBaWgL9i-0ZUQUFUYoHZchKnuErjYicV_HsMLSAxMN1wz7139yB0SvAlwUxdRU444zmmLMeYsyKHPTQmXIq84ILuozEGAbkkVI3QUYxLnCip6CEaMUWkZJyN0cPsJdjWddnK1s70ts4qE2rn18H3tuqd77Ihum6RJWTj-uCzla9tGzPfZP7N1aZ3G5vFPtgYj9FBY9poT3Z1gp5vb56md_n8cXY_vZ7nFSfQ540kjQICRUnBSG6gNKIoMUBBJREmPWKNKKvGlKwiYBWvawYFrlStKBPYsAm62OamI18HG3u9crGybWs664eoKVAFVHBQCT3_gy79ELp0XaIKAZJJxhJFt1QVfIzBNnod3MqEd02w_lStt6p1Uq2_VGtIQ2e76KFM8n5Gvt0mgG2BmFrdwobf3f_EfgDcVokX</recordid><startdate>20240301</startdate><enddate>20240301</enddate><creator>Kok, Cindy Y.</creator><creator>Ghossein, George</creator><creator>Igoor, Sindhu</creator><creator>Rao, Renuka</creator><creator>Titus, Tracy</creator><creator>Tsurusaki, Shinya</creator><creator>Chong, James JH</creator><creator>Kizana, Eddy</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><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>7QP</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7266-6720</orcidid><orcidid>https://orcid.org/0000-0002-2592-4555</orcidid><orcidid>https://orcid.org/0000-0002-4161-0820</orcidid><orcidid>https://orcid.org/0000-0002-9536-1989</orcidid><orcidid>https://orcid.org/0000-0002-5201-4856</orcidid><orcidid>https://orcid.org/0000-0003-3086-7097</orcidid></search><sort><creationdate>20240301</creationdate><title>Ghrelin mediated cardioprotection using in vitro models of oxidative stress</title><author>Kok, Cindy Y. ; 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However, the roles of ghrelin extend beyond regulating hunger. Our aim was to investigate the ability of ghrelin to protect against hydrogen peroxide (H
2
O
2
), a reactive oxygen species commonly associated with cardiac injury. An in vitro model of oxidative stress was developed using H
2
O
2
injured H9c2 cells. Despite lentiviral ghrelin overexpression, H9c2 cell viability and mitochondrial function were not protected following H
2
O
2
injury. We found that H9c2 cells lack expression of the preproghrelin cleavage enzyme prohormone convertase 1 (encoded by
PCSK1
), required to convert ghrelin to its active form. In contrast, we found that primary rat cardiomyocytes do express
PCSK1
and were protected from H
2
O
2
injury by lentiviral ghrelin overexpression. In conclusion, we have shown that ghrelin expression can protect primary rat cardiomyocytes against H
2
O
2
, though this effect was not observed in other cell types tested.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>38177343</pmid><doi>10.1038/s41434-023-00435-9</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-7266-6720</orcidid><orcidid>https://orcid.org/0000-0002-2592-4555</orcidid><orcidid>https://orcid.org/0000-0002-4161-0820</orcidid><orcidid>https://orcid.org/0000-0002-9536-1989</orcidid><orcidid>https://orcid.org/0000-0002-5201-4856</orcidid><orcidid>https://orcid.org/0000-0003-3086-7097</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Gene therapy, 2024-03, Vol.31 (3-4), p.165-174 |
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| language | eng |
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| source | Springer Nature |
| subjects | 13/100 13/106 13/2 13/44 14/34 38/35 631/61/201 692/699/75 Animal models Animals Apoptosis Biomedical and Life Sciences Biomedicine Cardiomyocytes Cell Biology Cell viability Food intake Gene Expression Gene Therapy Ghrelin Ghrelin - genetics Ghrelin - metabolism Ghrelin - pharmacology Hormones Human Genetics Humans Hunger Hydrogen peroxide Hydrogen Peroxide - pharmacology In vitro Myocytes, Cardiac - metabolism Nanotechnology Oxidative Stress Proprotein convertases Rats Reactive oxygen species Reactive Oxygen Species - metabolism Reactive Oxygen Species - pharmacology Signal Transduction |
| title | Ghrelin mediated cardioprotection using in vitro models of oxidative stress |
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