Possible Involvement of F1F0-ATP synthase and Intracellular ATP in Keratinocyte Differentiation in normal skin and skin lesions
The F1F0-ATP synthase, an enzyme complex, is mainly located on the mitochondrial inner membrane or sometimes cytomembrane to generate or hydrolyze ATP, play a role in cell proliferation. This study focused on the role of F1F0-ATP synthase in keratinocyte differentiation, and its relationship with in...
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description | The F1F0-ATP synthase, an enzyme complex, is mainly located on the mitochondrial inner membrane or sometimes cytomembrane to generate or hydrolyze ATP, play a role in cell proliferation. This study focused on the role of F1F0-ATP synthase in keratinocyte differentiation, and its relationship with intracellular and extracellular ATP (InATP and ExATP). The F1F0-ATP synthase β subunit (ATP5B) expression in various skin tissues and confluence-dependent HaCaT differentiation models was detected. ATP5B expression increased with keratinocyte and HaCaT cell differentiation in normal skin, some epidermis hyper-proliferative diseases, squamous cell carcinoma, and the HaCaT cell differentiation model. The impact of InATP and ExATP content on HaCaT differentiation was reflected by the expression of the differentiation marker involucrin. Inhibition of F1F0-ATP synthase blocked HaCaT cell differentiation, which was associated with a decrease of InATP content, but not with changes of ExATP. Our results revealed that F1F0-ATP synthase expression is associated with the process of keratinocyte differentiation which may possibly be related to InATP synthesis. |
doi_str_mv | 10.1038/srep42672 |
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This study focused on the role of F1F0-ATP synthase in keratinocyte differentiation, and its relationship with intracellular and extracellular ATP (InATP and ExATP). The F1F0-ATP synthase β subunit (ATP5B) expression in various skin tissues and confluence-dependent HaCaT differentiation models was detected. ATP5B expression increased with keratinocyte and HaCaT cell differentiation in normal skin, some epidermis hyper-proliferative diseases, squamous cell carcinoma, and the HaCaT cell differentiation model. The impact of InATP and ExATP content on HaCaT differentiation was reflected by the expression of the differentiation marker involucrin. Inhibition of F1F0-ATP synthase blocked HaCaT cell differentiation, which was associated with a decrease of InATP content, but not with changes of ExATP. Our results revealed that F1F0-ATP synthase expression is associated with the process of keratinocyte differentiation which may possibly be related to InATP synthesis.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep42672</identifier><identifier>PMID: 28209970</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/51 ; 38/77 ; 631/67/327 ; 692/53/2422 ; Adenosine Triphosphate - biosynthesis ; ATP synthase ; Binding sites ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - metabolism ; Carcinoma, Squamous Cell - pathology ; Cell Differentiation ; Cell Line, Transformed ; Cell proliferation ; Dermatitis - genetics ; Dermatitis - metabolism ; Dermatitis - pathology ; Epidermis ; Gene Expression Regulation ; Humanities and Social Sciences ; Humans ; Intracellular ; Keratinocytes - cytology ; Keratinocytes - metabolism ; Keratoacanthoma - genetics ; Keratoacanthoma - metabolism ; Keratoacanthoma - pathology ; Keratosis, Seborrheic - genetics ; Keratosis, Seborrheic - metabolism ; Keratosis, Seborrheic - pathology ; Metabolism ; Mitochondria ; Mitochondria - metabolism ; Mitochondrial Membranes - metabolism ; Mitochondrial Proton-Translocating ATPases - genetics ; Mitochondrial Proton-Translocating ATPases - metabolism ; multidisciplinary ; Physiology ; Protein Precursors - genetics ; Protein Precursors - metabolism ; Prurigo - genetics ; Prurigo - metabolism ; Prurigo - pathology ; Psoriasis ; Psoriasis - genetics ; Psoriasis - metabolism ; Psoriasis - pathology ; Science ; Skin - cytology ; Skin - metabolism ; Skin diseases ; Skin Neoplasms - genetics ; Skin Neoplasms - metabolism ; Skin Neoplasms - pathology ; Squamous cell carcinoma ; Warts - genetics ; Warts - metabolism ; Warts - pathology</subject><ispartof>Scientific reports, 2017-02, Vol.7 (1), p.42672-42672, Article 42672</ispartof><rights>The Author(s) 2017</rights><rights>Copyright Nature Publishing Group Feb 2017</rights><rights>Copyright © 2017, The Author(s) 2017 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-72f39e64a9febdb913ea6d65e898e971c7d9c6798b30cd107dbb1e18ccf747c23</citedby><cites>FETCH-LOGICAL-c478t-72f39e64a9febdb913ea6d65e898e971c7d9c6798b30cd107dbb1e18ccf747c23</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/PMC5314331/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5314331/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28209970$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xiaoyun, Xie</creatorcontrib><creatorcontrib>Chaofei, Han</creatorcontrib><creatorcontrib>Weiqi, Zeng</creatorcontrib><creatorcontrib>Chen, Chen</creatorcontrib><creatorcontrib>Lixia, Lu</creatorcontrib><creatorcontrib>Queping, Liu</creatorcontrib><creatorcontrib>Cong, Peng</creatorcontrib><creatorcontrib>Shuang, Zhao</creatorcontrib><creatorcontrib>Juan, Su</creatorcontrib><creatorcontrib>Xiang, Chen</creatorcontrib><title>Possible Involvement of F1F0-ATP synthase and Intracellular ATP in Keratinocyte Differentiation in normal skin and skin lesions</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>The F1F0-ATP synthase, an enzyme complex, is mainly located on the mitochondrial inner membrane or sometimes cytomembrane to generate or hydrolyze ATP, play a role in cell proliferation. This study focused on the role of F1F0-ATP synthase in keratinocyte differentiation, and its relationship with intracellular and extracellular ATP (InATP and ExATP). The F1F0-ATP synthase β subunit (ATP5B) expression in various skin tissues and confluence-dependent HaCaT differentiation models was detected. ATP5B expression increased with keratinocyte and HaCaT cell differentiation in normal skin, some epidermis hyper-proliferative diseases, squamous cell carcinoma, and the HaCaT cell differentiation model. The impact of InATP and ExATP content on HaCaT differentiation was reflected by the expression of the differentiation marker involucrin. Inhibition of F1F0-ATP synthase blocked HaCaT cell differentiation, which was associated with a decrease of InATP content, but not with changes of ExATP. 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biosynthesis</topic><topic>ATP synthase</topic><topic>Binding sites</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - metabolism</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell Differentiation</topic><topic>Cell Line, Transformed</topic><topic>Cell proliferation</topic><topic>Dermatitis - genetics</topic><topic>Dermatitis - metabolism</topic><topic>Dermatitis - pathology</topic><topic>Epidermis</topic><topic>Gene Expression Regulation</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Intracellular</topic><topic>Keratinocytes - cytology</topic><topic>Keratinocytes - metabolism</topic><topic>Keratoacanthoma - genetics</topic><topic>Keratoacanthoma - metabolism</topic><topic>Keratoacanthoma - pathology</topic><topic>Keratosis, Seborrheic - genetics</topic><topic>Keratosis, Seborrheic - metabolism</topic><topic>Keratosis, Seborrheic - pathology</topic><topic>Metabolism</topic><topic>Mitochondria</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondrial Membranes - metabolism</topic><topic>Mitochondrial Proton-Translocating ATPases - genetics</topic><topic>Mitochondrial Proton-Translocating ATPases - metabolism</topic><topic>multidisciplinary</topic><topic>Physiology</topic><topic>Protein Precursors - genetics</topic><topic>Protein Precursors - metabolism</topic><topic>Prurigo - genetics</topic><topic>Prurigo - metabolism</topic><topic>Prurigo - pathology</topic><topic>Psoriasis</topic><topic>Psoriasis - genetics</topic><topic>Psoriasis - metabolism</topic><topic>Psoriasis - pathology</topic><topic>Science</topic><topic>Skin - cytology</topic><topic>Skin - metabolism</topic><topic>Skin diseases</topic><topic>Skin Neoplasms - genetics</topic><topic>Skin Neoplasms - metabolism</topic><topic>Skin Neoplasms - pathology</topic><topic>Squamous cell carcinoma</topic><topic>Warts - genetics</topic><topic>Warts - metabolism</topic><topic>Warts - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xiaoyun, Xie</creatorcontrib><creatorcontrib>Chaofei, Han</creatorcontrib><creatorcontrib>Weiqi, Zeng</creatorcontrib><creatorcontrib>Chen, Chen</creatorcontrib><creatorcontrib>Lixia, Lu</creatorcontrib><creatorcontrib>Queping, Liu</creatorcontrib><creatorcontrib>Cong, Peng</creatorcontrib><creatorcontrib>Shuang, Zhao</creatorcontrib><creatorcontrib>Juan, Su</creatorcontrib><creatorcontrib>Xiang, Chen</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xiaoyun, Xie</au><au>Chaofei, Han</au><au>Weiqi, Zeng</au><au>Chen, Chen</au><au>Lixia, Lu</au><au>Queping, Liu</au><au>Cong, Peng</au><au>Shuang, Zhao</au><au>Juan, Su</au><au>Xiang, Chen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Possible Involvement of F1F0-ATP synthase and Intracellular ATP in Keratinocyte Differentiation in normal skin and skin lesions</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2017-02-17</date><risdate>2017</risdate><volume>7</volume><issue>1</issue><spage>42672</spage><epage>42672</epage><pages>42672-42672</pages><artnum>42672</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>The F1F0-ATP synthase, an enzyme complex, is mainly located on the mitochondrial inner membrane or sometimes cytomembrane to generate or hydrolyze ATP, play a role in cell proliferation. This study focused on the role of F1F0-ATP synthase in keratinocyte differentiation, and its relationship with intracellular and extracellular ATP (InATP and ExATP). The F1F0-ATP synthase β subunit (ATP5B) expression in various skin tissues and confluence-dependent HaCaT differentiation models was detected. ATP5B expression increased with keratinocyte and HaCaT cell differentiation in normal skin, some epidermis hyper-proliferative diseases, squamous cell carcinoma, and the HaCaT cell differentiation model. The impact of InATP and ExATP content on HaCaT differentiation was reflected by the expression of the differentiation marker involucrin. Inhibition of F1F0-ATP synthase blocked HaCaT cell differentiation, which was associated with a decrease of InATP content, but not with changes of ExATP. Our results revealed that F1F0-ATP synthase expression is associated with the process of keratinocyte differentiation which may possibly be related to InATP synthesis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>28209970</pmid><doi>10.1038/srep42672</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 13/51 38/77 631/67/327 692/53/2422 Adenosine Triphosphate - biosynthesis ATP synthase Binding sites Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - pathology Cell Differentiation Cell Line, Transformed Cell proliferation Dermatitis - genetics Dermatitis - metabolism Dermatitis - pathology Epidermis Gene Expression Regulation Humanities and Social Sciences Humans Intracellular Keratinocytes - cytology Keratinocytes - metabolism Keratoacanthoma - genetics Keratoacanthoma - metabolism Keratoacanthoma - pathology Keratosis, Seborrheic - genetics Keratosis, Seborrheic - metabolism Keratosis, Seborrheic - pathology Metabolism Mitochondria Mitochondria - metabolism Mitochondrial Membranes - metabolism Mitochondrial Proton-Translocating ATPases - genetics Mitochondrial Proton-Translocating ATPases - metabolism multidisciplinary Physiology Protein Precursors - genetics Protein Precursors - metabolism Prurigo - genetics Prurigo - metabolism Prurigo - pathology Psoriasis Psoriasis - genetics Psoriasis - metabolism Psoriasis - pathology Science Skin - cytology Skin - metabolism Skin diseases Skin Neoplasms - genetics Skin Neoplasms - metabolism Skin Neoplasms - pathology Squamous cell carcinoma Warts - genetics Warts - metabolism Warts - pathology |
title | Possible Involvement of F1F0-ATP synthase and Intracellular ATP in Keratinocyte Differentiation in normal skin and skin lesions |
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