The Expression of the Endogenous mTORC1 Inhibitor Sestrin 2 Is Induced by UVB and Balanced with the Expression Level of Sestrin 1
Sestrin 2 (SESN2) is an evolutionarily conserved regulator of mechanistic target of rapamycin complex 1 (mTORC1) which controls central cellular processes such as protein translation and autophagy. Previous studies have suggested that SESN2 itself is subjected to regulation at multiple levels. Here,...
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| creator | Mlitz, Veronika Gendronneau, Gaelle Berlin, Irina Buchberger, Maria Eckhart, Leopold Tschachler, Erwin |
| description | Sestrin 2 (SESN2) is an evolutionarily conserved regulator of mechanistic target of rapamycin complex 1 (mTORC1) which controls central cellular processes such as protein translation and autophagy. Previous studies have suggested that SESN2 itself is subjected to regulation at multiple levels. Here, we investigated the expression of SESN2 in the skin and in isolated skin cells. SESN2 was detected by immunofluorescence analysis in fibroblasts and keratinocytes of human skin. Differentiation of epidermal keratinocytes was not associated with altered SESN2 expression and siRNA-mediated knockdown of SESN2 did not impair stratum corneum formation in vitro. However, SESN2 was increased in both cell types when the expression of its paralog SESN1 was blocked by siRNA-mediated knock down, indicating a compensatory mechanism for the control of expression. Irradiation with UVB but not with UVA significantly increased SESN2 expression in both keratinocytes and fibroblasts. Upregulation of SESN2 expression could be completely blocked by suppression of p53. These results suggest that SESN2 is dispensable for normal epidermal keratinization but involved in the UVB stress response of skin cells. |
| doi_str_mv | 10.1371/journal.pone.0166832 |
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Previous studies have suggested that SESN2 itself is subjected to regulation at multiple levels. Here, we investigated the expression of SESN2 in the skin and in isolated skin cells. SESN2 was detected by immunofluorescence analysis in fibroblasts and keratinocytes of human skin. Differentiation of epidermal keratinocytes was not associated with altered SESN2 expression and siRNA-mediated knockdown of SESN2 did not impair stratum corneum formation in vitro. However, SESN2 was increased in both cell types when the expression of its paralog SESN1 was blocked by siRNA-mediated knock down, indicating a compensatory mechanism for the control of expression. Irradiation with UVB but not with UVA significantly increased SESN2 expression in both keratinocytes and fibroblasts. Upregulation of SESN2 expression could be completely blocked by suppression of p53. These results suggest that SESN2 is dispensable for normal epidermal keratinization but involved in the UVB stress response of skin cells.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0166832</identifier><identifier>PMID: 27861561</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Aged ; Analysis ; Antigens ; Autophagy ; Biology ; Biology and Life Sciences ; Cancer ; Cellular stress response ; Deoxyribonucleic acid ; Dermatology ; DNA ; DNA damage ; Drosophila melanogaster ; Fibroblasts ; Fibroblasts - metabolism ; Fibroblasts - radiation effects ; Gene Expression Regulation - radiation effects ; Gene Knockdown Techniques ; Heat-Shock Proteins - genetics ; Heat-Shock Proteins - metabolism ; Homeostasis ; Humans ; Immunofluorescence ; Irradiation ; Keratinization ; Keratinocytes ; Keratinocytes - metabolism ; Keratinocytes - radiation effects ; Mammals ; Mechanistic Target of Rapamycin Complex 1 ; Medicine and Health Sciences ; Middle Aged ; Multiprotein Complexes - antagonists & inhibitors ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Oxidative stress ; p53 Protein ; Phagocytosis ; Physical sciences ; Proteins ; Rapamycin ; Research and analysis methods ; RNA, Small Interfering - genetics ; Rodents ; siRNA ; Skin ; Stratum corneum ; Stress response ; TOR protein ; TOR Serine-Threonine Kinases - antagonists & inhibitors ; Tumor proteins ; Ultraviolet radiation ; Ultraviolet Rays ; Young Adult</subject><ispartof>PloS one, 2016-11, Vol.11 (11), p.e0166832-e0166832</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Mlitz 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. 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Previous studies have suggested that SESN2 itself is subjected to regulation at multiple levels. Here, we investigated the expression of SESN2 in the skin and in isolated skin cells. SESN2 was detected by immunofluorescence analysis in fibroblasts and keratinocytes of human skin. Differentiation of epidermal keratinocytes was not associated with altered SESN2 expression and siRNA-mediated knockdown of SESN2 did not impair stratum corneum formation in vitro. However, SESN2 was increased in both cell types when the expression of its paralog SESN1 was blocked by siRNA-mediated knock down, indicating a compensatory mechanism for the control of expression. Irradiation with UVB but not with UVA significantly increased SESN2 expression in both keratinocytes and fibroblasts. Upregulation of SESN2 expression could be completely blocked by suppression of p53. These results suggest that SESN2 is dispensable for normal epidermal keratinization but involved in the UVB stress response of skin cells.</description><subject>Adult</subject><subject>Aged</subject><subject>Analysis</subject><subject>Antigens</subject><subject>Autophagy</subject><subject>Biology</subject><subject>Biology and Life Sciences</subject><subject>Cancer</subject><subject>Cellular stress response</subject><subject>Deoxyribonucleic acid</subject><subject>Dermatology</subject><subject>DNA</subject><subject>DNA damage</subject><subject>Drosophila melanogaster</subject><subject>Fibroblasts</subject><subject>Fibroblasts - metabolism</subject><subject>Fibroblasts - radiation effects</subject><subject>Gene Expression Regulation - radiation effects</subject><subject>Gene Knockdown Techniques</subject><subject>Heat-Shock Proteins - genetics</subject><subject>Heat-Shock Proteins - metabolism</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Immunofluorescence</subject><subject>Irradiation</subject><subject>Keratinization</subject><subject>Keratinocytes</subject><subject>Keratinocytes - metabolism</subject><subject>Keratinocytes - radiation effects</subject><subject>Mammals</subject><subject>Mechanistic Target of Rapamycin Complex 1</subject><subject>Medicine and Health Sciences</subject><subject>Middle Aged</subject><subject>Multiprotein Complexes - antagonists & inhibitors</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Oxidative stress</subject><subject>p53 Protein</subject><subject>Phagocytosis</subject><subject>Physical sciences</subject><subject>Proteins</subject><subject>Rapamycin</subject><subject>Research and analysis methods</subject><subject>RNA, Small Interfering - genetics</subject><subject>Rodents</subject><subject>siRNA</subject><subject>Skin</subject><subject>Stratum corneum</subject><subject>Stress response</subject><subject>TOR protein</subject><subject>TOR Serine-Threonine Kinases - antagonists & inhibitors</subject><subject>Tumor proteins</subject><subject>Ultraviolet radiation</subject><subject>Ultraviolet Rays</subject><subject>Young 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Expression of the Endogenous mTORC1 Inhibitor Sestrin 2 Is Induced by UVB and Balanced with the Expression Level of Sestrin 1</title><author>Mlitz, Veronika ; Gendronneau, Gaelle ; Berlin, Irina ; Buchberger, Maria ; Eckhart, Leopold ; Tschachler, Erwin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c725t-471eff192188ffba82433cf6d948b4e3edd87053ca5b8a043c7499e69b0932433</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Analysis</topic><topic>Antigens</topic><topic>Autophagy</topic><topic>Biology</topic><topic>Biology and Life Sciences</topic><topic>Cancer</topic><topic>Cellular stress response</topic><topic>Deoxyribonucleic acid</topic><topic>Dermatology</topic><topic>DNA</topic><topic>DNA damage</topic><topic>Drosophila melanogaster</topic><topic>Fibroblasts</topic><topic>Fibroblasts - metabolism</topic><topic>Fibroblasts - 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One</addtitle><date>2016-11-18</date><risdate>2016</risdate><volume>11</volume><issue>11</issue><spage>e0166832</spage><epage>e0166832</epage><pages>e0166832-e0166832</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Sestrin 2 (SESN2) is an evolutionarily conserved regulator of mechanistic target of rapamycin complex 1 (mTORC1) which controls central cellular processes such as protein translation and autophagy. Previous studies have suggested that SESN2 itself is subjected to regulation at multiple levels. Here, we investigated the expression of SESN2 in the skin and in isolated skin cells. SESN2 was detected by immunofluorescence analysis in fibroblasts and keratinocytes of human skin. Differentiation of epidermal keratinocytes was not associated with altered SESN2 expression and siRNA-mediated knockdown of SESN2 did not impair stratum corneum formation in vitro. However, SESN2 was increased in both cell types when the expression of its paralog SESN1 was blocked by siRNA-mediated knock down, indicating a compensatory mechanism for the control of expression. Irradiation with UVB but not with UVA significantly increased SESN2 expression in both keratinocytes and fibroblasts. Upregulation of SESN2 expression could be completely blocked by suppression of p53. These results suggest that SESN2 is dispensable for normal epidermal keratinization but involved in the UVB stress response of skin cells.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27861561</pmid><doi>10.1371/journal.pone.0166832</doi><tpages>e0166832</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; PubMed Central(OpenAccess); PLoS - Public Library of Sciencem (Open Access); Directory of Open Access Journals(OpenAccess); Free E-Journal (出版社公開部分のみ）; Free Full-Text Journals in Chemistry |
| subjects | Adult Aged Analysis Antigens Autophagy Biology Biology and Life Sciences Cancer Cellular stress response Deoxyribonucleic acid Dermatology DNA DNA damage Drosophila melanogaster Fibroblasts Fibroblasts - metabolism Fibroblasts - radiation effects Gene Expression Regulation - radiation effects Gene Knockdown Techniques Heat-Shock Proteins - genetics Heat-Shock Proteins - metabolism Homeostasis Humans Immunofluorescence Irradiation Keratinization Keratinocytes Keratinocytes - metabolism Keratinocytes - radiation effects Mammals Mechanistic Target of Rapamycin Complex 1 Medicine and Health Sciences Middle Aged Multiprotein Complexes - antagonists & inhibitors Nuclear Proteins - genetics Nuclear Proteins - metabolism Oxidative stress p53 Protein Phagocytosis Physical sciences Proteins Rapamycin Research and analysis methods RNA, Small Interfering - genetics Rodents siRNA Skin Stratum corneum Stress response TOR protein TOR Serine-Threonine Kinases - antagonists & inhibitors Tumor proteins Ultraviolet radiation Ultraviolet Rays Young Adult |
| title | The Expression of the Endogenous mTORC1 Inhibitor Sestrin 2 Is Induced by UVB and Balanced with the Expression Level of Sestrin 1 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-01T08%3A12%3A27IST&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=The%20Expression%20of%20the%20Endogenous%20mTORC1%20Inhibitor%20Sestrin%202%20Is%20Induced%20by%20UVB%20and%20Balanced%20with%20the%20Expression%20Level%20of%20Sestrin%201&rft.jtitle=PloS%20one&rft.au=Mlitz,%20Veronika&rft.date=2016-11-18&rft.volume=11&rft.issue=11&rft.spage=e0166832&rft.epage=e0166832&rft.pages=e0166832-e0166832&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0166832&rft_dat=%3Cgale_plos_%3EA471881676%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=1841403276&rft_id=info:pmid/27861561&rft_galeid=A471881676&rft_doaj_id=oai_doaj_org_article_1eb2b39dd6814c328f92dfa6336cbded&rfr_iscdi=true |