Developmental relationship between junctional epithelium and epithelial rests of Malassez
(K17) is thought to be a candidate target gene for regulation by Lymphoid Enhancer Factor-1 (Lef-1) K17 is a marker that distinguishes junctional epithelium (JE) from epithelial rests of Malassez (ERM). However, the relationship of Lef-1 to K17 is not clear in this context. Moreover, the expression...
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Veröffentlicht in: | The International journal of developmental biology 2024, Vol.68 (1), p.39-45 |
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description | (K17) is thought to be a candidate target gene for regulation by Lymphoid Enhancer Factor-1 (Lef-1)
K17 is a marker that distinguishes junctional epithelium (JE) from epithelial rests of Malassez (ERM). However, the relationship of Lef-1 to K17 is not clear in this context. Moreover, the expression of other keratins such as K5, K6, K7 and K16 is not reported. Therefore, the aim of our study was to assay the expression of K5, K6, K7, K14, K16, K17 and Lef-1 in postnatal developing teeth, and clarify the corresponding immunophenotypes of the JE and ERM. Upper jaws of Wistar rats aged from postnatal (PN) day 3.5 to PN21 were used and processed for immunohistochemistry. K5 and K14 were intensely expressed in inner enamel epithelium (IEE), reduced enamel epithelium (REE), ERM and JE. There was no staining for K16 in the tissue, except for strong staining in the oral epithelium. Specifically, at PN3.5 and PN7, K17 was initially strongly expressed and then negative in the IEE. At PN16 and PN21, both REE and ERM were strongly stained for K17, whereas K17 was negative in the JE. In addition, K6, K7 and Lef-1 were not detected in any tissue investigated. REE and ERM have an identical keratin expression pattern before eruption, while JE differs from ERM in the expression of K17 after eruption. The expression of K17 does not coincide with that of Lef-1. These data indicate that JE has a unique phenotype different from ERM, which is of odontogenic origin. |
doi_str_mv | 10.1387/ijdb.230243sl |
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K17 is a marker that distinguishes junctional epithelium (JE) from epithelial rests of Malassez (ERM). However, the relationship of Lef-1 to K17 is not clear in this context. Moreover, the expression of other keratins such as K5, K6, K7 and K16 is not reported. Therefore, the aim of our study was to assay the expression of K5, K6, K7, K14, K16, K17 and Lef-1 in postnatal developing teeth, and clarify the corresponding immunophenotypes of the JE and ERM. Upper jaws of Wistar rats aged from postnatal (PN) day 3.5 to PN21 were used and processed for immunohistochemistry. K5 and K14 were intensely expressed in inner enamel epithelium (IEE), reduced enamel epithelium (REE), ERM and JE. There was no staining for K16 in the tissue, except for strong staining in the oral epithelium. Specifically, at PN3.5 and PN7, K17 was initially strongly expressed and then negative in the IEE. At PN16 and PN21, both REE and ERM were strongly stained for K17, whereas K17 was negative in the JE. In addition, K6, K7 and Lef-1 were not detected in any tissue investigated. REE and ERM have an identical keratin expression pattern before eruption, while JE differs from ERM in the expression of K17 after eruption. The expression of K17 does not coincide with that of Lef-1. These data indicate that JE has a unique phenotype different from ERM, which is of odontogenic origin.</description><identifier>ISSN: 0214-6282</identifier><identifier>EISSN: 1696-3547</identifier><identifier>DOI: 10.1387/ijdb.230243sl</identifier><identifier>PMID: 38591692</identifier><language>eng</language><publisher>Spain: University of the Basque Country Press</publisher><subject>Animals ; Dental enamel ; Epithelial Attachment - metabolism ; Epithelium ; Epithelium - metabolism ; Immunohistochemistry ; Keratin ; Keratins - metabolism ; LEF protein ; Phenotypes ; Rats ; Rats, Wistar ; Rest ; Staining ; Teeth</subject><ispartof>The International journal of developmental biology, 2024, Vol.68 (1), p.39-45</ispartof><rights>Copyright University of the Basque Country Press 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38591692$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Shubo</creatorcontrib><creatorcontrib>Li, Shufang</creatorcontrib><creatorcontrib>Cao, Mingguo</creatorcontrib><title>Developmental relationship between junctional epithelium and epithelial rests of Malassez</title><title>The International journal of developmental biology</title><addtitle>Int J Dev Biol</addtitle><description>(K17) is thought to be a candidate target gene for regulation by Lymphoid Enhancer Factor-1 (Lef-1)
K17 is a marker that distinguishes junctional epithelium (JE) from epithelial rests of Malassez (ERM). However, the relationship of Lef-1 to K17 is not clear in this context. Moreover, the expression of other keratins such as K5, K6, K7 and K16 is not reported. Therefore, the aim of our study was to assay the expression of K5, K6, K7, K14, K16, K17 and Lef-1 in postnatal developing teeth, and clarify the corresponding immunophenotypes of the JE and ERM. Upper jaws of Wistar rats aged from postnatal (PN) day 3.5 to PN21 were used and processed for immunohistochemistry. K5 and K14 were intensely expressed in inner enamel epithelium (IEE), reduced enamel epithelium (REE), ERM and JE. There was no staining for K16 in the tissue, except for strong staining in the oral epithelium. Specifically, at PN3.5 and PN7, K17 was initially strongly expressed and then negative in the IEE. At PN16 and PN21, both REE and ERM were strongly stained for K17, whereas K17 was negative in the JE. In addition, K6, K7 and Lef-1 were not detected in any tissue investigated. REE and ERM have an identical keratin expression pattern before eruption, while JE differs from ERM in the expression of K17 after eruption. The expression of K17 does not coincide with that of Lef-1. These data indicate that JE has a unique phenotype different from ERM, which is of odontogenic origin.</description><subject>Animals</subject><subject>Dental enamel</subject><subject>Epithelial Attachment - metabolism</subject><subject>Epithelium</subject><subject>Epithelium - metabolism</subject><subject>Immunohistochemistry</subject><subject>Keratin</subject><subject>Keratins - metabolism</subject><subject>LEF protein</subject><subject>Phenotypes</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Rest</subject><subject>Staining</subject><subject>Teeth</subject><issn>0214-6282</issn><issn>1696-3547</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkLtPwzAQxi0EoqUwsqJILCwpti-2kxGVp1TEAgNT5CRnNZHzIE5A8NfjPujAdPrufvfp7iPknNE5g1hdl1WRzTlQHoGzB2TKZCJDEJE6JFPKWRRKHvMJOXGuol7TWB2TCcQi8SCfkvdb_ETbdjU2g7ZBj1YPZdu4VdkFGQ5fiE1QjU2-bvo5duWwQluOdaCbYi83m25wQWuCZ221c_hzSo6Mtg7PdnVG3u7vXheP4fLl4WlxswxzYHIIDSArRFJowygkjAnFhABesDwxBkyGMRSJKXTGFGRKZJkEGYHmRoKIY6phRq62vl3ffoz-irQuXY7W6gbb0aVAQVAVQaQ8evkPrdqx939tKAZSMeCeCrdU3rfO9WjSri9r3X-njKbrzNN15ulf5p6_2LmOWY3Fnv4LGX4B3vJ-iA</recordid><startdate>2024</startdate><enddate>2024</enddate><creator>Li, Shubo</creator><creator>Li, Shufang</creator><creator>Cao, Mingguo</creator><general>University of the Basque Country Press</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>7QL</scope><scope>7QP</scope><scope>7TK</scope><scope>7TM</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>2024</creationdate><title>Developmental relationship between junctional epithelium and epithelial rests of Malassez</title><author>Li, Shubo ; Li, Shufang ; Cao, Mingguo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c316t-f3e1d59daf1039115715532d1c9ff3fbe83d9fdab173b75bb63643a2f635880a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Dental enamel</topic><topic>Epithelial Attachment - metabolism</topic><topic>Epithelium</topic><topic>Epithelium - metabolism</topic><topic>Immunohistochemistry</topic><topic>Keratin</topic><topic>Keratins - metabolism</topic><topic>LEF protein</topic><topic>Phenotypes</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Rest</topic><topic>Staining</topic><topic>Teeth</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Shubo</creatorcontrib><creatorcontrib>Li, Shufang</creatorcontrib><creatorcontrib>Cao, Mingguo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The International journal of developmental biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Shubo</au><au>Li, Shufang</au><au>Cao, Mingguo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Developmental relationship between junctional epithelium and epithelial rests of Malassez</atitle><jtitle>The International journal of developmental biology</jtitle><addtitle>Int J Dev Biol</addtitle><date>2024</date><risdate>2024</risdate><volume>68</volume><issue>1</issue><spage>39</spage><epage>45</epage><pages>39-45</pages><issn>0214-6282</issn><eissn>1696-3547</eissn><abstract>(K17) is thought to be a candidate target gene for regulation by Lymphoid Enhancer Factor-1 (Lef-1)
K17 is a marker that distinguishes junctional epithelium (JE) from epithelial rests of Malassez (ERM). However, the relationship of Lef-1 to K17 is not clear in this context. Moreover, the expression of other keratins such as K5, K6, K7 and K16 is not reported. Therefore, the aim of our study was to assay the expression of K5, K6, K7, K14, K16, K17 and Lef-1 in postnatal developing teeth, and clarify the corresponding immunophenotypes of the JE and ERM. Upper jaws of Wistar rats aged from postnatal (PN) day 3.5 to PN21 were used and processed for immunohistochemistry. K5 and K14 were intensely expressed in inner enamel epithelium (IEE), reduced enamel epithelium (REE), ERM and JE. There was no staining for K16 in the tissue, except for strong staining in the oral epithelium. Specifically, at PN3.5 and PN7, K17 was initially strongly expressed and then negative in the IEE. At PN16 and PN21, both REE and ERM were strongly stained for K17, whereas K17 was negative in the JE. In addition, K6, K7 and Lef-1 were not detected in any tissue investigated. REE and ERM have an identical keratin expression pattern before eruption, while JE differs from ERM in the expression of K17 after eruption. The expression of K17 does not coincide with that of Lef-1. These data indicate that JE has a unique phenotype different from ERM, which is of odontogenic origin.</abstract><cop>Spain</cop><pub>University of the Basque Country Press</pub><pmid>38591692</pmid><doi>10.1387/ijdb.230243sl</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Dental enamel Epithelial Attachment - metabolism Epithelium Epithelium - metabolism Immunohistochemistry Keratin Keratins - metabolism LEF protein Phenotypes Rats Rats, Wistar Rest Staining Teeth |
title | Developmental relationship between junctional epithelium and epithelial rests of Malassez |
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