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HIF-1α, VEGF, and EGFR: contributing factors in the pathogenesis of necrotizing sialometaplasia

Objectives Necrotizing sialometaplasia (NS) is an uncommon reactive lesion involving the minor salivary glands. This study aimed to investigate the expression of hypoxia‐inducible factor alpha (HIF‐1α), vascular endothelial growth factor (VEGF), and epithelial growth factor receptor (EGFR) in the pa...

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Published in:Oral diseases 2014-07, Vol.20 (5), p.440-445
Main Authors: Allon, I, Kaplan, I, Allon, DM, Vered, H, Shlomi, B, Hirshberg, A
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cited_by cdi_FETCH-LOGICAL-c3639-20563444ea7e347f08164ab743a45eb094b79ecb95e402c8523dc412a8a36e463
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container_end_page 445
container_issue 5
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container_title Oral diseases
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creator Allon, I
Kaplan, I
Allon, DM
Vered, H
Shlomi, B
Hirshberg, A
description Objectives Necrotizing sialometaplasia (NS) is an uncommon reactive lesion involving the minor salivary glands. This study aimed to investigate the expression of hypoxia‐inducible factor alpha (HIF‐1α), vascular endothelial growth factor (VEGF), and epithelial growth factor receptor (EGFR) in the pathogenesis of NS. Methods Paraffin‐embedded tissue sections from 10 cases of NS were immunohistochemically stained for HIF‐1α, VEGF, and EGFR. A semiquantitative morphometric analysis was performed and compared with normal palatal salivary glands and traumatic ulcerations. Results Hypoxia‐inducible factor alpha staining was observed in most elements of the affected area, the acini and ducts of the involved salivary glands as well as in the inflammatory infiltrate, the endothelial cells, and stromal cells. HIF‐1α was almost absent in the control glands (P 
doi_str_mv 10.1111/odi.12149
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This study aimed to investigate the expression of hypoxia‐inducible factor alpha (HIF‐1α), vascular endothelial growth factor (VEGF), and epithelial growth factor receptor (EGFR) in the pathogenesis of NS. Methods Paraffin‐embedded tissue sections from 10 cases of NS were immunohistochemically stained for HIF‐1α, VEGF, and EGFR. A semiquantitative morphometric analysis was performed and compared with normal palatal salivary glands and traumatic ulcerations. Results Hypoxia‐inducible factor alpha staining was observed in most elements of the affected area, the acini and ducts of the involved salivary glands as well as in the inflammatory infiltrate, the endothelial cells, and stromal cells. HIF‐1α was almost absent in the control glands (P &lt; 0.0001). VEGF staining was positive in the stromal capillaries and in the inflammatory infiltrate. The expression was higher in cases of NS compared with the normal salivary glands (P &lt; 0.001). EGFR was expressed in the surface epithelium, the pseudo‐epitheliomatous hyperplasia, and the islands of squamous metaplasia. VEGF expression in traumatic ulcerations was lower than that in cases of NS. Conclusion This study provides molecular evidence to the role of hypoxia in NS; HIF‐1α, the main regulator of hypoxia, was expressed in the infarcted salivary glands, EGFR in the metaplastic epithelium and VEGF in the stromal capillaries, all three components are the key factors induced by hypoxia.</description><identifier>ISSN: 1354-523X</identifier><identifier>EISSN: 1601-0825</identifier><identifier>DOI: 10.1111/odi.12149</identifier><identifier>PMID: 23837804</identifier><language>eng</language><publisher>Denmark: Blackwell Publishing Ltd</publisher><subject>Adult ; Aged ; Dentistry ; epithelial growth factor receptor (EGFR) ; Female ; Humans ; hypoxia ; Hypoxia-Inducible Factor 1, alpha Subunit - physiology ; hypoxia-inducible factor alpha (HIF-1α) ; Immunohistochemistry ; Male ; Middle Aged ; necrotizing sialometaplasia ; Receptor, Epidermal Growth Factor - physiology ; Salivary Glands - chemistry ; Sialometaplasia, Necrotizing - etiology ; vascular endothelial growth factor (VEGF) ; Vascular Endothelial Growth Factor A - physiology</subject><ispartof>Oral diseases, 2014-07, Vol.20 (5), p.440-445</ispartof><rights>2013 John Wiley &amp; Sons A/S. Published by John Wiley &amp; Sons Ltd</rights><rights>2013 John Wiley &amp; Sons A/S. Published by John Wiley &amp; Sons Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3639-20563444ea7e347f08164ab743a45eb094b79ecb95e402c8523dc412a8a36e463</citedby><cites>FETCH-LOGICAL-c3639-20563444ea7e347f08164ab743a45eb094b79ecb95e402c8523dc412a8a36e463</cites></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/23837804$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Allon, I</creatorcontrib><creatorcontrib>Kaplan, I</creatorcontrib><creatorcontrib>Allon, DM</creatorcontrib><creatorcontrib>Vered, H</creatorcontrib><creatorcontrib>Shlomi, B</creatorcontrib><creatorcontrib>Hirshberg, A</creatorcontrib><title>HIF-1α, VEGF, and EGFR: contributing factors in the pathogenesis of necrotizing sialometaplasia</title><title>Oral diseases</title><addtitle>Oral Dis</addtitle><description>Objectives Necrotizing sialometaplasia (NS) is an uncommon reactive lesion involving the minor salivary glands. This study aimed to investigate the expression of hypoxia‐inducible factor alpha (HIF‐1α), vascular endothelial growth factor (VEGF), and epithelial growth factor receptor (EGFR) in the pathogenesis of NS. Methods Paraffin‐embedded tissue sections from 10 cases of NS were immunohistochemically stained for HIF‐1α, VEGF, and EGFR. A semiquantitative morphometric analysis was performed and compared with normal palatal salivary glands and traumatic ulcerations. Results Hypoxia‐inducible factor alpha staining was observed in most elements of the affected area, the acini and ducts of the involved salivary glands as well as in the inflammatory infiltrate, the endothelial cells, and stromal cells. HIF‐1α was almost absent in the control glands (P &lt; 0.0001). VEGF staining was positive in the stromal capillaries and in the inflammatory infiltrate. The expression was higher in cases of NS compared with the normal salivary glands (P &lt; 0.001). EGFR was expressed in the surface epithelium, the pseudo‐epitheliomatous hyperplasia, and the islands of squamous metaplasia. VEGF expression in traumatic ulcerations was lower than that in cases of NS. Conclusion This study provides molecular evidence to the role of hypoxia in NS; HIF‐1α, the main regulator of hypoxia, was expressed in the infarcted salivary glands, EGFR in the metaplastic epithelium and VEGF in the stromal capillaries, all three components are the key factors induced by hypoxia.</description><subject>Adult</subject><subject>Aged</subject><subject>Dentistry</subject><subject>epithelial growth factor receptor (EGFR)</subject><subject>Female</subject><subject>Humans</subject><subject>hypoxia</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - physiology</subject><subject>hypoxia-inducible factor alpha (HIF-1α)</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Middle Aged</subject><subject>necrotizing sialometaplasia</subject><subject>Receptor, Epidermal Growth Factor - physiology</subject><subject>Salivary Glands - chemistry</subject><subject>Sialometaplasia, Necrotizing - etiology</subject><subject>vascular endothelial growth factor (VEGF)</subject><subject>Vascular Endothelial Growth Factor A - physiology</subject><issn>1354-523X</issn><issn>1601-0825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNp1kElOAzEQRS0EYl5wAeQlSHTwUD2xQ0BCJAYxszPuTjUYOu3QdgThVlyEM2EIsKM29Rfvf1V9QtY46_Aw23ZgOlxwyGfIIk8Yj1gm4tmgZQxRLOTtAlly7pExnuZSzJMFITOZZgwWyd1hvxvxj_cten3Q625R3QxoEOc7tLSNb00x9qa5p5UuvW0dNQ31D0hH2j_Ye2zQGUdtRRssW-vN2xfqjK7tEL0e1TroFTJX6drh6s9eJlfdg8u9w-jotNff2z2KSpnIPBIsTiQAoE5RQlqxjCegixSkhhgLlkOR5lgWeYzARJmFrwYlcKEzLROERC6TjWnuqLXPY3ReDY0rsa51g3bsFI8lcMZA5AHdnKLhaOdarNSoNUPdThRn6qtQFQpV34UGdv0ndlwMcfBH_jYYgO0p8GJqnPyfpE73-7-R0dRhnMfXP4dun1SSyjRWNyc9BWeX8vrk-FxdyE_K-o19</recordid><startdate>201407</startdate><enddate>201407</enddate><creator>Allon, I</creator><creator>Kaplan, I</creator><creator>Allon, DM</creator><creator>Vered, H</creator><creator>Shlomi, B</creator><creator>Hirshberg, A</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>7X8</scope></search><sort><creationdate>201407</creationdate><title>HIF-1α, VEGF, and EGFR: contributing factors in the pathogenesis of necrotizing sialometaplasia</title><author>Allon, I ; Kaplan, I ; Allon, DM ; Vered, H ; Shlomi, B ; Hirshberg, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3639-20563444ea7e347f08164ab743a45eb094b79ecb95e402c8523dc412a8a36e463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Dentistry</topic><topic>epithelial growth factor receptor (EGFR)</topic><topic>Female</topic><topic>Humans</topic><topic>hypoxia</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - physiology</topic><topic>hypoxia-inducible factor alpha (HIF-1α)</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Middle Aged</topic><topic>necrotizing sialometaplasia</topic><topic>Receptor, Epidermal Growth Factor - physiology</topic><topic>Salivary Glands - chemistry</topic><topic>Sialometaplasia, Necrotizing - etiology</topic><topic>vascular endothelial growth factor (VEGF)</topic><topic>Vascular Endothelial Growth Factor A - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Allon, I</creatorcontrib><creatorcontrib>Kaplan, I</creatorcontrib><creatorcontrib>Allon, DM</creatorcontrib><creatorcontrib>Vered, H</creatorcontrib><creatorcontrib>Shlomi, B</creatorcontrib><creatorcontrib>Hirshberg, A</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Oral diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Allon, I</au><au>Kaplan, I</au><au>Allon, DM</au><au>Vered, H</au><au>Shlomi, B</au><au>Hirshberg, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HIF-1α, VEGF, and EGFR: contributing factors in the pathogenesis of necrotizing sialometaplasia</atitle><jtitle>Oral diseases</jtitle><addtitle>Oral Dis</addtitle><date>2014-07</date><risdate>2014</risdate><volume>20</volume><issue>5</issue><spage>440</spage><epage>445</epage><pages>440-445</pages><issn>1354-523X</issn><eissn>1601-0825</eissn><abstract>Objectives Necrotizing sialometaplasia (NS) is an uncommon reactive lesion involving the minor salivary glands. This study aimed to investigate the expression of hypoxia‐inducible factor alpha (HIF‐1α), vascular endothelial growth factor (VEGF), and epithelial growth factor receptor (EGFR) in the pathogenesis of NS. Methods Paraffin‐embedded tissue sections from 10 cases of NS were immunohistochemically stained for HIF‐1α, VEGF, and EGFR. A semiquantitative morphometric analysis was performed and compared with normal palatal salivary glands and traumatic ulcerations. Results Hypoxia‐inducible factor alpha staining was observed in most elements of the affected area, the acini and ducts of the involved salivary glands as well as in the inflammatory infiltrate, the endothelial cells, and stromal cells. HIF‐1α was almost absent in the control glands (P &lt; 0.0001). VEGF staining was positive in the stromal capillaries and in the inflammatory infiltrate. The expression was higher in cases of NS compared with the normal salivary glands (P &lt; 0.001). EGFR was expressed in the surface epithelium, the pseudo‐epitheliomatous hyperplasia, and the islands of squamous metaplasia. VEGF expression in traumatic ulcerations was lower than that in cases of NS. Conclusion This study provides molecular evidence to the role of hypoxia in NS; HIF‐1α, the main regulator of hypoxia, was expressed in the infarcted salivary glands, EGFR in the metaplastic epithelium and VEGF in the stromal capillaries, all three components are the key factors induced by hypoxia.</abstract><cop>Denmark</cop><pub>Blackwell Publishing Ltd</pub><pmid>23837804</pmid><doi>10.1111/odi.12149</doi><tpages>6</tpages></addata></record>
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source Wiley-Blackwell Read & Publish Collection
subjects Adult
Aged
Dentistry
epithelial growth factor receptor (EGFR)
Female
Humans
hypoxia
Hypoxia-Inducible Factor 1, alpha Subunit - physiology
hypoxia-inducible factor alpha (HIF-1α)
Immunohistochemistry
Male
Middle Aged
necrotizing sialometaplasia
Receptor, Epidermal Growth Factor - physiology
Salivary Glands - chemistry
Sialometaplasia, Necrotizing - etiology
vascular endothelial growth factor (VEGF)
Vascular Endothelial Growth Factor A - physiology
title HIF-1α, VEGF, and EGFR: contributing factors in the pathogenesis of necrotizing sialometaplasia
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