Histopathology and selective biomarker expression in human meibomian glands
Background/aimsMeibomian gland dysfunction (MGD) is the most common form of evaporative dry eye disease, but its pathogenesis is poorly understood. This study examined the histopathological features of meibomian gland (MG) tissue from cadaver donors to identify potential pathogenic processes that un...
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| Veröffentlicht in: | British journal of ophthalmology 2020-07, Vol.104 (7), p.999-1004 |
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| description | Background/aimsMeibomian gland dysfunction (MGD) is the most common form of evaporative dry eye disease, but its pathogenesis is poorly understood. This study examined the histopathological features of meibomian gland (MG) tissue from cadaver donors to identify potential pathogenic processes that underlie MGD in humans.MethodsHistological analyses was performed on the MGs in the tarsal plates dissected from four cadaver donors, two young and two old adults, including a 36-year-old female (36F) and three males aged 30, 63 and 64 years (30M, 63M and 64M).ResultsThe MGs of 36F displayed normal anatomy and structure, whereas the MGs of 30M showed severe ductal obstruction with mild distortion. The obstruction was caused by increased cytokeratin levels in association with hyperproliferation, but not hyperkeratinisation. In two older males, moderate to severe MG atrophy was noted. Cell proliferation was significantly reduced in the MG acini of the two older donors as measured by Ki67 labelling index (6.0%±3.4% and 7.9%±2.8% in 63M and 64M, respectively) when compared with that of the two younger donors (23.2%±5.5% and 16.9%±4.8% in 30M and 36F, respectively) (p |
| doi_str_mv | 10.1136/bjophthalmol-2019-314466 |
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This study examined the histopathological features of meibomian gland (MG) tissue from cadaver donors to identify potential pathogenic processes that underlie MGD in humans.MethodsHistological analyses was performed on the MGs in the tarsal plates dissected from four cadaver donors, two young and two old adults, including a 36-year-old female (36F) and three males aged 30, 63 and 64 years (30M, 63M and 64M).ResultsThe MGs of 36F displayed normal anatomy and structure, whereas the MGs of 30M showed severe ductal obstruction with mild distortion. The obstruction was caused by increased cytokeratin levels in association with hyperproliferation, but not hyperkeratinisation. In two older males, moderate to severe MG atrophy was noted. Cell proliferation was significantly reduced in the MG acini of the two older donors as measured by Ki67 labelling index (6.0%±3.4% and 7.9%±2.8% in 63M and 64M, respectively) when compared with that of the two younger donors (23.2%±5.5% and 16.9%±4.8% in 30M and 36F, respectively) (p<0.001). The expression patterns of meibocyte differentiation biomarkers were similar in the older and younger donors.ConclusionOur histopathological study, based on a small sample size, suggests potentially distinct pathogenic mechanisms in MGD. In the young male adult, hyperproliferation and aberrant differentiation of the central ductal epithelia may lead to the obstruction by overproduced cytokeratins. In contrast, in older adults, decreased cell proliferation in acinar basal epithelia could be a contributing factor leading to MG glandular atrophy.</description><identifier>ISSN: 0007-1161</identifier><identifier>EISSN: 1468-2079</identifier><identifier>DOI: 10.1136/bjophthalmol-2019-314466</identifier><identifier>PMID: 31585964</identifier><language>eng</language><publisher>England: BMJ Publishing Group LTD</publisher><subject>Adult ; Antibodies ; Antigens ; Atrophy ; Biomarkers ; Biomarkers - metabolism ; Cell growth ; Cell Proliferation ; Clinical Science ; Dry Eye Syndromes - metabolism ; Dry Eye Syndromes - pathology ; Female ; Histology ; Humans ; Immunoenzyme Techniques ; Keratin-16 - metabolism ; Keratin-17 - metabolism ; Keratin-6 - metabolism ; Ki-67 Antigen - metabolism ; Lipids ; Male ; Meibomian Gland Dysfunction - metabolism ; Meibomian Gland Dysfunction - pathology ; Meibomian Glands - metabolism ; Meibomian Glands - pathology ; Middle Aged ; Older people ; Pathogenesis ; Tissue Donors ; Young adults</subject><ispartof>British journal of ophthalmology, 2020-07, Vol.104 (7), p.999-1004</ispartof><rights>Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</rights><rights>2020 Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ . Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b558t-219e22f63cc132645a3b081d62e35a1dd9226e524d7412adfa567f416d51a6683</citedby><cites>FETCH-LOGICAL-b558t-219e22f63cc132645a3b081d62e35a1dd9226e524d7412adfa567f416d51a6683</cites><orcidid>0000-0002-5622-1326</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7361036/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7361036/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31585964$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Reneker, Lixing W</creatorcontrib><creatorcontrib>Irlmeier, Rebecca T</creatorcontrib><creatorcontrib>Shui, Ying-Bo</creatorcontrib><creatorcontrib>Liu, Ying</creatorcontrib><creatorcontrib>Huang, Andrew J W</creatorcontrib><title>Histopathology and selective biomarker expression in human meibomian glands</title><title>British journal of ophthalmology</title><addtitle>Br J Ophthalmol</addtitle><description>Background/aimsMeibomian gland dysfunction (MGD) is the most common form of evaporative dry eye disease, but its pathogenesis is poorly understood. This study examined the histopathological features of meibomian gland (MG) tissue from cadaver donors to identify potential pathogenic processes that underlie MGD in humans.MethodsHistological analyses was performed on the MGs in the tarsal plates dissected from four cadaver donors, two young and two old adults, including a 36-year-old female (36F) and three males aged 30, 63 and 64 years (30M, 63M and 64M).ResultsThe MGs of 36F displayed normal anatomy and structure, whereas the MGs of 30M showed severe ductal obstruction with mild distortion. The obstruction was caused by increased cytokeratin levels in association with hyperproliferation, but not hyperkeratinisation. In two older males, moderate to severe MG atrophy was noted. Cell proliferation was significantly reduced in the MG acini of the two older donors as measured by Ki67 labelling index (6.0%±3.4% and 7.9%±2.8% in 63M and 64M, respectively) when compared with that of the two younger donors (23.2%±5.5% and 16.9%±4.8% in 30M and 36F, respectively) (p<0.001). The expression patterns of meibocyte differentiation biomarkers were similar in the older and younger donors.ConclusionOur histopathological study, based on a small sample size, suggests potentially distinct pathogenic mechanisms in MGD. In the young male adult, hyperproliferation and aberrant differentiation of the central ductal epithelia may lead to the obstruction by overproduced cytokeratins. In contrast, in older adults, decreased cell proliferation in acinar basal epithelia could be a contributing factor leading to MG glandular atrophy.</description><subject>Adult</subject><subject>Antibodies</subject><subject>Antigens</subject><subject>Atrophy</subject><subject>Biomarkers</subject><subject>Biomarkers - metabolism</subject><subject>Cell growth</subject><subject>Cell Proliferation</subject><subject>Clinical Science</subject><subject>Dry Eye Syndromes - metabolism</subject><subject>Dry Eye Syndromes - pathology</subject><subject>Female</subject><subject>Histology</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>Keratin-16 - metabolism</subject><subject>Keratin-17 - metabolism</subject><subject>Keratin-6 - metabolism</subject><subject>Ki-67 Antigen - metabolism</subject><subject>Lipids</subject><subject>Male</subject><subject>Meibomian Gland Dysfunction - metabolism</subject><subject>Meibomian Gland Dysfunction - pathology</subject><subject>Meibomian Glands - metabolism</subject><subject>Meibomian Glands - pathology</subject><subject>Middle Aged</subject><subject>Older people</subject><subject>Pathogenesis</subject><subject>Tissue Donors</subject><subject>Young adults</subject><issn>0007-1161</issn><issn>1468-2079</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>9YT</sourceid><sourceid>ACMMV</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqNkUtP3TAQhS3UCm6Bv4AiddNNWo8fk2RTqUKlVEXqBtaWk0xufJvEqZ2g8u8xuoAoK1Z-fedojg9jGfDPABK_1Ds_90tvh9EPueBQ5RKUQjxgG1BYpquiesc2nPMiB0A4Yh9i3KWjQCgO2ZEEXeoK1Yb9unRx8bNdej_47V1mpzaLNFCzuFvKaudHG_5QyOjfHChG56fMTVm_jnbKRnK1H13abYekiyfsfWeHSKeP6zG7ufh-fX6ZX_3-8fP821Vea10uuYCKhOhQNg1IgUpbWfMSWhQktYW2rYRA0kK1hQJh285qLDoF2GqwiKU8Zl_3vvNaj9Q2NC3BDmYOLg17Z7x15v-XyfVm629NIRG4xGTw6dEg-L8rxcWMLjY0pBTk12iE5Ok7QWqZ0I-v0J1fw5TiGaGkFKIoKpGock81wccYqHseBrh5aMy8bMw8NGb2jSXp2cswz8KnihIg90A97t5uew8zIqd7</recordid><startdate>20200701</startdate><enddate>20200701</enddate><creator>Reneker, Lixing W</creator><creator>Irlmeier, Rebecca T</creator><creator>Shui, Ying-Bo</creator><creator>Liu, Ying</creator><creator>Huang, Andrew J W</creator><general>BMJ Publishing Group LTD</general><general>BMJ Publishing Group</general><scope>9YT</scope><scope>ACMMV</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5622-1326</orcidid></search><sort><creationdate>20200701</creationdate><title>Histopathology and selective biomarker expression in human meibomian glands</title><author>Reneker, Lixing W ; Irlmeier, Rebecca T ; Shui, Ying-Bo ; Liu, Ying ; Huang, Andrew J W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b558t-219e22f63cc132645a3b081d62e35a1dd9226e524d7412adfa567f416d51a6683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adult</topic><topic>Antibodies</topic><topic>Antigens</topic><topic>Atrophy</topic><topic>Biomarkers</topic><topic>Biomarkers - metabolism</topic><topic>Cell growth</topic><topic>Cell Proliferation</topic><topic>Clinical Science</topic><topic>Dry Eye Syndromes - metabolism</topic><topic>Dry Eye Syndromes - pathology</topic><topic>Female</topic><topic>Histology</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>Keratin-16 - metabolism</topic><topic>Keratin-17 - metabolism</topic><topic>Keratin-6 - metabolism</topic><topic>Ki-67 Antigen - metabolism</topic><topic>Lipids</topic><topic>Male</topic><topic>Meibomian Gland Dysfunction - metabolism</topic><topic>Meibomian Gland Dysfunction - pathology</topic><topic>Meibomian Glands - metabolism</topic><topic>Meibomian Glands - pathology</topic><topic>Middle Aged</topic><topic>Older people</topic><topic>Pathogenesis</topic><topic>Tissue Donors</topic><topic>Young adults</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Reneker, Lixing W</creatorcontrib><creatorcontrib>Irlmeier, Rebecca T</creatorcontrib><creatorcontrib>Shui, Ying-Bo</creatorcontrib><creatorcontrib>Liu, Ying</creatorcontrib><creatorcontrib>Huang, Andrew J W</creatorcontrib><collection>BMJ Open Access Journals</collection><collection>BMJ Journals:Open Access</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>Medical Database (Alumni Edition)</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 Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of ophthalmology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Reneker, Lixing W</au><au>Irlmeier, Rebecca T</au><au>Shui, Ying-Bo</au><au>Liu, Ying</au><au>Huang, Andrew J W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Histopathology and selective biomarker expression in human meibomian glands</atitle><jtitle>British journal of ophthalmology</jtitle><addtitle>Br J Ophthalmol</addtitle><date>2020-07-01</date><risdate>2020</risdate><volume>104</volume><issue>7</issue><spage>999</spage><epage>1004</epage><pages>999-1004</pages><issn>0007-1161</issn><eissn>1468-2079</eissn><abstract>Background/aimsMeibomian gland dysfunction (MGD) is the most common form of evaporative dry eye disease, but its pathogenesis is poorly understood. This study examined the histopathological features of meibomian gland (MG) tissue from cadaver donors to identify potential pathogenic processes that underlie MGD in humans.MethodsHistological analyses was performed on the MGs in the tarsal plates dissected from four cadaver donors, two young and two old adults, including a 36-year-old female (36F) and three males aged 30, 63 and 64 years (30M, 63M and 64M).ResultsThe MGs of 36F displayed normal anatomy and structure, whereas the MGs of 30M showed severe ductal obstruction with mild distortion. The obstruction was caused by increased cytokeratin levels in association with hyperproliferation, but not hyperkeratinisation. In two older males, moderate to severe MG atrophy was noted. Cell proliferation was significantly reduced in the MG acini of the two older donors as measured by Ki67 labelling index (6.0%±3.4% and 7.9%±2.8% in 63M and 64M, respectively) when compared with that of the two younger donors (23.2%±5.5% and 16.9%±4.8% in 30M and 36F, respectively) (p<0.001). The expression patterns of meibocyte differentiation biomarkers were similar in the older and younger donors.ConclusionOur histopathological study, based on a small sample size, suggests potentially distinct pathogenic mechanisms in MGD. In the young male adult, hyperproliferation and aberrant differentiation of the central ductal epithelia may lead to the obstruction by overproduced cytokeratins. In contrast, in older adults, decreased cell proliferation in acinar basal epithelia could be a contributing factor leading to MG glandular atrophy.</abstract><cop>England</cop><pub>BMJ Publishing Group LTD</pub><pmid>31585964</pmid><doi>10.1136/bjophthalmol-2019-314466</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0002-5622-1326</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Antibodies Antigens Atrophy Biomarkers Biomarkers - metabolism Cell growth Cell Proliferation Clinical Science Dry Eye Syndromes - metabolism Dry Eye Syndromes - pathology Female Histology Humans Immunoenzyme Techniques Keratin-16 - metabolism Keratin-17 - metabolism Keratin-6 - metabolism Ki-67 Antigen - metabolism Lipids Male Meibomian Gland Dysfunction - metabolism Meibomian Gland Dysfunction - pathology Meibomian Glands - metabolism Meibomian Glands - pathology Middle Aged Older people Pathogenesis Tissue Donors Young adults |
| title | Histopathology and selective biomarker expression in human meibomian glands |
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