Repair of naphthalene-induced acute tracheal injury by basal cells depends on β-catenin
Objectives Little is known about the role of Wnt/β-catenin in postnatal airway homeostasis and basal cell function. This study aimed to investigate the role of Wnt signaling in the self-renewal of basal cells and the involvement of β-catenin in tracheal repair after naphthalene-induced injury. Metho...
Gespeichert in:
Veröffentlicht in: | The Journal of thoracic and cardiovascular surgery 2014-07, Vol.148 (1), p.322-332 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 332 |
---|---|
container_issue | 1 |
container_start_page | 322 |
container_title | The Journal of thoracic and cardiovascular surgery |
container_volume | 148 |
creator | Hsu, Han-Shui, MD, PhD Liu, Chen-Chi, MD Lin, Jiun-Han, MS Hsu, Tien-Wei, MS Su, Kelly, BS Hung, Shih-Chieh, MD, PhD |
description | Objectives Little is known about the role of Wnt/β-catenin in postnatal airway homeostasis and basal cell function. This study aimed to investigate the role of Wnt signaling in the self-renewal of basal cells and the involvement of β-catenin in tracheal repair after naphthalene-induced injury. Methods Mice were treated with naphthalene and injected with 4-hydroxytamoxifen. Injury and repair of the tracheal epithelium after naphthalene-mediated secretory cell depletion was assessed by a immunohistochemical study. The involvement of Wnt and β-catenin signaling in basal cell proliferation was investigated during in vitro expansion. Results Immunohistochemical analysis of tracheal epithelium in wild-type mice showed a reduction in the number of Clara cell secretory protein (CCSP+) and forkhead box transcription factor (Fox-J1+) cells on days 2 to 5 after naphthalene-induced injury; this cell population was regenerated by day 10. After flush labeling, bromodeoxyuridine-positive (BrdU+) cells and Ki67+ cells were observed in tracheal epithelium on days 2 to 5 but not on days 10 and 21. Confocal microscopy visualizing K5+ and BrdU+ cells showed that Wnt3a promotes proliferation of K5+ cells. Immunohistochemical analysis of K5+ and CCSP+ in tracheal epithelial cells from wild-type littermate and K5-Cre–mediated β-catenin knock-out mice showed that on day 3, the number of CCSP+ cells was decreased in all mice. On day 10, CCSP+ cells were present in wild-type littermate mice but absent in conditional knock-out mice. Conclusions Basal cells serve as stem cells in the tracheal epithelium, regenerating and maintaining tracheal epithelial cells in a mouse model of tracheal injury. β-Catenin is required for proliferation and self-renewal of tracheal epithelial cells. |
doi_str_mv | 10.1016/j.jtcvs.2013.10.039 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1537593871</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0022522313012646</els_id><sourcerecordid>1537593871</sourcerecordid><originalsourceid>FETCH-LOGICAL-c459t-4aad2932dbe36b78a2b77b295b3f6e03622b0097ba88c33493fd5680d70ef2133</originalsourceid><addsrcrecordid>eNqFkctq3TAQhkVpaE7TPkGhaNmNT0aSbdmLFkroJRAopC1kJ3QZc-T6yK5kB85r5UH6TJV70iyyCQgGDf8_l28IecNgy4DV5_22n-1t2nJgIme2INpnZMOglUXdVDfPyQaA86LiXJySlyn1ACCBtS_IKS95A5LJDbm5xkn7SMeOBj3t5p0eMGDhg1ssOqrtMiOdo7Y71AP1oV_igZr8dMp_i8OQqMMJg0t0DPTPXWH1jMGHV-Sk00PC1_fxjPz8_OnHxdfi6tuXy4uPV4Utq3YuSq0dbwV3BkVtZKO5kdLwtjKiqxFEzbmBvJLRTWOFKFvRuapuwEnAjjMhzsi7Y90pjr8XTLPa-7TOpQOOS1KsErJqRSNZloqj1MYxpYidmqLf63hQDNSKVPXqH1K1Il2TGWl2vb1vsJg9ugfPf4ZZ8P4owLzmrceokvUYMj4f0c7Kjf6JBh8e-e3gg7d6-IUHTP24xJAJKqYSV6C-r1ddj8oEMF6XtfgLn76d8w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1537593871</pqid></control><display><type>article</type><title>Repair of naphthalene-induced acute tracheal injury by basal cells depends on β-catenin</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>ScienceDirect Journals (5 years ago - present)</source><creator>Hsu, Han-Shui, MD, PhD ; Liu, Chen-Chi, MD ; Lin, Jiun-Han, MS ; Hsu, Tien-Wei, MS ; Su, Kelly, BS ; Hung, Shih-Chieh, MD, PhD</creator><creatorcontrib>Hsu, Han-Shui, MD, PhD ; Liu, Chen-Chi, MD ; Lin, Jiun-Han, MS ; Hsu, Tien-Wei, MS ; Su, Kelly, BS ; Hung, Shih-Chieh, MD, PhD</creatorcontrib><description>Objectives Little is known about the role of Wnt/β-catenin in postnatal airway homeostasis and basal cell function. This study aimed to investigate the role of Wnt signaling in the self-renewal of basal cells and the involvement of β-catenin in tracheal repair after naphthalene-induced injury. Methods Mice were treated with naphthalene and injected with 4-hydroxytamoxifen. Injury and repair of the tracheal epithelium after naphthalene-mediated secretory cell depletion was assessed by a immunohistochemical study. The involvement of Wnt and β-catenin signaling in basal cell proliferation was investigated during in vitro expansion. Results Immunohistochemical analysis of tracheal epithelium in wild-type mice showed a reduction in the number of Clara cell secretory protein (CCSP+) and forkhead box transcription factor (Fox-J1+) cells on days 2 to 5 after naphthalene-induced injury; this cell population was regenerated by day 10. After flush labeling, bromodeoxyuridine-positive (BrdU+) cells and Ki67+ cells were observed in tracheal epithelium on days 2 to 5 but not on days 10 and 21. Confocal microscopy visualizing K5+ and BrdU+ cells showed that Wnt3a promotes proliferation of K5+ cells. Immunohistochemical analysis of K5+ and CCSP+ in tracheal epithelial cells from wild-type littermate and K5-Cre–mediated β-catenin knock-out mice showed that on day 3, the number of CCSP+ cells was decreased in all mice. On day 10, CCSP+ cells were present in wild-type littermate mice but absent in conditional knock-out mice. Conclusions Basal cells serve as stem cells in the tracheal epithelium, regenerating and maintaining tracheal epithelial cells in a mouse model of tracheal injury. β-Catenin is required for proliferation and self-renewal of tracheal epithelial cells.</description><identifier>ISSN: 0022-5223</identifier><identifier>EISSN: 1097-685X</identifier><identifier>DOI: 10.1016/j.jtcvs.2013.10.039</identifier><identifier>PMID: 24280717</identifier><language>eng</language><publisher>United States: Mosby, Inc</publisher><subject>Animals ; beta Catenin - genetics ; beta Catenin - metabolism ; Cardiothoracic Surgery ; Cell Proliferation - drug effects ; Cells, Cultured ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Epithelial Cells - pathology ; Forkhead Transcription Factors - metabolism ; Keratin-15 ; Keratin-5 - genetics ; Keratin-5 - metabolism ; Ki-67 Antigen - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Naphthalenes - toxicity ; Regeneration - drug effects ; Respiratory Mucosa - drug effects ; Respiratory Mucosa - metabolism ; Respiratory Mucosa - pathology ; Stem Cells - drug effects ; Stem Cells - metabolism ; Stem Cells - pathology ; Time Factors ; Trachea - drug effects ; Trachea - metabolism ; Trachea - pathology ; Uteroglobin - metabolism ; Wnt Signaling Pathway - drug effects</subject><ispartof>The Journal of thoracic and cardiovascular surgery, 2014-07, Vol.148 (1), p.322-332</ispartof><rights>The American Association for Thoracic Surgery</rights><rights>2014 The American Association for Thoracic Surgery</rights><rights>Copyright © 2014 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-4aad2932dbe36b78a2b77b295b3f6e03622b0097ba88c33493fd5680d70ef2133</citedby><cites>FETCH-LOGICAL-c459t-4aad2932dbe36b78a2b77b295b3f6e03622b0097ba88c33493fd5680d70ef2133</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jtcvs.2013.10.039$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24280717$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hsu, Han-Shui, MD, PhD</creatorcontrib><creatorcontrib>Liu, Chen-Chi, MD</creatorcontrib><creatorcontrib>Lin, Jiun-Han, MS</creatorcontrib><creatorcontrib>Hsu, Tien-Wei, MS</creatorcontrib><creatorcontrib>Su, Kelly, BS</creatorcontrib><creatorcontrib>Hung, Shih-Chieh, MD, PhD</creatorcontrib><title>Repair of naphthalene-induced acute tracheal injury by basal cells depends on β-catenin</title><title>The Journal of thoracic and cardiovascular surgery</title><addtitle>J Thorac Cardiovasc Surg</addtitle><description>Objectives Little is known about the role of Wnt/β-catenin in postnatal airway homeostasis and basal cell function. This study aimed to investigate the role of Wnt signaling in the self-renewal of basal cells and the involvement of β-catenin in tracheal repair after naphthalene-induced injury. Methods Mice were treated with naphthalene and injected with 4-hydroxytamoxifen. Injury and repair of the tracheal epithelium after naphthalene-mediated secretory cell depletion was assessed by a immunohistochemical study. The involvement of Wnt and β-catenin signaling in basal cell proliferation was investigated during in vitro expansion. Results Immunohistochemical analysis of tracheal epithelium in wild-type mice showed a reduction in the number of Clara cell secretory protein (CCSP+) and forkhead box transcription factor (Fox-J1+) cells on days 2 to 5 after naphthalene-induced injury; this cell population was regenerated by day 10. After flush labeling, bromodeoxyuridine-positive (BrdU+) cells and Ki67+ cells were observed in tracheal epithelium on days 2 to 5 but not on days 10 and 21. Confocal microscopy visualizing K5+ and BrdU+ cells showed that Wnt3a promotes proliferation of K5+ cells. Immunohistochemical analysis of K5+ and CCSP+ in tracheal epithelial cells from wild-type littermate and K5-Cre–mediated β-catenin knock-out mice showed that on day 3, the number of CCSP+ cells was decreased in all mice. On day 10, CCSP+ cells were present in wild-type littermate mice but absent in conditional knock-out mice. Conclusions Basal cells serve as stem cells in the tracheal epithelium, regenerating and maintaining tracheal epithelial cells in a mouse model of tracheal injury. β-Catenin is required for proliferation and self-renewal of tracheal epithelial cells.</description><subject>Animals</subject><subject>beta Catenin - genetics</subject><subject>beta Catenin - metabolism</subject><subject>Cardiothoracic Surgery</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells, Cultured</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - pathology</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Keratin-15</subject><subject>Keratin-5 - genetics</subject><subject>Keratin-5 - metabolism</subject><subject>Ki-67 Antigen - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Naphthalenes - toxicity</subject><subject>Regeneration - drug effects</subject><subject>Respiratory Mucosa - drug effects</subject><subject>Respiratory Mucosa - metabolism</subject><subject>Respiratory Mucosa - pathology</subject><subject>Stem Cells - drug effects</subject><subject>Stem Cells - metabolism</subject><subject>Stem Cells - pathology</subject><subject>Time Factors</subject><subject>Trachea - drug effects</subject><subject>Trachea - metabolism</subject><subject>Trachea - pathology</subject><subject>Uteroglobin - metabolism</subject><subject>Wnt Signaling Pathway - drug effects</subject><issn>0022-5223</issn><issn>1097-685X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctq3TAQhkVpaE7TPkGhaNmNT0aSbdmLFkroJRAopC1kJ3QZc-T6yK5kB85r5UH6TJV70iyyCQgGDf8_l28IecNgy4DV5_22n-1t2nJgIme2INpnZMOglUXdVDfPyQaA86LiXJySlyn1ACCBtS_IKS95A5LJDbm5xkn7SMeOBj3t5p0eMGDhg1ssOqrtMiOdo7Y71AP1oV_igZr8dMp_i8OQqMMJg0t0DPTPXWH1jMGHV-Sk00PC1_fxjPz8_OnHxdfi6tuXy4uPV4Utq3YuSq0dbwV3BkVtZKO5kdLwtjKiqxFEzbmBvJLRTWOFKFvRuapuwEnAjjMhzsi7Y90pjr8XTLPa-7TOpQOOS1KsErJqRSNZloqj1MYxpYidmqLf63hQDNSKVPXqH1K1Il2TGWl2vb1vsJg9ugfPf4ZZ8P4owLzmrceokvUYMj4f0c7Kjf6JBh8e-e3gg7d6-IUHTP24xJAJKqYSV6C-r1ddj8oEMF6XtfgLn76d8w</recordid><startdate>20140701</startdate><enddate>20140701</enddate><creator>Hsu, Han-Shui, MD, PhD</creator><creator>Liu, Chen-Chi, MD</creator><creator>Lin, Jiun-Han, MS</creator><creator>Hsu, Tien-Wei, MS</creator><creator>Su, Kelly, BS</creator><creator>Hung, Shih-Chieh, MD, PhD</creator><general>Mosby, Inc</general><scope>6I.</scope><scope>AAFTH</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>20140701</creationdate><title>Repair of naphthalene-induced acute tracheal injury by basal cells depends on β-catenin</title><author>Hsu, Han-Shui, MD, PhD ; Liu, Chen-Chi, MD ; Lin, Jiun-Han, MS ; Hsu, Tien-Wei, MS ; Su, Kelly, BS ; Hung, Shih-Chieh, MD, PhD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-4aad2932dbe36b78a2b77b295b3f6e03622b0097ba88c33493fd5680d70ef2133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>beta Catenin - genetics</topic><topic>beta Catenin - metabolism</topic><topic>Cardiothoracic Surgery</topic><topic>Cell Proliferation - drug effects</topic><topic>Cells, Cultured</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelial Cells - pathology</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>Keratin-15</topic><topic>Keratin-5 - genetics</topic><topic>Keratin-5 - metabolism</topic><topic>Ki-67 Antigen - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Naphthalenes - toxicity</topic><topic>Regeneration - drug effects</topic><topic>Respiratory Mucosa - drug effects</topic><topic>Respiratory Mucosa - metabolism</topic><topic>Respiratory Mucosa - pathology</topic><topic>Stem Cells - drug effects</topic><topic>Stem Cells - metabolism</topic><topic>Stem Cells - pathology</topic><topic>Time Factors</topic><topic>Trachea - drug effects</topic><topic>Trachea - metabolism</topic><topic>Trachea - pathology</topic><topic>Uteroglobin - metabolism</topic><topic>Wnt Signaling Pathway - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hsu, Han-Shui, MD, PhD</creatorcontrib><creatorcontrib>Liu, Chen-Chi, MD</creatorcontrib><creatorcontrib>Lin, Jiun-Han, MS</creatorcontrib><creatorcontrib>Hsu, Tien-Wei, MS</creatorcontrib><creatorcontrib>Su, Kelly, BS</creatorcontrib><creatorcontrib>Hung, Shih-Chieh, MD, PhD</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect: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>MEDLINE - Academic</collection><jtitle>The Journal of thoracic and cardiovascular surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hsu, Han-Shui, MD, PhD</au><au>Liu, Chen-Chi, MD</au><au>Lin, Jiun-Han, MS</au><au>Hsu, Tien-Wei, MS</au><au>Su, Kelly, BS</au><au>Hung, Shih-Chieh, MD, PhD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Repair of naphthalene-induced acute tracheal injury by basal cells depends on β-catenin</atitle><jtitle>The Journal of thoracic and cardiovascular surgery</jtitle><addtitle>J Thorac Cardiovasc Surg</addtitle><date>2014-07-01</date><risdate>2014</risdate><volume>148</volume><issue>1</issue><spage>322</spage><epage>332</epage><pages>322-332</pages><issn>0022-5223</issn><eissn>1097-685X</eissn><abstract>Objectives Little is known about the role of Wnt/β-catenin in postnatal airway homeostasis and basal cell function. This study aimed to investigate the role of Wnt signaling in the self-renewal of basal cells and the involvement of β-catenin in tracheal repair after naphthalene-induced injury. Methods Mice were treated with naphthalene and injected with 4-hydroxytamoxifen. Injury and repair of the tracheal epithelium after naphthalene-mediated secretory cell depletion was assessed by a immunohistochemical study. The involvement of Wnt and β-catenin signaling in basal cell proliferation was investigated during in vitro expansion. Results Immunohistochemical analysis of tracheal epithelium in wild-type mice showed a reduction in the number of Clara cell secretory protein (CCSP+) and forkhead box transcription factor (Fox-J1+) cells on days 2 to 5 after naphthalene-induced injury; this cell population was regenerated by day 10. After flush labeling, bromodeoxyuridine-positive (BrdU+) cells and Ki67+ cells were observed in tracheal epithelium on days 2 to 5 but not on days 10 and 21. Confocal microscopy visualizing K5+ and BrdU+ cells showed that Wnt3a promotes proliferation of K5+ cells. Immunohistochemical analysis of K5+ and CCSP+ in tracheal epithelial cells from wild-type littermate and K5-Cre–mediated β-catenin knock-out mice showed that on day 3, the number of CCSP+ cells was decreased in all mice. On day 10, CCSP+ cells were present in wild-type littermate mice but absent in conditional knock-out mice. Conclusions Basal cells serve as stem cells in the tracheal epithelium, regenerating and maintaining tracheal epithelial cells in a mouse model of tracheal injury. β-Catenin is required for proliferation and self-renewal of tracheal epithelial cells.</abstract><cop>United States</cop><pub>Mosby, Inc</pub><pmid>24280717</pmid><doi>10.1016/j.jtcvs.2013.10.039</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0022-5223 |
ispartof | The Journal of thoracic and cardiovascular surgery, 2014-07, Vol.148 (1), p.322-332 |
issn | 0022-5223 1097-685X |
language | eng |
recordid | cdi_proquest_miscellaneous_1537593871 |
source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; ScienceDirect Journals (5 years ago - present) |
subjects | Animals beta Catenin - genetics beta Catenin - metabolism Cardiothoracic Surgery Cell Proliferation - drug effects Cells, Cultured Epithelial Cells - drug effects Epithelial Cells - metabolism Epithelial Cells - pathology Forkhead Transcription Factors - metabolism Keratin-15 Keratin-5 - genetics Keratin-5 - metabolism Ki-67 Antigen - metabolism Mice Mice, Inbred C57BL Mice, Transgenic Naphthalenes - toxicity Regeneration - drug effects Respiratory Mucosa - drug effects Respiratory Mucosa - metabolism Respiratory Mucosa - pathology Stem Cells - drug effects Stem Cells - metabolism Stem Cells - pathology Time Factors Trachea - drug effects Trachea - metabolism Trachea - pathology Uteroglobin - metabolism Wnt Signaling Pathway - drug effects |
title | Repair of naphthalene-induced acute tracheal injury by basal cells depends on β-catenin |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-15T08%3A02%3A40IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Repair%20of%20naphthalene-induced%20acute%20tracheal%20injury%20by%20basal%20cells%20depends%20on%20%CE%B2-catenin&rft.jtitle=The%20Journal%20of%20thoracic%20and%20cardiovascular%20surgery&rft.au=Hsu,%20Han-Shui,%20MD,%20PhD&rft.date=2014-07-01&rft.volume=148&rft.issue=1&rft.spage=322&rft.epage=332&rft.pages=322-332&rft.issn=0022-5223&rft.eissn=1097-685X&rft_id=info:doi/10.1016/j.jtcvs.2013.10.039&rft_dat=%3Cproquest_cross%3E1537593871%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1537593871&rft_id=info:pmid/24280717&rft_els_id=S0022522313012646&rfr_iscdi=true |