The role of Fas-mediated apoptosis in otitis media: Observations in the lpr/ lpr mouse
Apoptosis, or programmed cell death, is a critical regulatory mechanism involved in the function, homeostasis and stimulus response of many organ systems. In the middle ear, apoptosis could participate in mucosal remodeling or leukocyte clearance during otitis media (OM). Fas is a death receptor tha...
Gespeichert in:
| Veröffentlicht in: | Hearing research 2005-09, Vol.207 (1), p.110-116 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 116 |
|---|---|
| container_issue | 1 |
| container_start_page | 110 |
| container_title | Hearing research |
| container_volume | 207 |
| creator | Rivkin, Alexander Z. Palacios, Sean D. Pak, Kwang Bennett, Thecla Ryan, Allen F. |
| description | Apoptosis, or programmed cell death, is a critical regulatory mechanism involved in the function, homeostasis and stimulus response of many organ systems. In the middle ear, apoptosis could participate in mucosal remodeling or leukocyte clearance during otitis media (OM).
Fas is a death receptor that can contribute to apoptosis in a variety of cell types. To assess the role of Fas signaling in OM, we probed for expression of Fas and Fas ligand (FasL) by polymerase chain reaction (PCR) during bacterial OM in the rat. In addition, we assessed the response of the middle ear to endotoxin, an inflammatory bacterial product that has been used as a model for otitis media in the mouse, in normal and Fas deficient mice. We saw evidence of increased expression of Fas and Fas ligand during bacterial OM. Moreover, the intensity of the mucosal response to endotoxin was significantly greater and the resolution of the response was prolonged in Fas deficient mice. Prolonged resolution of mucosal hyperplasia may reflect reduced apoptosis of the hyperplastic mucosal cells. Elucidation of the pathways that regulate the mucosal hyperplastic response during otitis media brings us closer to manipulating them in the interest of reducing the chronic complications of this disease. |
| doi_str_mv | 10.1016/j.heares.2005.04.010 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_68591843</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0378595505001577</els_id><sourcerecordid>68591843</sourcerecordid><originalsourceid>FETCH-LOGICAL-c390t-a9ae2d984f4ff618075c5fd6c96d8c88df3537cc2643bb970bf19ce8441132f93</originalsourceid><addsrcrecordid>eNp9kE1LxDAQhoMouq7-A5Fe9NaaNEmbeBBE_IIFL-o1pOkEs3SbmmQF_71Zd8Gbl2RgnnmZeRA6I7gimDRXy-oDdIBY1RjzCrMKE7yHZkS0ouRCkn00w3RTS86P0HGMS4wJp6w-REeEy1a0vJmh99cPKIIfoPC2eNCxXEHvdIK-0JOfko8uFm4sfHIpV7_N6-KlixC-dHJ-_O2mnDFM4WrzFCu_jnCCDqweIpzu_jl6e7h_vXsqFy-Pz3e3i9JQiVOppYa6l4JZZm1DBG654bZvjGx6YYToLeW0NaZuGO062eLOEmlAMEYIra2kc3S5zZ2C_1xDTGrlooFh0CPkPVQjuCSC0QyyLWiCjzGAVVNwKx2-FcFq41Mt1dan2vhUmKnsM4-d7_LXXT7-b2gnMAMXO0BHowcb9Ghc_ONaUnMmSeZuthxkG18OgorGwWiy0AAmqd67_zf5AX-slSQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>68591843</pqid></control><display><type>article</type><title>The role of Fas-mediated apoptosis in otitis media: Observations in the lpr/ lpr mouse</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Rivkin, Alexander Z. ; Palacios, Sean D. ; Pak, Kwang ; Bennett, Thecla ; Ryan, Allen F.</creator><creatorcontrib>Rivkin, Alexander Z. ; Palacios, Sean D. ; Pak, Kwang ; Bennett, Thecla ; Ryan, Allen F.</creatorcontrib><description>Apoptosis, or programmed cell death, is a critical regulatory mechanism involved in the function, homeostasis and stimulus response of many organ systems. In the middle ear, apoptosis could participate in mucosal remodeling or leukocyte clearance during otitis media (OM).
Fas is a death receptor that can contribute to apoptosis in a variety of cell types. To assess the role of Fas signaling in OM, we probed for expression of Fas and Fas ligand (FasL) by polymerase chain reaction (PCR) during bacterial OM in the rat. In addition, we assessed the response of the middle ear to endotoxin, an inflammatory bacterial product that has been used as a model for otitis media in the mouse, in normal and Fas deficient mice. We saw evidence of increased expression of Fas and Fas ligand during bacterial OM. Moreover, the intensity of the mucosal response to endotoxin was significantly greater and the resolution of the response was prolonged in Fas deficient mice. Prolonged resolution of mucosal hyperplasia may reflect reduced apoptosis of the hyperplastic mucosal cells. Elucidation of the pathways that regulate the mucosal hyperplastic response during otitis media brings us closer to manipulating them in the interest of reducing the chronic complications of this disease.</description><identifier>ISSN: 0378-5955</identifier><identifier>EISSN: 1878-5891</identifier><identifier>DOI: 10.1016/j.heares.2005.04.010</identifier><identifier>PMID: 15978756</identifier><identifier>CODEN: HERED3</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Animals ; Apoptosis ; Apoptosis - genetics ; Apoptosis - physiology ; Base Sequence ; Biological and medical sciences ; Chromosome aberrations ; Disease Models, Animal ; DNA - genetics ; Ear, auditive nerve, cochleovestibular tract, facial nerve: diseases, semeiology ; Fas ; Fas ligand ; Fas Ligand Protein ; fas Receptor ; Medical genetics ; Medical sciences ; Membrane Glycoproteins - genetics ; Membrane Glycoproteins - physiology ; Mice ; Mice, Inbred CBA ; Mice, Inbred MRL lpr ; Middle ear ; Non tumoral diseases ; Otitis media ; Otitis Media - genetics ; Otitis Media - pathology ; Otorhinolaryngology. Stomatology ; Polymerase Chain Reaction ; Rats ; Rats, Sprague-Dawley ; Receptors, Tumor Necrosis Factor - genetics ; Receptors, Tumor Necrosis Factor - physiology ; Tumor Necrosis Factors - genetics ; Tumor Necrosis Factors - physiology</subject><ispartof>Hearing research, 2005-09, Vol.207 (1), p.110-116</ispartof><rights>2005 Elsevier B.V.</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-a9ae2d984f4ff618075c5fd6c96d8c88df3537cc2643bb970bf19ce8441132f93</citedby><cites>FETCH-LOGICAL-c390t-a9ae2d984f4ff618075c5fd6c96d8c88df3537cc2643bb970bf19ce8441132f93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0378595505001577$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17125491$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15978756$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rivkin, Alexander Z.</creatorcontrib><creatorcontrib>Palacios, Sean D.</creatorcontrib><creatorcontrib>Pak, Kwang</creatorcontrib><creatorcontrib>Bennett, Thecla</creatorcontrib><creatorcontrib>Ryan, Allen F.</creatorcontrib><title>The role of Fas-mediated apoptosis in otitis media: Observations in the lpr/ lpr mouse</title><title>Hearing research</title><addtitle>Hear Res</addtitle><description>Apoptosis, or programmed cell death, is a critical regulatory mechanism involved in the function, homeostasis and stimulus response of many organ systems. In the middle ear, apoptosis could participate in mucosal remodeling or leukocyte clearance during otitis media (OM).
Fas is a death receptor that can contribute to apoptosis in a variety of cell types. To assess the role of Fas signaling in OM, we probed for expression of Fas and Fas ligand (FasL) by polymerase chain reaction (PCR) during bacterial OM in the rat. In addition, we assessed the response of the middle ear to endotoxin, an inflammatory bacterial product that has been used as a model for otitis media in the mouse, in normal and Fas deficient mice. We saw evidence of increased expression of Fas and Fas ligand during bacterial OM. Moreover, the intensity of the mucosal response to endotoxin was significantly greater and the resolution of the response was prolonged in Fas deficient mice. Prolonged resolution of mucosal hyperplasia may reflect reduced apoptosis of the hyperplastic mucosal cells. Elucidation of the pathways that regulate the mucosal hyperplastic response during otitis media brings us closer to manipulating them in the interest of reducing the chronic complications of this disease.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis - physiology</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Chromosome aberrations</subject><subject>Disease Models, Animal</subject><subject>DNA - genetics</subject><subject>Ear, auditive nerve, cochleovestibular tract, facial nerve: diseases, semeiology</subject><subject>Fas</subject><subject>Fas ligand</subject><subject>Fas Ligand Protein</subject><subject>fas Receptor</subject><subject>Medical genetics</subject><subject>Medical sciences</subject><subject>Membrane Glycoproteins - genetics</subject><subject>Membrane Glycoproteins - physiology</subject><subject>Mice</subject><subject>Mice, Inbred CBA</subject><subject>Mice, Inbred MRL lpr</subject><subject>Middle ear</subject><subject>Non tumoral diseases</subject><subject>Otitis media</subject><subject>Otitis Media - genetics</subject><subject>Otitis Media - pathology</subject><subject>Otorhinolaryngology. Stomatology</subject><subject>Polymerase Chain Reaction</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Tumor Necrosis Factor - genetics</subject><subject>Receptors, Tumor Necrosis Factor - physiology</subject><subject>Tumor Necrosis Factors - genetics</subject><subject>Tumor Necrosis Factors - physiology</subject><issn>0378-5955</issn><issn>1878-5891</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1LxDAQhoMouq7-A5Fe9NaaNEmbeBBE_IIFL-o1pOkEs3SbmmQF_71Zd8Gbl2RgnnmZeRA6I7gimDRXy-oDdIBY1RjzCrMKE7yHZkS0ouRCkn00w3RTS86P0HGMS4wJp6w-REeEy1a0vJmh99cPKIIfoPC2eNCxXEHvdIK-0JOfko8uFm4sfHIpV7_N6-KlixC-dHJ-_O2mnDFM4WrzFCu_jnCCDqweIpzu_jl6e7h_vXsqFy-Pz3e3i9JQiVOppYa6l4JZZm1DBG654bZvjGx6YYToLeW0NaZuGO062eLOEmlAMEYIra2kc3S5zZ2C_1xDTGrlooFh0CPkPVQjuCSC0QyyLWiCjzGAVVNwKx2-FcFq41Mt1dan2vhUmKnsM4-d7_LXXT7-b2gnMAMXO0BHowcb9Ghc_ONaUnMmSeZuthxkG18OgorGwWiy0AAmqd67_zf5AX-slSQ</recordid><startdate>20050901</startdate><enddate>20050901</enddate><creator>Rivkin, Alexander Z.</creator><creator>Palacios, Sean D.</creator><creator>Pak, Kwang</creator><creator>Bennett, Thecla</creator><creator>Ryan, Allen F.</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</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><scope>8BM</scope></search><sort><creationdate>20050901</creationdate><title>The role of Fas-mediated apoptosis in otitis media: Observations in the lpr/ lpr mouse</title><author>Rivkin, Alexander Z. ; Palacios, Sean D. ; Pak, Kwang ; Bennett, Thecla ; Ryan, Allen F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-a9ae2d984f4ff618075c5fd6c96d8c88df3537cc2643bb970bf19ce8441132f93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Apoptosis - physiology</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Chromosome aberrations</topic><topic>Disease Models, Animal</topic><topic>DNA - genetics</topic><topic>Ear, auditive nerve, cochleovestibular tract, facial nerve: diseases, semeiology</topic><topic>Fas</topic><topic>Fas ligand</topic><topic>Fas Ligand Protein</topic><topic>fas Receptor</topic><topic>Medical genetics</topic><topic>Medical sciences</topic><topic>Membrane Glycoproteins - genetics</topic><topic>Membrane Glycoproteins - physiology</topic><topic>Mice</topic><topic>Mice, Inbred CBA</topic><topic>Mice, Inbred MRL lpr</topic><topic>Middle ear</topic><topic>Non tumoral diseases</topic><topic>Otitis media</topic><topic>Otitis Media - genetics</topic><topic>Otitis Media - pathology</topic><topic>Otorhinolaryngology. Stomatology</topic><topic>Polymerase Chain Reaction</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Tumor Necrosis Factor - genetics</topic><topic>Receptors, Tumor Necrosis Factor - physiology</topic><topic>Tumor Necrosis Factors - genetics</topic><topic>Tumor Necrosis Factors - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rivkin, Alexander Z.</creatorcontrib><creatorcontrib>Palacios, Sean D.</creatorcontrib><creatorcontrib>Pak, Kwang</creatorcontrib><creatorcontrib>Bennett, Thecla</creatorcontrib><creatorcontrib>Ryan, Allen F.</creatorcontrib><collection>Pascal-Francis</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><collection>ComDisDome</collection><jtitle>Hearing research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rivkin, Alexander Z.</au><au>Palacios, Sean D.</au><au>Pak, Kwang</au><au>Bennett, Thecla</au><au>Ryan, Allen F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of Fas-mediated apoptosis in otitis media: Observations in the lpr/ lpr mouse</atitle><jtitle>Hearing research</jtitle><addtitle>Hear Res</addtitle><date>2005-09-01</date><risdate>2005</risdate><volume>207</volume><issue>1</issue><spage>110</spage><epage>116</epage><pages>110-116</pages><issn>0378-5955</issn><eissn>1878-5891</eissn><coden>HERED3</coden><abstract>Apoptosis, or programmed cell death, is a critical regulatory mechanism involved in the function, homeostasis and stimulus response of many organ systems. In the middle ear, apoptosis could participate in mucosal remodeling or leukocyte clearance during otitis media (OM).
Fas is a death receptor that can contribute to apoptosis in a variety of cell types. To assess the role of Fas signaling in OM, we probed for expression of Fas and Fas ligand (FasL) by polymerase chain reaction (PCR) during bacterial OM in the rat. In addition, we assessed the response of the middle ear to endotoxin, an inflammatory bacterial product that has been used as a model for otitis media in the mouse, in normal and Fas deficient mice. We saw evidence of increased expression of Fas and Fas ligand during bacterial OM. Moreover, the intensity of the mucosal response to endotoxin was significantly greater and the resolution of the response was prolonged in Fas deficient mice. Prolonged resolution of mucosal hyperplasia may reflect reduced apoptosis of the hyperplastic mucosal cells. Elucidation of the pathways that regulate the mucosal hyperplastic response during otitis media brings us closer to manipulating them in the interest of reducing the chronic complications of this disease.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>15978756</pmid><doi>10.1016/j.heares.2005.04.010</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0378-5955 |
| ispartof | Hearing research, 2005-09, Vol.207 (1), p.110-116 |
| issn | 0378-5955 1878-5891 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_68591843 |
| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals Apoptosis Apoptosis - genetics Apoptosis - physiology Base Sequence Biological and medical sciences Chromosome aberrations Disease Models, Animal DNA - genetics Ear, auditive nerve, cochleovestibular tract, facial nerve: diseases, semeiology Fas Fas ligand Fas Ligand Protein fas Receptor Medical genetics Medical sciences Membrane Glycoproteins - genetics Membrane Glycoproteins - physiology Mice Mice, Inbred CBA Mice, Inbred MRL lpr Middle ear Non tumoral diseases Otitis media Otitis Media - genetics Otitis Media - pathology Otorhinolaryngology. Stomatology Polymerase Chain Reaction Rats Rats, Sprague-Dawley Receptors, Tumor Necrosis Factor - genetics Receptors, Tumor Necrosis Factor - physiology Tumor Necrosis Factors - genetics Tumor Necrosis Factors - physiology |
| title | The role of Fas-mediated apoptosis in otitis media: Observations in the lpr/ lpr mouse |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-02T01%3A21%3A16IST&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=The%20role%20of%20Fas-mediated%20apoptosis%20in%20otitis%20media:%20Observations%20in%20the%20lpr/%20lpr%20mouse&rft.jtitle=Hearing%20research&rft.au=Rivkin,%20Alexander%20Z.&rft.date=2005-09-01&rft.volume=207&rft.issue=1&rft.spage=110&rft.epage=116&rft.pages=110-116&rft.issn=0378-5955&rft.eissn=1878-5891&rft.coden=HERED3&rft_id=info:doi/10.1016/j.heares.2005.04.010&rft_dat=%3Cproquest_cross%3E68591843%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=68591843&rft_id=info:pmid/15978756&rft_els_id=S0378595505001577&rfr_iscdi=true |