Impairment of corneal epithelial wound healing in a TRPV1-deficient mouse
To examine whether the absence or blockage of an ion channel receptor, transient receptor potential vanilloid subtype 1 (TRPV1), affects the healing of an epithelial injury using an experimental model of an epithelial defect in animal cornea. The expression of TRPV1 in the corneal epithelium was exa...
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| Veröffentlicht in: | Investigative ophthalmology & visual science 2014-04, Vol.55 (5), p.3295-3302 |
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| container_title | Investigative ophthalmology & visual science |
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| creator | Sumioka, Takayoshi Okada, Yuka Reinach, Peter S Shirai, Kumi Miyajima, Masayasu Yamanaka, Osamu Saika, Shizuya |
| description | To examine whether the absence or blockage of an ion channel receptor, transient receptor potential vanilloid subtype 1 (TRPV1), affects the healing of an epithelial injury using an experimental model of an epithelial defect in animal cornea.
The expression of TRPV1 in the corneal epithelium was examined using immunohistochemistry in mice and rats. The migration of the corneal epithelium was examined in epithelium-debrided rat cornea in organ culture in the presence or absence of a TRPV1 agonist or its antagonist. Epithelial migration and cell proliferation following the debridement were examined in the cornea of a TRPV1-null mouse. Real-time RT-PCR was performed in samples of healing corneas to analyze the expression pattern of epithelial migration-related components (i.e., IL-6, substance P, and TGF-β1).
TRPV1 was detected mainly in the basal layer of mouse or rat corneal epithelium. Adding a TRPV1 receptor agonist to the culture medium enhanced epithelial healing in the rat cornea, and a TRPV1 antagonist retarded it in organ culture. The loss of TRPV1 did not affect the histology of the mouse cornea. In vivo analysis showed the loss of TRPV1-impaired re-epithelialization of the debrided area of the corneal epithelium by the suppression of both cell migration and proliferation. The lack of TRPV1 suppressed the expression of IL-6 and substance P but not of TGF-β1 in response to epithelial debridement in mice.
TRPV1 signal is required for the upregulation of IL-6 and substance P and the healing of debrided corneal epithelium in mice. |
| doi_str_mv | 10.1167/iovs.13-13077 |
| format | Article |
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The expression of TRPV1 in the corneal epithelium was examined using immunohistochemistry in mice and rats. The migration of the corneal epithelium was examined in epithelium-debrided rat cornea in organ culture in the presence or absence of a TRPV1 agonist or its antagonist. Epithelial migration and cell proliferation following the debridement were examined in the cornea of a TRPV1-null mouse. Real-time RT-PCR was performed in samples of healing corneas to analyze the expression pattern of epithelial migration-related components (i.e., IL-6, substance P, and TGF-β1).
TRPV1 was detected mainly in the basal layer of mouse or rat corneal epithelium. Adding a TRPV1 receptor agonist to the culture medium enhanced epithelial healing in the rat cornea, and a TRPV1 antagonist retarded it in organ culture. The loss of TRPV1 did not affect the histology of the mouse cornea. In vivo analysis showed the loss of TRPV1-impaired re-epithelialization of the debrided area of the corneal epithelium by the suppression of both cell migration and proliferation. The lack of TRPV1 suppressed the expression of IL-6 and substance P but not of TGF-β1 in response to epithelial debridement in mice.
TRPV1 signal is required for the upregulation of IL-6 and substance P and the healing of debrided corneal epithelium in mice.</description><identifier>ISSN: 1552-5783</identifier><identifier>EISSN: 1552-5783</identifier><identifier>DOI: 10.1167/iovs.13-13077</identifier><identifier>PMID: 24781945</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Cell Proliferation ; Disease Models, Animal ; Epithelium, Corneal - injuries ; Epithelium, Corneal - metabolism ; Epithelium, Corneal - pathology ; Eye Injuries - genetics ; Eye Injuries - metabolism ; Eye Injuries - pathology ; Gene Expression Regulation ; Immunohistochemistry ; Mice ; Mice, Knockout ; RNA - genetics ; TRPV Cation Channels - biosynthesis ; TRPV Cation Channels - deficiency ; TRPV Cation Channels - genetics ; Wound Healing - genetics</subject><ispartof>Investigative ophthalmology & visual science, 2014-04, Vol.55 (5), p.3295-3302</ispartof><rights>Copyright 2014 The Association for Research in Vision and Ophthalmology, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c398t-54e27fc7249d75bd3f2854e14060f8f708bc9e3ce104dd2824de17939660bb783</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24781945$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sumioka, Takayoshi</creatorcontrib><creatorcontrib>Okada, Yuka</creatorcontrib><creatorcontrib>Reinach, Peter S</creatorcontrib><creatorcontrib>Shirai, Kumi</creatorcontrib><creatorcontrib>Miyajima, Masayasu</creatorcontrib><creatorcontrib>Yamanaka, Osamu</creatorcontrib><creatorcontrib>Saika, Shizuya</creatorcontrib><title>Impairment of corneal epithelial wound healing in a TRPV1-deficient mouse</title><title>Investigative ophthalmology & visual science</title><addtitle>Invest Ophthalmol Vis Sci</addtitle><description>To examine whether the absence or blockage of an ion channel receptor, transient receptor potential vanilloid subtype 1 (TRPV1), affects the healing of an epithelial injury using an experimental model of an epithelial defect in animal cornea.
The expression of TRPV1 in the corneal epithelium was examined using immunohistochemistry in mice and rats. The migration of the corneal epithelium was examined in epithelium-debrided rat cornea in organ culture in the presence or absence of a TRPV1 agonist or its antagonist. Epithelial migration and cell proliferation following the debridement were examined in the cornea of a TRPV1-null mouse. Real-time RT-PCR was performed in samples of healing corneas to analyze the expression pattern of epithelial migration-related components (i.e., IL-6, substance P, and TGF-β1).
TRPV1 was detected mainly in the basal layer of mouse or rat corneal epithelium. Adding a TRPV1 receptor agonist to the culture medium enhanced epithelial healing in the rat cornea, and a TRPV1 antagonist retarded it in organ culture. The loss of TRPV1 did not affect the histology of the mouse cornea. In vivo analysis showed the loss of TRPV1-impaired re-epithelialization of the debrided area of the corneal epithelium by the suppression of both cell migration and proliferation. The lack of TRPV1 suppressed the expression of IL-6 and substance P but not of TGF-β1 in response to epithelial debridement in mice.
TRPV1 signal is required for the upregulation of IL-6 and substance P and the healing of debrided corneal epithelium in mice.</description><subject>Animals</subject><subject>Cell Proliferation</subject><subject>Disease Models, Animal</subject><subject>Epithelium, Corneal - injuries</subject><subject>Epithelium, Corneal - metabolism</subject><subject>Epithelium, Corneal - pathology</subject><subject>Eye Injuries - genetics</subject><subject>Eye Injuries - metabolism</subject><subject>Eye Injuries - pathology</subject><subject>Gene Expression Regulation</subject><subject>Immunohistochemistry</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>RNA - genetics</subject><subject>TRPV Cation Channels - biosynthesis</subject><subject>TRPV Cation Channels - deficiency</subject><subject>TRPV Cation Channels - genetics</subject><subject>Wound Healing - genetics</subject><issn>1552-5783</issn><issn>1552-5783</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkEtPwzAQhC0EoqVw5Ipy5JLitZ04PqKKR6VKIFS4Wom9pkZ5EScg_j0pLYjTjkbfjnaHkHOgc4BUXvnmI8yBx8CplAdkCknC4kRm_PCfnpCTEN4oZQCMHpMJEzIDJZIpWS6rNvddhXUfNS4yTVdjXkbY-n6DpR_lZzPUNtqMrq9fI19HebR-enyB2KLzxm8Xq2YIeEqOXF4GPNvPGXm-vVkv7uPVw91ycb2KDVdZHycCmXRGMqGsTArLHctGDwRNqcucpFlhFHKDQIW1LGPCIkjFVZrSohh_mZHLXW7bNe8Dhl5XPhgsy7zG8Q4NCaecURBqROMdaromhA6dbjtf5d2XBqq37eltexq4_mlv5C_20UNRof2jf-vi3yy7ai8</recordid><startdate>20140429</startdate><enddate>20140429</enddate><creator>Sumioka, Takayoshi</creator><creator>Okada, Yuka</creator><creator>Reinach, Peter S</creator><creator>Shirai, Kumi</creator><creator>Miyajima, Masayasu</creator><creator>Yamanaka, Osamu</creator><creator>Saika, Shizuya</creator><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>20140429</creationdate><title>Impairment of corneal epithelial wound healing in a TRPV1-deficient mouse</title><author>Sumioka, Takayoshi ; Okada, Yuka ; Reinach, Peter S ; Shirai, Kumi ; Miyajima, Masayasu ; Yamanaka, Osamu ; Saika, Shizuya</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c398t-54e27fc7249d75bd3f2854e14060f8f708bc9e3ce104dd2824de17939660bb783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Cell Proliferation</topic><topic>Disease Models, Animal</topic><topic>Epithelium, Corneal - injuries</topic><topic>Epithelium, Corneal - metabolism</topic><topic>Epithelium, Corneal - pathology</topic><topic>Eye Injuries - genetics</topic><topic>Eye Injuries - metabolism</topic><topic>Eye Injuries - pathology</topic><topic>Gene Expression Regulation</topic><topic>Immunohistochemistry</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>RNA - genetics</topic><topic>TRPV Cation Channels - biosynthesis</topic><topic>TRPV Cation Channels - deficiency</topic><topic>TRPV Cation Channels - genetics</topic><topic>Wound Healing - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sumioka, Takayoshi</creatorcontrib><creatorcontrib>Okada, Yuka</creatorcontrib><creatorcontrib>Reinach, Peter S</creatorcontrib><creatorcontrib>Shirai, Kumi</creatorcontrib><creatorcontrib>Miyajima, Masayasu</creatorcontrib><creatorcontrib>Yamanaka, Osamu</creatorcontrib><creatorcontrib>Saika, Shizuya</creatorcontrib><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>Investigative ophthalmology & visual science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sumioka, Takayoshi</au><au>Okada, Yuka</au><au>Reinach, Peter S</au><au>Shirai, Kumi</au><au>Miyajima, Masayasu</au><au>Yamanaka, Osamu</au><au>Saika, Shizuya</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impairment of corneal epithelial wound healing in a TRPV1-deficient mouse</atitle><jtitle>Investigative ophthalmology & visual science</jtitle><addtitle>Invest Ophthalmol Vis Sci</addtitle><date>2014-04-29</date><risdate>2014</risdate><volume>55</volume><issue>5</issue><spage>3295</spage><epage>3302</epage><pages>3295-3302</pages><issn>1552-5783</issn><eissn>1552-5783</eissn><abstract>To examine whether the absence or blockage of an ion channel receptor, transient receptor potential vanilloid subtype 1 (TRPV1), affects the healing of an epithelial injury using an experimental model of an epithelial defect in animal cornea.
The expression of TRPV1 in the corneal epithelium was examined using immunohistochemistry in mice and rats. The migration of the corneal epithelium was examined in epithelium-debrided rat cornea in organ culture in the presence or absence of a TRPV1 agonist or its antagonist. Epithelial migration and cell proliferation following the debridement were examined in the cornea of a TRPV1-null mouse. Real-time RT-PCR was performed in samples of healing corneas to analyze the expression pattern of epithelial migration-related components (i.e., IL-6, substance P, and TGF-β1).
TRPV1 was detected mainly in the basal layer of mouse or rat corneal epithelium. Adding a TRPV1 receptor agonist to the culture medium enhanced epithelial healing in the rat cornea, and a TRPV1 antagonist retarded it in organ culture. The loss of TRPV1 did not affect the histology of the mouse cornea. In vivo analysis showed the loss of TRPV1-impaired re-epithelialization of the debrided area of the corneal epithelium by the suppression of both cell migration and proliferation. The lack of TRPV1 suppressed the expression of IL-6 and substance P but not of TGF-β1 in response to epithelial debridement in mice.
TRPV1 signal is required for the upregulation of IL-6 and substance P and the healing of debrided corneal epithelium in mice.</abstract><cop>United States</cop><pmid>24781945</pmid><doi>10.1167/iovs.13-13077</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Cell Proliferation Disease Models, Animal Epithelium, Corneal - injuries Epithelium, Corneal - metabolism Epithelium, Corneal - pathology Eye Injuries - genetics Eye Injuries - metabolism Eye Injuries - pathology Gene Expression Regulation Immunohistochemistry Mice Mice, Knockout RNA - genetics TRPV Cation Channels - biosynthesis TRPV Cation Channels - deficiency TRPV Cation Channels - genetics Wound Healing - genetics |
| title | Impairment of corneal epithelial wound healing in a TRPV1-deficient mouse |
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