Ecrg4 attenuates the inflammatory proliferative response of mucosal epithelial cells to infection.
We report an inverse relationship between expression of the orphan candidate tumor suppressor gene esophageal cancer related gene 4 (Ecrg4), and the mucosal epithelial cell response to infection in the middle ear (ME). First, we found constitutive Ecrg4 mRNA expression in normal, quiescent ME mucosa...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2013-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3634077?pdf=render |
| _version_ | 1828172438728343552 |
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| author | Arwa Kurabi Kwang Pak Xitong Dang Raul Coimbra Brian P Eliceiri Allen F Ryan Andrew Baird |
| author_facet | Arwa Kurabi Kwang Pak Xitong Dang Raul Coimbra Brian P Eliceiri Allen F Ryan Andrew Baird |
| author_sort | Arwa Kurabi |
| collection | DOAJ |
| description | We report an inverse relationship between expression of the orphan candidate tumor suppressor gene esophageal cancer related gene 4 (Ecrg4), and the mucosal epithelial cell response to infection in the middle ear (ME). First, we found constitutive Ecrg4 mRNA expression in normal, quiescent ME mucosa that was confirmed by immunostainning of mucosal epithelial cells and immunoblotting of tissue lysates for the 14 kDa Ecrg4 protein. Upon experimental ME infection, Ecrg4 gene expression rapidly decreased by over 80%, between 3 to 48 hrs, post infection. When explants of this infected mucosa were placed in culture and transduced with an adenovirus (AD) encoding Ecrg4 gene (ADEcrg4), the proliferative and migratory responses of mucosal cells were significantly inhibited. ADEcrg4 transduction of control explants from uninfected MEs had no effect on basal growth and migration. Over-expression of Ecrg4 in vivo, by pre-injecting MEs with ADEcrg4 48 hrs prior to infection, prevented the natural down-regulation of Ecrg4, reduced mucosal proliferation and prevented inflammatory cell infiltration normally observed after infection. Taken together, these data support a hypothesis that Ecrg4 plays a role in coordinating the inflammatory and proliferative response to infection of mucosal epithelium suggesting a possible mechanism for its putative anti-tumor activity. |
| first_indexed | 2024-04-12T03:40:18Z |
| format | Article |
| id | doaj.art-c6310f3ebc5447ab8325eb724f796d58 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-04-12T03:40:18Z |
| publishDate | 2013-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-c6310f3ebc5447ab8325eb724f796d582022-12-22T03:49:18ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0184e6139410.1371/journal.pone.0061394Ecrg4 attenuates the inflammatory proliferative response of mucosal epithelial cells to infection.Arwa KurabiKwang PakXitong DangRaul CoimbraBrian P EliceiriAllen F RyanAndrew BairdWe report an inverse relationship between expression of the orphan candidate tumor suppressor gene esophageal cancer related gene 4 (Ecrg4), and the mucosal epithelial cell response to infection in the middle ear (ME). First, we found constitutive Ecrg4 mRNA expression in normal, quiescent ME mucosa that was confirmed by immunostainning of mucosal epithelial cells and immunoblotting of tissue lysates for the 14 kDa Ecrg4 protein. Upon experimental ME infection, Ecrg4 gene expression rapidly decreased by over 80%, between 3 to 48 hrs, post infection. When explants of this infected mucosa were placed in culture and transduced with an adenovirus (AD) encoding Ecrg4 gene (ADEcrg4), the proliferative and migratory responses of mucosal cells were significantly inhibited. ADEcrg4 transduction of control explants from uninfected MEs had no effect on basal growth and migration. Over-expression of Ecrg4 in vivo, by pre-injecting MEs with ADEcrg4 48 hrs prior to infection, prevented the natural down-regulation of Ecrg4, reduced mucosal proliferation and prevented inflammatory cell infiltration normally observed after infection. Taken together, these data support a hypothesis that Ecrg4 plays a role in coordinating the inflammatory and proliferative response to infection of mucosal epithelium suggesting a possible mechanism for its putative anti-tumor activity.http://europepmc.org/articles/PMC3634077?pdf=render |
| spellingShingle | Arwa Kurabi Kwang Pak Xitong Dang Raul Coimbra Brian P Eliceiri Allen F Ryan Andrew Baird Ecrg4 attenuates the inflammatory proliferative response of mucosal epithelial cells to infection. PLoS ONE |
| title | Ecrg4 attenuates the inflammatory proliferative response of mucosal epithelial cells to infection. |
| title_full | Ecrg4 attenuates the inflammatory proliferative response of mucosal epithelial cells to infection. |
| title_fullStr | Ecrg4 attenuates the inflammatory proliferative response of mucosal epithelial cells to infection. |
| title_full_unstemmed | Ecrg4 attenuates the inflammatory proliferative response of mucosal epithelial cells to infection. |
| title_short | Ecrg4 attenuates the inflammatory proliferative response of mucosal epithelial cells to infection. |
| title_sort | ecrg4 attenuates the inflammatory proliferative response of mucosal epithelial cells to infection |
| url | http://europepmc.org/articles/PMC3634077?pdf=render |
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