Claudin-18: unexpected regulator of lung alveolar epithelial cell proliferation
Claudin 18 (CLDN18) is a tight junction protein that is highly expressed in the lung. While mice lacking CLDN18 exhibit the expected loss of epithelial integrity in the lung, these animals also have unexpectedly large lungs. In this issue of the JCI, Zhou, Flodby, and colleagues reveal that the incr...
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| Veröffentlicht in: | The Journal of clinical investigation 2018-03, Vol.128 (3), p.903-905 |
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| description | Claudin 18 (CLDN18) is a tight junction protein that is highly expressed in the lung. While mice lacking CLDN18 exhibit the expected loss of epithelial integrity in the lung, these animals also have unexpectedly large lungs. In this issue of the JCI, Zhou, Flodby, and colleagues reveal that the increased lung size of Cldn18-/- mice is the result of increased type 2 alveolar epithelial (AT2) cell proliferation. This increase in proliferation was shown to be driven by translocation of the transcriptional regulator Yes-associated protein (YAP) to the nucleus and subsequent induction of proliferative pathways. CLDN18-deficent mice also had increased frequency of lung adenocarcinomas. Together, the results of this study advance our understanding of the mechanisms that likely regulate homeostasis of the normal lung as well as promote the proliferative state of malignant cells found in lung adenocarcinomas thought to originate from AT2 cells. |
| doi_str_mv | 10.1172/JCI99799 |
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While mice lacking CLDN18 exhibit the expected loss of epithelial integrity in the lung, these animals also have unexpectedly large lungs. In this issue of the JCI, Zhou, Flodby, and colleagues reveal that the increased lung size of Cldn18-/- mice is the result of increased type 2 alveolar epithelial (AT2) cell proliferation. This increase in proliferation was shown to be driven by translocation of the transcriptional regulator Yes-associated protein (YAP) to the nucleus and subsequent induction of proliferative pathways. CLDN18-deficent mice also had increased frequency of lung adenocarcinomas. 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While mice lacking CLDN18 exhibit the expected loss of epithelial integrity in the lung, these animals also have unexpectedly large lungs. In this issue of the JCI, Zhou, Flodby, and colleagues reveal that the increased lung size of Cldn18-/- mice is the result of increased type 2 alveolar epithelial (AT2) cell proliferation. This increase in proliferation was shown to be driven by translocation of the transcriptional regulator Yes-associated protein (YAP) to the nucleus and subsequent induction of proliferative pathways. CLDN18-deficent mice also had increased frequency of lung adenocarcinomas. Together, the results of this study advance our understanding of the mechanisms that likely regulate homeostasis of the normal lung as well as promote the proliferative state of malignant cells found in lung adenocarcinomas thought to originate from AT2 cells.</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>Alveolar Epithelial Cells</subject><subject>Alveoli</subject><subject>Animals</subject><subject>Biomedical research</subject><subject>Carcinogenesis</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Cell Cycle Proteins</subject><subject>Cell growth</subject><subject>Cell Proliferation</subject><subject>Claudins</subject><subject>Conflicts of interest</subject><subject>Development and progression</subject><subject>Epithelial cells</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Homeostasis</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Lung diseases</subject><subject>Lungs</subject><subject>Mice</subject><subject>Phosphoproteins</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Stem Cells</subject><subject>Tight Junctions</subject><subject>Transcription</subject><subject>Transport proteins</subject><subject>Yes-associated 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unexpected regulator of lung alveolar epithelial cell proliferation</title><author>Kotton, Darrell N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c643t-7010d37e51982807b979faa706e4fe8d089b457e455a6526eb5e529dc3a276aa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adaptor Proteins, Signal Transducing</topic><topic>Alveolar Epithelial Cells</topic><topic>Alveoli</topic><topic>Animals</topic><topic>Biomedical research</topic><topic>Carcinogenesis</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>Cell Cycle Proteins</topic><topic>Cell growth</topic><topic>Cell Proliferation</topic><topic>Claudins</topic><topic>Conflicts of interest</topic><topic>Development and progression</topic><topic>Epithelial cells</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Homeostasis</topic><topic>Kinases</topic><topic>Lung cancer</topic><topic>Lung diseases</topic><topic>Lungs</topic><topic>Mice</topic><topic>Phosphoproteins</topic><topic>Proteins</topic><topic>Rodents</topic><topic>Stem Cells</topic><topic>Tight Junctions</topic><topic>Transcription</topic><topic>Transport proteins</topic><topic>Yes-associated protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kotton, Darrell N</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Nursing and Allied Health Journals</collection><collection>ProQuest Health and 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| subjects | Adaptor Proteins, Signal Transducing Alveolar Epithelial Cells Alveoli Animals Biomedical research Carcinogenesis Care and treatment Cell cycle Cell Cycle Proteins Cell growth Cell Proliferation Claudins Conflicts of interest Development and progression Epithelial cells Gene expression Genetic aspects Health aspects Homeostasis Kinases Lung cancer Lung diseases Lungs Mice Phosphoproteins Proteins Rodents Stem Cells Tight Junctions Transcription Transport proteins Yes-associated protein |
| title | Claudin-18: unexpected regulator of lung alveolar epithelial cell proliferation |
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