ArticleOncogene2004
HST-1/FGF-4 plays a critical role in crypt cell survival and facilitates epithelial cell restitution and proliferation.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- Geranylgeranyl Transferase Inhibitors Mitigate Intestinal Radiation Toxicity.International journal of radiation oncology, biology, physics · 2026Article
- Fibroblast Growth Factors for Nonalcoholic Fatty Liver Disease: Opportunities and Challenges.International journal of molecular sciences · 2023Review
- ERK Activity Imaging During Migration of Living Cells In Vitro and In Vivo.International journal of molecular sciences · 2019Review
- Activation of Erk in ileal epithelial cells engaged in ischemic-injury repair.Scientific reports · 2017Article
- Protected graft copolymer-formulated fibroblast growth factors mitigate the lethality of partial body irradiation injury.PloS one · 2017Article
- Research resource: Comprehensive expression atlas of the fibroblast growth factor system in adult mouse.Molecular endocrinology (Baltimore, Md.) · 2010Article
- Progress in researches about focal adhesion kinase in gastrointestinal tract.World journal of gastroenterology · 2009Review
- Smad3 knockout mice exhibit impaired intestinal mucosal healing.Laboratory investigation; a journal of technical methods and pathology · 2008Article
- Cellular and molecular mechanisms of the epithelial repair in IBD.Digestive diseases and sciences · 2005Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fibroblast growth factor-4 (HST-1/FGF-4) is a heparin-binding growth factor that influences on epithelial and many other cells through interaction with FGF receptors. It has been demonstrated that the HST-1/FGF-4 gene protects mice from lethal irradiation by preventing bone marrow damage and intestinal tract damage. However, the radioprotective mechanism is unknown. In this study, we have investigated the expression of Hst-1/Fgf-4 in mouse small intestine after irradiation, and determined the role of HST-1/FGF-4 in mouse intestinal crypt cell survival and epithelial cell proliferation and restitution. We found the induction of endogenous Hst-1/Fgf-4 expression in intestine when mice are exposed to 9.0 Gy irradiation. Laser-captured microdissection (LCM) coupled with RT-PCR analysis revealed that expression of Hst-1/Fgf-4 was found in epithelial cell of the villi and crypt cells. Pretreatment of HST-1/FGF-4 caused an increase in the number of surviving crypt cells, and clearly suppresses the radiation-induced apoptosis of the crypt cells. Moreover, exogenous HST-1/FGF-4 enhances epithelial cell restitution and proliferation in an in vitro model. These data suggest that HST-1/FGF-4 is induced by irradiation injury, and that HST-1/FGF-4 will find a therapeutic role in the prevention of intestinal cell toxicity following intensive chemotherapy and radiation therapy protocols, and in allogenic cell transplantation.
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