Keratinocyte growth factor is an endogenous stimulant of rabbit gastric epithelial cell proliferation and migration in primary culture

Takahashi, Momoko; Ota, Satoshi; Ogura, Kohei; Hamada, Eiji; Shimada, Tomiko; Terano, Akira; Omata, M

doi:10.1016/0016-5085(95)27335-2

Cited by 5 publications

(8 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Messenger RNA for the KGF receptor is induced in the epidermis. 143 These results are in line with a study by Takahashi et al, 144 who could show KGF mRNA in fibroblasts but not epithelial cells.…”

Section: Keratinocyte Growth Factor (Kgf)supporting

confidence: 88%

“…This cytokine seems to specifically act on epithelial cells, inducing proliferation, differentiation and migration. [143][144][145] After skin injury mRNA transcription for KGF is induced in the dermis of the wound margin and in the hypodermis below the wound ground. Messenger RNA for the KGF receptor is induced in the epidermis.…”

Section: Keratinocyte Growth Factor (Kgf)mentioning

confidence: 99%

See 1 more Smart Citation

Prophylaxis and treatment of chemo- and radiotherapy-induced oral mucositis – are there new strategies?

Karthaus

Rosenthal

Ganser

1999

Bone Marrow Transplant

View full text Add to dashboard Cite

Summary:Oral mucositis is a major dose-limiting toxic effect of intensive cancer chemotherapy. Oral complications may lead to dose reduction or delay in further cancer treatment. Mucositis can be caused directly by cytotoxic effects and indirectly by sustained neutropenia after cytostatic therapy. An impaired mucosal barrier predisposes to life-threatening septic complications during aplasia. The prevalence of an oral focus in febrile neutropenia has been reported in up to 30% of cases and also reduces quality of life. The basic strategies aim at pain relief and prevention of bacterial and fungal infectious complications. However, no effective causal prophylaxis or treatment of oral mucositis is widely accepted. The introduction of cytokines, eg granulocytemacrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) for oral mucositis may be particularly effective and offer a new and hopeful approach. At present, the optimal growth factor, best schedule, effective dosage and best mode of application is not known.

show abstract

Section: Keratinocyte Growth Factor (Kgf)supporting

confidence: 88%

Section: Keratinocyte Growth Factor (Kgf)mentioning

confidence: 99%

Prophylaxis and treatment of chemo- and radiotherapy-induced oral mucositis – are there new strategies?

Karthaus

Rosenthal

Ganser

1999

Bone Marrow Transplant

View full text Add to dashboard Cite

show abstract

“…When administered parenterally to adult animals, KGF increases wet weight of intestine and stomach, exerts a positive influence on stem cell proliferation from the foregut to the colon, and causes a dramatic increase of cholesterol and triglyceride circulating levels (11,13). Some of these results were confirmed using rabbit gastric epithelial monolayers in which KGF stimulates cell proliferation and migration by itself or in combination with other mitogens (14). Another study (15) demonstrated that KGF-induced hypertriglyceridemia results mainly from stimulation of hepatic lipolysis.…”

mentioning

confidence: 83%

“…For comparative purposes, HGF (Calbiochem, La Jolla, CA, U.S.A.) was also added at 3, 10, 20 ng/mL to jejunal and colonic explants. The dosages used in this study were proven to stimulate proliferation and migration of gastric epithelial cells in primary culture (14).…”

Section: Methodsmentioning

confidence: 99%

Functional Characterization of the Keratinocyte Growth Factor System in Human Fetal Gastrointestinal Tract

et al. 2000

View full text Add to dashboard Cite

Keratinocyte growth factor (KGF) is a paracrine growth factor whose mRNA has been detected in human adult and rodent gut tissues together with its associated receptor. Our objectives were to assess the presence of immunoreactive KGF ligand and receptor proteins in human fetal gastrointestinal (GI) tract segments and to evaluate the role of exogenous KGF on cell proliferation and intestinal digestive functions. KGF (26 -28 kD doublet) was identified in esophagus, stomach, small intestine, and colon by Western blot. Its receptor (135 kD) was ubiquitously detected in proliferative and differentiated epithelial cells of each GI segment by use of indirect immunofluorescence (anti-bek, anti-K-sam). The addition of KGF to explants cultured in serum-free conditions greatly stimulated DNA synthesis in all GI tract tissues. The growth factor up-regulated intestinal sucrase-isomaltase and ␥-glutamyl-transpeptidase activities in jejunal explants, whereas it down-regulated these activities in colon explants. It is suggested that the KGF system likely represents an important paracrine pathway that is able to stimulate cell proliferation in all segments of the human fetal GI tract and to differentially regulate intestinal digestive functions. KGF or FGF-7 is a member of the heparin-binding growth factor family [reviewed by Baird and Klagsbrun (1)]. This growth factor is able to stimulate the proliferation of epithelial cells and to positively influence their polarization/differentiation status in culture (2-4). Its associated receptor (KGF-R) is virtually identical to the K-sam protein found in KATO-III cells and gastric carcinomas (5, 6), which is the product of an alternative transcript of the FGFR-2/bek gene. Splicing of the mRNA alters a small region of the extracellular domain of the receptor and confers increased capacity for KGF binding (7). One study (8) clearly demonstrated that the bek gene is expressed in great amounts in diverse epithelia (skin, intestine, stomach, kidney) of the mouse embryo and that the alternative transcript encoding the KGF-R represents the major form found in these tissues. Some other important features characterize this growth factor: 1) KGF is exclusively synthesized by mesenchymal cells and exerts its action on epithelial cells (9, 10) via KGF-R, and 2) as opposed to other growth factor receptors [epidermal growth factor/transforming growth factor (EGF/TGF␣), hepatocyte growth factor (HGF), insulin-like growth factor (IGF) associated with basolateral membranes of epithelial cells, KGF-R is also present in the cytoplasm (6).During the last years, attention has been focused on the possible implication of this paracrine growth factor in the regulation of GI physiology. Indeed, the observations that KGF and KGF-R mRNA are present in all segments of the adult rat GI tract and hepatocytes (11) as well as in fetal rat stomach (12) supported the concept that the KGF system could be involved in normal development and maintenance of digestive organs. When administered parenterally to adult animals, K...

show abstract

“…tors [46,47]. In this situation matrix metalloproteinase production is too low to cause degradation of the lamina propria matrix, while epithelial growth factors are able to stimulate crypt cell growth followed by hyperplasia [48].…”

Section: Immunological Findingsmentioning

confidence: 99%

In vitro Model of the Pathogenesis of Celiac Disease

Oberhuber

Schwarzenhofer²,

Vogelsang³

1998

Dig Dis

View full text Add to dashboard Cite

The in vitro challenge of duodenal mucosa with gliadin is a useful model to reproduce the immunological features of celiac disease (CD) and allows the study of early pathogenetic events in this disease. With this model it was shown that antigens such as ICAM-1 and HLA-DR are upregulated as early as 1–2 h after gliadin challenge in patients with CD. After 24 h the lamina propria contained CD4+ T cells expressing the IL-2 receptor α-chain, which is a sign of activation. Intraepithelial lymphocytes increased in number and showed proliferative activity. After in vitro stimulation with gliadin, endomysial antibodies were found in the supernatant of the cultured mucosa from patients with CD following a gluten-free diet. This supported the notion that endomysial antibodies are at least in part produced locally. The model was also successfully used to identify toxic constituents of gliadin. Presently, organ culture is not commonly used for diagnostic purposes.

show abstract

Keratinocyte growth factor is an endogenous stimulant of rabbit gastric epithelial cell proliferation and migration in primary culture

Cited by 5 publications

References 0 publications

Prophylaxis and treatment of chemo- and radiotherapy-induced oral mucositis – are there new strategies?

Prophylaxis and treatment of chemo- and radiotherapy-induced oral mucositis – are there new strategies?

Functional Characterization of the Keratinocyte Growth Factor System in Human Fetal Gastrointestinal Tract

In vitro Model of the Pathogenesis of Celiac Disease

Contact Info

Product

Resources

About