Keratinocyte growth factor prevents ischemia-induced delayed neuronal death in the hippocampal CA1 field of the gerbil brain

Sadohara, Tomohiro; Sugahara, Kazuhiro; Urashima, Yukari; Terasaki, Hidenori; Iyama, Ken Ichi

doi:10.1097/00001756-200101220-00022

Cited by 14 publications

(6 citation statements)

References 21 publications

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“…Recent studies have shown an anti-apoptotic effect of KGF on various tissues such as epidermal cells [29], neural cells [30] and hepatocytes [31]. In this study KGF could have exerted such a role on transplanted cells in the early days after transplantation, a time at which some loss of tissue is known to occur [32].…”

Section: Effect Of Kgf On Beta Cell and Ductal Cell Proliferationmentioning

confidence: 72%

Keratinocyte growth factor and beta-cell differentiation in human fetal pancreatic endocrine precursor cells

et al. 2003

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Aims and hypothesis. Keratinocyte growth factor (KGF) is a member of the heparin-binding fibroblast growth factor family with a high degree of specificity for epithelial cells in vitro and in vivo. Our aim was to study the effect of KGF on beta-cell growth and differentiation on islet-like cell clusters derived from human fetal pancreas. Methods. We investigated the effects of KGF, in vitro, on beta-cell differentiation from undifferentiated pancreatic precursor cells and in vivo after transplantating human fetal pancreatic cells into athymic rats treated with KGF. Results. Treatment of islet-like cell clusters with KGF in vitro did not change the number of insulin producing cells, as measured by the measurement of insulin content or DNA. The in vivo treatment of recipient rats with KGF increased the number of beta cells within the grafts 8 weeks after transplantation. At this time, glucose-stimulated insulin secretion was evaluated by glucose stimulation tests in rats bearing the transplants. Measurements of human C-peptide concentrations after glucose challenge showed that the newly differentiated beta cells in the KGF-treated group were functionally competent as opposed to the control group, where the graft failed to release insulin appropriately. Conclusion/interpretation. These findings suggest that in vivo, KGF is capable of inducing human fetal beta-cell expansion. The growth promoting effect of KGF on beta cells occurred mainly through the activation of ductal cell proliferation and their subsequent differentiation into beta cells. [Diabetologia (2003) 46:822-829]

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Section: Effect Of Kgf On Beta Cell and Ductal Cell Proliferationmentioning

confidence: 72%

Keratinocyte growth factor and beta-cell differentiation in human fetal pancreatic endocrine precursor cells

et al. 2003

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“…OPN binding to α4β1 integrin has been implicated in the organization of endothelial cells in the developing vasculature, the extravasation of immune cells into tissues, and the emigration of neuroblasts[37]. Fibroblast growth factor-7 (FGF7 or KGF), which was increased 173-fold in our study, is known to mediate cell proliferation and motility, protect against cell death,[38] and has been shown to limit ischemia-induced neuronal death[39]. We also found a 44-fold increase in olfactomedin-1 (Olfm1), which has been implicated in neuronal differentiation, axon extension and cell survival[40].…”

Section: Discussionmentioning

confidence: 96%

Induction of neuro-protective/regenerative genes in stem cells infiltrating post-ischemic brain tissue

Yılmaz

Alexander

Yılmaz

et al. 2010

Exp & Trans Stroke Med

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Background-Although the therapeutic potential of bone marrow-derived stromal stem cells (BMSC) has been demonstrated in different experimental models of ischemic stroke, it remains unclear how stem cells (SC) induce neuroprotection following stroke. In this study, we describe a novel method for isolating BMSC that infiltrate postischemic brain tissue and use this method to identify the genes that are persistently activated or depressed in BMSC that infiltrate brain tissue following ischemic stroke.Methods-Ischemic strokes were induced in C57BL/6 mice by middle cerebral artery occlusion for 1 h, followed by reperfusion. BMSC were isolated from H-2 Kb-tsA58 (immortomouse™) mice, and were administered (i.v.) 24 h after reperfusion. At the peak of therapeutic improvement (14 days after the ischemic insult), infarcted brain tissue was isolated, and the BMSC were isolated by culturing at 33°C. Microarray analysis and RT-PCR were performed to compare differential gene expression between naïve and infiltrating BMSC populations.Results-Z-scoring revealed dramatic differences in the expression of extracellular genes between naïve and infiltrating BMSC. Pair-wise analysis detected 80 extracellular factor genes that were up-regulated (≥ 2 fold, P < 0.05, Benjamini-Hochberg correction) between naïve and infiltrated BMSC. Although several anticipated neuroregenerative, nerve guidance and angiogenic factor (e.g., bFGF, bone morphogenetic protein, angiopoietins, neural growth factor) genes exhibited an increased expression, a remarkable induction of genes for nerve guidance survival (e.g., cytokine receptor-like factor 1, glypican 1, Dickkopf homolog 2, osteopontin) was also noted.Conclusions-BMSC infiltrating the post-ischemic brain exhibit persistent epigenetic changes in gene expression for numerous extracellular genes, compared to their naïve counterparts. These genes are relevant to the neuroprotection, regeneration and angiogenesis previously described following stem cell therapy in animal models of ischemic stroke.

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“…We first investigated the effect of KGF in the prevention of b-cell apoptosis in the pancreas of STZ/KGF rats. Anti-apoptotic effects of KGF on various tissues such as epidermal cells (Jeschke et al 2002), neural cells (Sadohara et al 2001), and hepatocytes (Senaldi et al 1998) have been described in numerous studies. It is known that STZ induces b-cell death partly by stimulation of apoptosis (Yamamoto et al 1981, Cardinal et al 2001.…”

Section: Discussionmentioning

confidence: 99%

Early administration of keratinocyte growth factor improves β-cell regeneration in rat with streptozotocin-induced diabetes

Movassat

Portha

2007

Journal of Endocrinology

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The aim of our study was to investigate the ability of keratinocyte growth factor (KGF; palifermin) in regulating b-cell growth in normal newborn rats and in rats with neonatal diabetes. Wistar rats were injected with streptozotocin (STZ) to induce diabetes on the day of birth. From days 2 to 6 after birth, animals received a daily s.c. injection of KGF (STZ/KGF group) and at the dose of 3 mg/kg body weight or saline solution (STZ groups). A group of non-diabetic Wistar rats was treated either with saline (Wistar group) or with KGF from days 2 to 6 after birth at the dose of 3 mg/kg body weight (Wistar/KGF group). b-cell mass was measured at day 7 after birth in all groups. b-and ductal cells replication were measured in all groups and apoptosis was assessed in the pancreas of 2-, 4-, and 7-day-old STZ and STZ/KGF rats. The total b-cell mass of the 7-day-old KGF/STZ neonates was significantly increased compared with that of age-matched STZ rats. b-cell replication rate was decreased at day 2 in the STZ/KGF group and was similar in the 4-and 7-day-old rats from STZ and STZ/KGF groups. Duct cell replication was significantly increased in the pancreas of 2-and 4-day-old KGF/STZ neonates when compared with that of age-matched rats from STZ control group. The rate of apoptosis in the neonatal pancreases of STZ and KGF/STZ groups was not significantly different. In non-diabetic Wistar rats, KGF treatment led to a slight but significant increase in duct cell proliferation at day 2 without significant changes in the total b-cell mass in the 7-dayold rats. We provide evidence for a growth-promoting effect of KGF during b-cell regeneration in neonatal diabetic rats. KGF exerts strong mitogenic effect on the pancreatic duct cells, thus expanding the population of precursor cells that subsequently differentiate into insulin-producing b-cells.

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Keratinocyte growth factor prevents ischemia-induced delayed neuronal death in the hippocampal CA1 field of the gerbil brain

Cited by 14 publications

References 21 publications

Keratinocyte growth factor and beta-cell differentiation in human fetal pancreatic endocrine precursor cells

Keratinocyte growth factor and beta-cell differentiation in human fetal pancreatic endocrine precursor cells

Induction of neuro-protective/regenerative genes in stem cells infiltrating post-ischemic brain tissue

Early administration of keratinocyte growth factor improves β-cell regeneration in rat with streptozotocin-induced diabetes

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