Role of Fgf10 in cell proliferation in white adipose tissue

Konishi, Morichika; Asaki, Toshiyuki; Koike, Naomi; Miwa, Hiroyuki; Miyake, Ayumi; Itoh, Nobuyuki

doi:10.1016/j.mce.2006.01.010

Cited by 35 publications

(35 citation statements)

References 21 publications

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“…It seems that only the blastema cells have a competence to Fgf signalling probably due to the presence of Fgf receptor expression (Poss et al, 2000). Although we did not assess the mitogenic activity of Fgf10a, it is reasonable to assume that this protein could possess a function overlapping with that of Fgf3 (Konishi et al, 2006;Shin et al, 2006).…”

Section: Functions Of Fgf3 and Fgf10a During Regenerationmentioning

confidence: 96%

“…A number of studies have suggested that Fgfs, including Fgf3 and Fgf10a, have mitogenic activity (Konishi et al, 2006;Shin et al, 2006;Wang et al, 2007;Itoh and Ornitz, 2008); however, their functions during fin regeneration have not yet been explored. In this study, we performed a gain-of-function analysis of fgf3 in the cultured blastema explants and demonstrated that Fgf3 promotes cell proliferation.…”

Section: Functions Of Fgf3 and Fgf10a During Regenerationmentioning

confidence: 99%

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Fgf signalling controls diverse aspects of fin regeneration

et al. 2016

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Studies have shown that fibroblast growth factor (Fgf ) signalling is necessary for appendage regeneration, but its exact function and the ligands involved during regeneration have not yet been elucidated. Here, we performed comprehensive expression analyses and identified fgf20a and fgf3/10a as major Fgf ligands in the wound epidermis and blastema, respectively. To reveal the target cells and processes of Fgf signalling, we performed a transplantation experiment of mesenchymal cells that express the dominantnegative Fgf receptor 1 (dnfgfr1) under control of the heat-shock promoter. This mosaic knockdown analysis suggested that Fgf signalling is directly required for fin ray mesenchyme to form the blastema at the early pre-blastema stage and to activate the regenerative cell proliferation at a later post-blastema stage. These results raised the possibility that the early epidermal Fgf20a and the later blastemal Fgf3/10a could be responsible for these respective processes. We demonstrated by gain-of-function analyses that Fgf20a induces the expression of distal blastema marker junbl, and that Fgf3 promotes blastema cell proliferation. Our study highlights that Fgfs in the wound epidermis and blastema have distinct functions to regulate fin regeneration cooperatively.

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Section: Functions Of Fgf3 and Fgf10a During Regenerationmentioning

confidence: 96%

Section: Functions Of Fgf3 and Fgf10a During Regenerationmentioning

confidence: 99%

Fgf signalling controls diverse aspects of fin regeneration

et al. 2016

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“…Interestingly, Fgf10 also stimulates cell proliferation in white adipose tissue (Konishi et al, 2006), and Fgf10-null embryos display impaired white adipose tissue formation (Asaki et al, 2004;Mailleux et al, 2002). A recent study demonstrated that postnatal day (P) 8 mouse lipofibroblasts expressing low levels of platelet derived growth factor receptor, alpha polypeptide (Pdgfra) express high levels of Fgf10 and its receptors Fgfr1b and Fgfr2b (McGowan and McCoy, 2015).…”

Section: Introductionmentioning

confidence: 99%

Evidence for the involvement of Fibroblast Growth Factor 10 in lipofibroblast formation during embryonic lung development

et al. 2015

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Lipid-containing alveolar interstitial fibroblasts (lipofibroblasts) are increasingly recognized as an important component of the epithelial stem cell niche in the rodent lung. Although lipofibroblasts were initially believed merely to assist type 2 alveolar epithelial cells in surfactant production during neonatal life, recent evidence suggests that these cells are indispensable for survival and growth of epithelial stem cells during adulthood. Despite increasing interest in lipofibroblast biology, little is known about their cellular origin or the molecular pathways controlling their formation during embryonic development. Here, we show that a population of lipid-droplet-containing stromal cells emerges in the developing mouse lung between E15.5 and E16.5. This is accompanied by significant upregulation, in the lung mesenchyme, of peroxisome proliferator-activated receptor gamma (master switch of lipogenesis), adipose differentiation-related protein (marker of mature lipofibroblasts) and fibroblast growth factor 10 (previously shown to identify a subpopulation of lipofibroblast progenitors). We also demonstrate that although only a subpopulation of total embryonic lipofibroblasts derives from Fgf10 + progenitor cells, in vivo knockdown of Fgfr2b ligand activity and reduction in Fgf10 expression lead to global reduction in the expression levels of lipofibroblast markers at E18.5. Constitutive Fgfr1b knockouts and mutants with conditional partial inactivation of Fgfr2b in the lung mesenchyme reveal the involvement of both receptors in lipofibroblast formation and suggest a possible compensation between the two receptors. We also provide data from human fetal lungs to demonstrate the relevance of our discoveries to humans. Our results reveal an essential role for Fgf10 signaling in the formation of lipofibroblasts during late lung development.

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“…ChREBP expression is also up-regulated by insulin and glucose in 3T3-L1 adipocytes [17]. Fibroblast growth factor 10 (FGF10), a member of the FGF family secreted by cultured 3T3-L1 preadipocytes, plays a crucial role in enhancing both adipogenesis and preadipocyte proliferation [18,19]. Clarification of the molecular mechanisms underlying RMI1 regulation and the physiological significance of this phenomenon will require further investigation into the relationship between RMI1 and glucose-responsive and adipogenesis-related molecules.…”

Section: Discussionmentioning

confidence: 99%

Glucose regulates RMI1 expression through the E2F pathways in adipose cells

et al. 2011

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RecQ-mediated genome instability 1 (RMI1) has been identified as a novel energy homeostasis-related molecule. While recent studies have suggested that change in RMI1 expression levels in adipose tissue may affect the body's energy balance, no reports have identified the mechanism behind this expression regulation. In the present study, we found that RMI1 expression increased on differentiation of 3T3-L1 fibroblasts to adipocytes. In addition, glucose stimulation induced RMI1 expression to approximately eight times the baseline level. Further, knockdown of either E2F5 or E2F8 mRNA using siRNA suppressed this glucose-induced up-regulation of RMI1 expression. These results suggest that RMI1 expression may be regulated by glucose, at least in part, via E2F expression.

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Role of Fgf10 in cell proliferation in white adipose tissue

Cited by 35 publications

References 21 publications

Fgf signalling controls diverse aspects of fin regeneration

Fgf signalling controls diverse aspects of fin regeneration

Evidence for the involvement of Fibroblast Growth Factor 10 in lipofibroblast formation during embryonic lung development

Glucose regulates RMI1 expression through the E2F pathways in adipose cells

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