Basic fibroblast growth factor stimulates the proliferation of human dermal fibroblasts via the ERK1/2 and JNK pathways

Makino, Takamitsu; Jinnin, Masatoshi; Muchemwa, Faith C.; Fukushima, Satoshi; Kogushi-Nishi, H.; Moriya, Chikako; Igata, Toshikatsu; Fujisawa, Akio; Johno, T.; Ihn, Hironobu

doi:10.1111/j.1365-2133.2009.09581.x

Cited by 91 publications

(62 citation statements)

References 46 publications

(40 reference statements)

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“…FGFR signaling activates MAPK p38, ERK1/2, JNK [Maher, 1999; Makino et al, 2010]. We investigated the contribution of these kinases to the establishment of cell “memory” of FGF stimulation.…”

Section: Resultsmentioning

confidence: 99%

Transitory FGF Treatment Results in the Long‐Lasting Suppression of the Proliferative Response to Repeated FGF Stimulation

Poole

Knowland

Cooper

et al. 2014

J of Cellular Biochemistry

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FGF applied as a single growth factor to quiescent mouse fibroblasts induces a round of DNA replication, however continuous stimulation results in arrest in the G1 phase of the next cell cycle. We hypothesized that FGF stimulation induces the establishment of cell memory, which prevents the proliferative response to repeated or continuous FGF application. When a 2-5 day quiescence period was introduced between primary and repeated FGF treatments, fibroblasts failed to efficiently replicate in response to secondary FGF application. The establishment of “FGF memory” during the first FGF stimulation did not require DNA synthesis, but was dependent on the activity of FGF receptors, MEK, p38 MAPK and NFκB signaling, and protein synthesis. While secondary stimulation resulted in strongly decreased replication rate, we did not observe any attenuation of morphological changes, Erk1/2 phosphorylation and cyclin D1 induction. However, secondary FGF stimulation failed to induce the expression of cyclin A, which is critical for the progression from G1 to S phase. Treatment of cells with a broad range histone deacetylase inhibitor during the primary FGF stimulation rescued the proliferative response to the secondary FGF treatment suggesting that the establishment of “FGF memory” may be based on epigenetic changes. We suggest that “FGF memory” can prevent the hyperplastic response to cell damage and inflammation, which are associated with an enhanced FGF production and secretion. “FGF memory” may present a natural obstacle to the efficient application of recombinant FGFs for the treament of ulcers, ischemias and wounds.

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Section: Resultsmentioning

confidence: 99%

Transitory FGF Treatment Results in the Long‐Lasting Suppression of the Proliferative Response to Repeated FGF Stimulation

Poole

Knowland

Cooper

et al. 2014

J of Cellular Biochemistry

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“…Gene expression levels of bFGF and α -SMA clearly showed that the fi broblastto-myofi broblast trans-differentiation was less pronounced in the vicinity of spider silk coated implants in comparison to uncoated implants. While bFGF induces the migration and proliferation of fi broblasts, [ 25 ] it also inhibits the formation of myofi broblasts by a) suppressing their trans-differentiation from fi broblasts [ 26 ] and b) enhancing the apoptosis of myofibroblasts-but not of fi broblasts. [ 27 ] Here, an 11-fold decrease of bFGF expression was observed in the periprosthetic tissue around silk-coated implants after three months, accompanied by a reduction of the fi broblast marker vimentin, a strongly reduced fi broblast number, and alpha smooth muscle actin ( α -SMA) production (Table 1 ).…”

Section: Impact Of Spider Silk Coating On Post-operative Infl Ammationmentioning

confidence: 99%

Spider Silk Coatings as a Bioshield to Reduce Periprosthetic Fibrous Capsule Formation

Zeplin

Maksimovikj

Jordan

et al. 2014

Adv Funct Materials

107

119

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“…The pharmacologic inhibition of the p42/44 pathway by its specific inhibitor PD was able to partially inhibit FGF-2 expression. Makino et al (31) showed that FGF-2 has the precise effect on proliferation of human dermal fibroblasts and that this effect is mediated by extracellular signal-related kinase (ERK). In this study the activation of p38 in cell signaling mediated by FGF-2 was also analyzed.…”

Section: Discussionmentioning

confidence: 99%

Studies on the Expression of Fibroblast Growth Factor-2 from Odontoblast-like Cells

Oliveira

Santos

2011

Journal of Endodontics

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Basic fibroblast growth factor stimulates the proliferation of human dermal fibroblasts via the ERK1/2 and JNK pathways

Abstract: This study indicates that ERK1/2 and JNK pathways play an important role in the bFGF-mediated effect in HDFs. This study also suggests that controlling ERK1/2 and/or JNK signalling may therefore be a new therapeutic approach for the treatment of chronic and untreatable skin ulcers.

Cited by 91 publications

References 46 publications

Transitory FGF Treatment Results in the Long‐Lasting Suppression of the Proliferative Response to Repeated FGF Stimulation

Transitory FGF Treatment Results in the Long‐Lasting Suppression of the Proliferative Response to Repeated FGF Stimulation

Spider Silk Coatings as a Bioshield to Reduce Periprosthetic Fibrous Capsule Formation

Studies on the Expression of Fibroblast Growth Factor-2 from Odontoblast-like Cells

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