bFGF Promotes the Migration of Human Dermal Fibroblasts under Diabetic Conditions through Reactive Oxygen Species Production via the PI3K/Akt-Rac1- JNK Pathways

Shi, Hongxue; Cheng, Yi; Ye, Jingjing; Cai, Pingtao; Zhang, Jinjing; Li, Rui; Yang, Ying; Wang, Zhouguang; Zhang, Hongyu; Cai, Lin; Lu, Xuemian; Jiang, Liping; Hu, Aiping; Zhu, Xiongwei; Zeng, Qian; Fu, Xiaobing; Li, Xiaokun; Xiao, Jian

doi:10.7150/ijbs.11921

Cited by 61 publications

(50 citation statements)

References 63 publications

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“…The PI3K/Akt signaling pathway plays important roles in regulating the cellular functions of various cell types, including cell proliferation, survival, and migration . bFGF, via activating the PI3K/Akt signaling pathway, stimulates proliferation and migration of different cell types . Our data showed that bFGF increased Akt phosphorylation and induced melanocyte migration (Fig.…”

Section: Discussionmentioning

confidence: 52%

“…Previous studies have reported that bFGF induces melanocyte migration , and that the PI3K/Akt‐Rac1‐JNK signaling pathways are involved in bFGF‐induced fibroblast migration . However, it was not known whether PI3K/Akt‐Rac1‐JNK signaling pathway is involved in bFGF‐induced melanocyte migration.…”

Section: Discussionmentioning

confidence: 99%

“…Basic fibroblast growth factor (bFGF) is a member of the fibroblast growth factor (FGF) family, which is composed of 18 FGFs and 4 FGF receptors . Our previous studies showed that bFGF promotes wound healing , reduces scar formation during wound healing process , and improves functional deficits in a spinal cord injury model as a potent mitogen that stimulates the migration, proliferation, and differentiation of cells of mesenchymal and neuroectodermal origin . Fibroblasts treated with bFGF showed increased activity of PI3K/Akt, Rho family proteins, and JNKs associated with cytoskeletal reorganization, leading to induction of fibroblast migration .…”

Section: Introductionmentioning

confidence: 99%

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Basic fibroblast growth factor promotes melanocyte migration via activating PI3K/Akt‐Rac1‐FAK‐JNK and ERK signaling pathways

et al. 2016

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Vitiligo is a depigmentation disorder characterized by loss of functional melanocytes of the skin epidermis. The pathogenesis of vitiligo remains elusive. The purpose of this study is to investigate the effects of basic fibroblast growth factor (bFGF) on melanocyte migration, including its biochemical mechanism using transwell assay in vitro. We found that melanocyte treated with bFGF showed a significant increase in migration and cytoskeletal rearrangement. These changes were associated with increased activation of PI3K/Akt, Rac1, FAK, JNK, and ERK. Likewise, reduction of PI3K/Akt, Rac1, FAK, JNK, and ERK activity using selective inhibitors or siRNA was associated with impediment of bFGF-induced melanocyte migration. In addition, activity of Rac1, FAK, and JNK was reduced in cells in which PI3K/Akt was inhibited, activity of FAK and JNK was reduced in cells in which the Rac1 was inhibited, and activity of JNK was reduced in cells in which the FAK was inhibited. Collectively, these data demonstrate that bFGF facilitated melanocyte migration via PI3K/Akt-Rac1-FAK-JNK and ERK signaling pathways. V C 2016 IUBMB Life, 68(9): [735][736][737][738][739][740][741][742][743][744][745][746][747] 2016

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Section: Discussionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Basic fibroblast growth factor promotes melanocyte migration via activating PI3K/Akt‐Rac1‐FAK‐JNK and ERK signaling pathways

et al. 2016

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“…PI3K-Akt could modulate the activity and functions of multiple downstream effectors [32,33]. In the present study, the activation of ERK1/2 was found to be attenuated as well when the activity of PI3K-Akt was inhibited by LY294002 or shRNA targeted to Akt, suggesting that the PI3K-Akt signal was required for the activation of ERK1/2 under conditions of mechanical stimulation.…”

Section: Discussionmentioning

confidence: 56%

Periodic Mechanical Stress Activates PKCδ-Dependent EGFR Mitogenic Signals in Rat Chondrocytes via PI3K-Akt and ERK1/2

Shen

Gao

et al. 2016

Cell Physiol Biochem

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Background/Aims: The present study aimed to analyze the mechanisms by which periodic mechanical stress is translated into biochemical signals, and to verify the important role of signaling molecules including phosphatidylinositol-3-kinase (PI3K)-Akt, protein kinase C (PKC), and epidermal growth factor receptor (EGFR) in chondrocyte proliferation. The effects of periodic mechanical stress on the mitogenesis of chondrocytes have been studied extensively in recent years. However, the mechanisms underlying the ability of chondrocytes to sense and respond to periodic mechanical stress need further investigation. Methods: Two steps were undertaken in the experiment. In the first step, the cells were pretreated with shRNA targeted to Akt or EGFR or PKCδ or control scrambled shRNA. Moreover, they were pretreated with LY294002, GF109203X, Gö6976, rottlerin, and AG1478. They were maintained under static conditions or periodic mechanical stress for 3 days, 8 h per day, prior to direct cell counting and CCK-8 assay, respectively. In the second step, the cells were pretreated with shRNA targeted to Akt or EGFR or PKCδ or control scrambled shRNA. Moreover, they were pretreated with LY294002, AG1478, and rottlerin. They were maintained under static conditions or periodic mechanical stress for 1 h prior to Western blot analysis. Results: Proliferation was inhibited by pretreatment with PKC or PKCδ inhibitor GF109203X or rottlerin and by short hairpin RNA (shRNA) targeted to PKCδ, but not by PKCα inhibitor Gö6976 in chondrocytes in response to periodic mechanical stress. Meantime, rottlerin and shRNA targeted to PKCδ also attenuated EGFR, Akt, and ERK1/2 activation. Furthermore, inhibiting EGFR activity by AG1478 and shRNA targeted to EGFR abrogated chondrocyte proliferation and phosphorylation levels of Akt and extracellular signal-regulated kinase (ERK)1/2 subjected to periodic mechanical stress, while the phosphorylation site of PKCδ was not affected. In addition, pretreatment with the PI3K-Akt-selective inhibitor LY294002 and shRNA targeted to Akt reduced periodic mechanical stress-induced chondrocyte proliferation and phosphorylation of ERK1/2, while the phosphorylation levels of EGFR and PKCδ were not inhibited. Conclusion: These findings suggested that periodic mechanical stress promoted chondrocyte proliferation through PKCδ-EGFR-PI3K-Akt-ERK1/2. They provide a stronger viewpoint for further investigations into chondrocyte mechanobiology under periodic mechanical stress and the ways to improve the quality of tissue-engineered cartilage.

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“…Studies have shown that bFGF is able to stimulate their migration, differentiation, proliferation, as well as preventing apoptosis, and ameliorating ischemic injury [Zhao et al, 2013;Cui et al, 2014;Shi et al, 2015]. Studies have shown that bFGF is able to stimulate their migration, differentiation, proliferation, as well as preventing apoptosis, and ameliorating ischemic injury [Zhao et al, 2013;Cui et al, 2014;Shi et al, 2015].…”

mentioning

confidence: 99%

Retracted: Suppression of Basic Fibroblast Growth Factor Expression by Antisense Oligonucleotides Inhibits Neural Stem Cell Proliferation and Differentiation in Rat models With Focal Cerebral Infarction

Che

Shi

et al. 2017

J of Cellular Biochemistry

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This study is designed to investigate the role of basic fibroblast growth factor (bFGF) antisense oligonucleotide (ASODN) on the proliferation and differentiation of neural stem cells (NSCs) in rat models with focal cerebral infarction (CI). Seventy-five Sprague-Dawlay (SD) rats were randomly divided into the control, sham, middle cerebral artery occlusion (MCAO), MCAO + nonsense oligonucleotide (NODN), and MCAO + ASODN groups. Proliferation and differentiation of NSCs were detected by bromodeoxyuridine (BrdU) and immunofluorescence staining, respectively. ELISA was performed to detect the expressions of endogenous factors that include insulin-like growth factor 1 (IGF-1), glial cell line derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF), transforming growth factor-α1 (TGF-α1), bFGF, and nerve growth factor (NGF). Results show significant neurological deficits and focal CI in the MCAO and MCAO + NODN groups. An obvious increase of NSC proliferation, reactive proliferation of astrocytes in CI areas, differentiation of newly proliferated NSCs into mature neuronal cells, and expressions of endogenous growth factors exhibited in the MCAO, MCAO + NODN and MCAO + ASODN groups. Compared to the MCAO and MACO + NODN groups, the MCAO + ASODN group showed a significant decrease NSC proliferation and differentiation in CI areas as well as decrease expressions of endogenous growth factors. These findings may offer insight to help us understand more as to how bFGF ASODN can effectively suppress the proliferation and differentiation of NSCs. These findings are expected to help contribute to research for new targets in the treatment of focal CI. J. Cell. Biochem. 118: 3875-3882, 2017. © 2017 Wiley Periodicals, Inc.

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bFGF Promotes the Migration of Human Dermal Fibroblasts under Diabetic Conditions through Reactive Oxygen Species Production via the PI3K/Akt-Rac1- JNK Pathways

Cited by 61 publications

References 63 publications

Basic fibroblast growth factor promotes melanocyte migration via activating PI3K/Akt‐Rac1‐FAK‐JNK and ERK signaling pathways

Basic fibroblast growth factor promotes melanocyte migration via activating PI3K/Akt‐Rac1‐FAK‐JNK and ERK signaling pathways

Periodic Mechanical Stress Activates PKCδ-Dependent EGFR Mitogenic Signals in Rat Chondrocytes via PI3K-Akt and ERK1/2

Retracted: Suppression of Basic Fibroblast Growth Factor Expression by Antisense Oligonucleotides Inhibits Neural Stem Cell Proliferation and Differentiation in Rat models With Focal Cerebral Infarction

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