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Fibroblast Growth Factor 9, Rabbit anti_Mouse, azide_free; WB_ELISA

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[#YSRTAAM17G] Fibroblast Growth Factor 9, Rabbit anti_Mouse, azide_free; WB_ELISA

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YSRTAAM17G | Fibroblast Growth Factor 9, Rabbit anti_Mouse, azide_free; WB_ELISA, 0.1 mg.
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(1) Fibroblast growth factor 9 activates anti-oxidative functions of Nrf2 through ERK signalling in striatal cell models of Huntington's disease.[TOP]

Pubmed ID :30391672
Publication Date : //
Huntington's disease (HD) is a heritable neurodegenerative disorder, and has been characterized as an increase of oxidative stress in brain regions. In our previous results, we showed fibroblast growth factor 9 (FGF9) provides neuroprotective functions to suppress cell death in HD striatal cells dominantly through ERK signalling. However, whether the working mechanism of FGF9 is related to anti-oxidative stress in HD is still unknown. In this study, STHdh (Q7) and STHdh (Q111) striatal knock-in cell lines were used to examine the neuroprotective effects of FGF9 against oxidative stress in HD. Results show that FGF9 alleviates oxidative stress induced by starvation in Q7 and Q111 cells. The treatment of FGF9 not only induces upregulation and activation of nuclear factor erythroid 2-like 2 (Nrf2), a critical transcription factor for anti-oxidative stress, but also further upregulates its downstream targets, such as superoxide dismutase 2, gamma-glutamylcysteine synthetase and glutathione reductase. Furthermore, blockage of the Nrf2 pathway abolishes the anti-oxidative functions of FGF9, and inhibition of ERK signalling reduces the activation of the FGF9-Nrf2 pathway, resulting in higher level of oxidative stress in HD cells. These results support the neuroprotective effects of FGF9 against oxidative stress through the ERK-Nrf2 pathway, and imply one of potential strategies for therapy of HD.

Authors : Yusuf Issa Olakunle, Chen Hsiu-Mei, Cheng Pei-Hsun, Chang Chih-Yi, Tsai Shaw-Jenq, Chuang Jih-Ing, Wu Chia-Ching, Huang Bu-Miin, Sun H Sunny, Yang Shang-Hsun,



(2) miR-4317 suppresses non-small cell lung cancer (NSCLC) by targeting fibroblast growth factor 9 (FGF9) and cyclin D2 (CCND2).[TOP]

Pubmed ID :30227870
Publication Date : //
Non-small cell lung cancer (NSCLC) is a leading cause of death worldwide. MicroRNAs (miRNAs) have been indicated as crucial actors in cancer biology. Accumulating evidence suggests that miRNAs can be used as diagnostic and prognostic markers for NSCLC.

Authors : He Xi, Chen Si-Yuan, Yang Zhao, Zhang Jie, Wang Wei, Liu Mei-Yue, Niu Yi, Wei Xiao-Mei, Li Hong-Min, Hu Wan-Ning, Sun Guo-Gui,



(3) Corrigendum to "Fibroblast Growth Factor-9 Activates c-Kit Progenitor Cells and Enhances Angiogenesis in the Infarcted Diabetic Heart".[TOP]

Pubmed ID :30210655
Publication Date : //
[This corrects the article DOI: 10.1155/2016/5810908.].

Authors : Singla Dinender K, Wang Jing,



(4) FGF9/FGFR2 increase cell proliferation by activating ERK1/2, Rb/E2F1, and cell cycle pathways in mouse Leydig tumor cells.[TOP]

Pubmed ID :30191630
Publication Date : //
Fibroblast growth factor 9 (FGF9) promotes cancer progression; however, its role in cell proliferation related to tumorigenesis remains elusive. We investigated how FGF9 affected MA-10 mouse Leydig tumor cell proliferation and found that FGF9 significantly induced cell proliferation by activating ERK1/2 and retinoblastoma (Rb) phosphorylations within 15 minutes. Subsequently, the expressions of E2F1 and the cell cycle regulators: cyclin D1, cyclin E1 and cyclin-dependent kinase 4 (CDK4) in G phase and cyclin A1, CDK2 and CDK1 in S-G /M phases were increased at 12 hours after FGF9 treatment; and cyclin B1 in G /M phases were induced at 24 hours after FGF9 stimulation, whereas the phosphorylations of p53, p21 and p27 were not affected by FGF9. Moreover, FGF9-induced effects were inhibited by MEK inhibitor PD98059, indicating FGF9 activated the Rb/E2F pathway to accelerate MA-10 cell proliferation by activating ERK1/2. Immunoprecipitation assay and ChIP-quantitative PCR results showed that FGF9-induced Rb phosphorylation led to the dissociation of Rb-E2F1 complexes and thereby enhanced the transactivations of E2F1 target genes, Cyclin D1, Cyclin E1 and Cyclin A1. Silencing of FGF receptor 2 (FGFR2) using lentiviral shRNA inhibited FGF9-induced ERK1/2 phosphorylation and cell proliferation, indicating that FGFR2 is the obligate receptor for FGF9 to bind and activate the signaling pathway in MA-10 cells. Furthermore, in a severe combined immunodeficiency mouse xenograft model, FGF9 significantly promoted MA-10 tumor growth, a consequence of increased cell proliferation and decreased apoptosis. Conclusively, FGF9 interacts with FGFR2 to activate ERK1/2, Rb/E2F1 and cell cycle pathways to induce MA-10 cell proliferation in vitro and tumor growth in vivo.

Authors : Chang Ming-Min, Lai Meng-Shao, Hong Siou-Ying, Pan Bo-Syong, Huang Hsin, Yang Shang-Hsun, Wu Chia-Ching, Sun H Sunny, Chuang Jih-Ing, Wang Chia-Yih, Huang Bu-Miin,



(5) Oil body bound oleosin-rhFGF9 fusion protein expressed in safflower (Carthamus tinctorius L.) stimulates hair growth and wound healing in mice.[TOP]

Pubmed ID :30157831
Publication Date : //
Fibroblast growth factor 9 (FGF9) is a heparin-binding growth factor, secreted by both mesothelial and epithelial cells, which participates in hair follicle regeneration, wound healing, and bone development. A suitable source of recombinant human FGF9 (rhFGF9) is needed for research into potential clinical applications. We present that expression of oleosin-rhFGF9 fusion protein in safflower (Carthamus tinctorius L.) seeds stimulates hair growth and wound healing.

Authors : Cai Jingbo, Wen Ruicheng, Li Wenqing, Wang Xiuran, Tian Haishan, Yi Shanyong, Zhang Linbo, Li Xiaokun, Jiang Chao, Li Haiyan,



(6) Role of FGF9 in sheep testis steroidogenesis during sexual maturation.[TOP]

Pubmed ID :30154034
Publication Date : //
Fibroblast growth factor 9 (FGF9) is an important signaling molecule in early gonadal development. Hu sheep are noted for reproductive precociousness and fertility. The present study was conducted to investigate the gene expression and functions of FGF9 in ovine testis steroidogenesis during sexual maturity. A 874 bp cDNA fragment of FGF9 was detected that included a 627 bp coding sequence, encoding 208 amino acids. The FGF9 amino acid sequence of sheep had high homology with this molecule of other mammalian species. Additionally, the abundance of FGF9 in ovine testis was greater (P <  0.05) at 9 months (M) and 24 M of age compared with those at 3 M. Immunohistochemistry further revealed that FGF9 mainly localized in the Leydig cells and that there were small amounts in elongating spermatids. The functions of FGF9 in sheep Leydig cells was investigated using a siRNA-FGF9. Secretion of T and abundance of testosterone synthesis-related enzymes in Leydig cells were inhibited (P <  0.05) by siRNA-FGF9. Thus, these results demonstrated FGF9 is an important regulator of testosterone biosynthesis in rams. Results of the present research provide a new perspective for genetic and molecular research on modulation of physiological mechanisms during sexual maturity in male sheep.

Authors : Gao Xiaoxiao, Yao Xiaolei, Yang Hua, Deng Kaiping, Guo Yixuan, Zhang Tingting, Zhang Guomin, Wang Feng,



(7) Systematic Analysis of Differential Expression Profile in Rheumatoid Arthritis Chondrocytes Using Next-Generation Sequencing and Bioinformatics Approaches.[TOP]

Pubmed ID :30123050
Publication Date : //
Cartilage destruction in rheumatoid arthritis (RA) occurs primarily in the pannus-cartilage interface. The close contact of the synovium-cartilage interface implicates crosstalk between synovial fibroblasts and chondrocytes. The aim of this study is to explore the differentially expressed genes and novel microRNA regulations potentially implicated in the dysregulated cartilage homeostasis in joint destruction of RA. Total RNAs were extracted from human primary cultured normal and RA chondrocytes for RNA and small RNA expression profiling using next-generation sequencing. Using systematic bioinformatics analyses, we identified 463 differentially expressed genes in RA chondrocytes were enriched in biological functions related to altered cell cycle process, inflammatory response and hypoxic stimulation. Moreover, fibroblast growth factor 9 (), kynureninase (), and regulator of cell cycle () were among the top dysregulated genes identified to be potentially affected in the RA joint microenvironment, having similar expression patterns observed in arrays of clinical RA synovial tissues from the Gene Expression Omnibus database. Additionally, among the 31 differentially expressed microRNAs and 10 candidate genes with potential microRNA-mRNA interactions in RA chondrocytes, the novel miR-140-3p- interaction was validated in different microRNA prediction databases, and proposed to participate in the pathogenesis of joint destruction through dysregulated cell growth in RA. The findings provide new perspectives for target genes in the management of cartilage destruction in RA.

Authors : Chen Yi-Jen, Chang Wei-An, Wu Ling-Yu, Hsu Ya-Ling, Chen Chia-Hsin, Kuo Po-Lin,



(8) [Expression of oleosin-rhFGF9 fusion protein in Carthamus tinctorius and determination of hair regeneration and wound repair potential in mice].[TOP]

Pubmed ID :30111028
Publication Date : //
The expression of fibroblast growth factor 9 (FGF9) recombinant fusion protein in Carthamus tinctorius was used to identify its effect on hair regrowth and wound repair system in mice, providing a basis for C. tinctorius as a plant bioreactor, and establishing a foundation for commercial applications of FGF9 fusion protein in hair regrowth and wound repair. The identified pOTBar-oleosin-rhFGF9 plasmid was transformed into Agrobacterium tumefaciens EHA105 by freeze-thaw method, and the oleosin-rhFGF9 gene was transformed into safflower leaves by A. tumefaciens mediated method. Transgenic safflower seedlings were then obtained by tissue culture. After basta screening, transgenic T₃ safflower seeds were obtained by grafting method, PCR verification and propagation. The expression of oleosin-rhFGF9 was detected by Western blot, and the content of oleosin-rhFGF9 fusion protein was 0.09% by using ELISA quantitative method. It was observed that 60 μg·L⁻¹ transgenic safflower oil had better effect on promoting NIH/3T3 cells proliferation in a certain dose-dependent manner. Sixty C57BL/6 mice were used to establish alopecia model and wound model respectively, and then were randomly divided into control group (treated with PBS or saline), negative group (treated with wild type safflower seed oil bodies, 60 g·L⁻¹), positive group (treated with FGF9, 0.054 g·L⁻¹), low dose group (treated with transgenic safflower oil bodies, 10 g·L⁻¹) and high dose group (treated with transgenic safflower oil bodies, 60 g·L⁻¹). The skin of all above-mentioned mice models were coated with soft adhesive manner every other day, 100 μL/time. After 15 days, the mice skin was cut and embedded for histological analysis. The hair regrowth experimental results showed that the hair of mice grew well, and the mice in high dose group had bushy hair, with significant effect on regeneration hair number as compared with the positive group. The healing was obvious in wound experiment, with significant healing effect in positive group, high dose group and low dose group as compared to blank control group. Furthermore, high dose group remarkably showed a better and higher healing effect than the positive group at day 5. Oleosin-rhFGF9 was successfully transformed into safflower, and T₃ transgenic safflower oil bodies expressed oleosin-rhFGF9 fusion protein were obtained, with the role of promoting hair regeneration and wound repair in mice.

Authors : Cai Jing-Bo, Li Wen-Qing, Wen Rui-Cheng, Jiang Chao, Li Xiao-Kun, Li Hai-Yan,



(9) A random forest classifier predicts recurrence risk in patients with ovarian cancer.[TOP]

Pubmed ID :30066910
Publication Date : //
Ovarian cancer (OC) is associated with a poor prognosis due to difficulties in early detection. The aims of the present study were to construct a recurrence risk prediction model and to reveal important OC genes or pathways. RNA sequencing data was obtained for 307 OC samples, and the corresponding clinical data were downloaded from The Cancer Genome Atlas database. Additionally, two validation datasets, GSE44104 (20 recurrent and 40 non‑recurrent OC samples) and GSE49997 (204 OC samples), were obtained from the Gene Expression Omnibus database. Differentially expressed genes were screened using the differential expression via distance synthesis algorithm, followed by gene ontology enrichment analysis and weighted gene coexpression network analysis (WGCNA). Furthermore, subnetwork analysis was conducted for the protein‑protein interaction (PPI) network using the BioNet package. Finally, a random forest classifier was constructed based on the subnetwork nodes, and its reliability was validated using the GSE44104 and GSE49997 validation datasets. A total of 44 upregulated and 117 downregulated genes were identified in the recurrent samples. Enrichment analysis indicated that cytochrome P450 family 17 subfamily A member 1 (CYP17A1) was associated with 'positive regulation of steroid hormone biosynthetic processes'. WGCNA identified turquoise and grey modules that were significantly correlated with status and prognosis. A significant PPI subnetwork containing 16 nodes was also identified, including: Transcription factor GATA‑4; fibroblast growth factor 9; aromatase; 3β‑hydroxysteroid dehydrogenase/δ5‑4‑isomerase type 2; corticosteroid 11β‑dehydrogenase isozyme 1; CYP17A1; pituitary homeobox 2; left‑right determination factor 1; homeobox protein ARX; estrogen receptor β; steroidogenic factor 1; forkhead box protein L2; myocardin; steroidogenic acute regulatory protein mitochondrial; vesicular inhibitory amino acid transporter; and twist‑related protein 1. A random forest classifier was constructed using the subnetwork nodes as feature genes, which exhibited a 92% true positive rate when classifying recurrent and non‑recurrent OC samples. The classifying efficiency of the random forest classifier was validated using the two other independent datasets. Overall, 44 upregulated and 117 downregulated genes associated with OC recurrence were identified. Furthermore, the 16 subnetwork node genes that were identified may be important molecules in OC recurrence.

Authors : Cheng Li, Li Lin, Wang Liling, Li Xiaofang, Xing Hui, Zhou Jinting,



(10) Fibroblast Growth Factor 9 Suppresses Striatal Cell Death Dominantly Through ERK Signaling in Huntington's Disease.[TOP]

Pubmed ID :30021209
Publication Date : //
Huntington's disease (HD) is a heritable neurodegenerative disorder, and there is no cure for HD to date. A type of fibroblast growth factor (FGF), FGF9, has been reported to play prosurvival roles in other neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease. However, the effects of FGF9 on HD is still unknown. With many similarities in the cellular and pathological mechanisms that eventually cause cell death in neurodegenerative diseases, we hypothesize that FGF9 might provide neuroprotective functions in HD.

Authors : Yusuf Issa Olakunle, Cheng Pei-Hsun, Chen Hsiu-Mei, Chang Yu-Fan, Chang Chih-Yi, Yang Han-In, Lin Chia-Wei, Tsai Shaw-Jenq, Chuang Jih-Ing, Wu Chia-Ching, Huang Bu-Miin, Sun H Sunny, Yang Shang-Hsun,