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Fibroblast Growth Factor 9, Rabbit anti_Mouse, Biotin; ELISA

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[#ACL9166B] Fibroblast Growth Factor 9, Rabbit anti_Mouse, Biotin; ELISA

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ACL9166B | Fibroblast Growth Factor 9, Rabbit anti_Mouse, Biotin; ELISA, 25 µg.
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(1) Resolution of bleomycin-induced murine pulmonary fibrosis via a splenic lymphocyte subpopulation.[TOP]

Pubmed ID :29690905
Publication Date : //
Idiopathic pulmonary fibrosis (IPF) is a progressive disease with high mortality, and the pathogenesis of the disease is still incompletely understood. Although lymphocytes, especially CD4CD25FoxP3 regulatory T cells (Tregs), have been implicated in the development of IPF, contradictory results have been reported regarding the contribution of Tregs to fibrosis both in animals and humans. The aim of this study was to investigate whether a specific T cell subset has therapeutic potential in inhibiting bleomycin (BLM)-induced murine pulmonary fibrosis.

Authors : Kamio Koichiro, Azuma Arata, Matsuda Kuniko, Usuki Jiro, Inomata Minoru, Morinaga Akemi, Kashiwada Takeru, Nishijima Nobuhiko, Itakura Shioto, Kokuho Nariaki, Atsumi Kenichiro, Hayashi Hiroki, Yamaguchi Tomoyoshi, Fujita Kazue, Saito Yoshinobu, Abe Shinji, Kubota Kaoru, Gemma Akihiko,



(2) Tumor associated macrophages support the growth of FGF9-induced lung adenocarcinoma by multiple mechanisms.[TOP]

Pubmed ID :29656749
Publication Date : //
Tumor-associated macrophages (TAMs) are known to promote tumorigenesis but the mechanism(s) remain elusive. We have developed a mouse model of lung cancer that is initiated through an inducible overexpression of fibroblast growth factor 9 (FGF9) in type-2 pneumocytes. Expression of FGF9 in adult lungs resulted in a rapid development of multiple adenocarcinoma-like tumor nodules, and is associated with an intense immunological reaction. The purpose of this study is to characterize the immune response to the FGF9-induced lung adenocarcinoma and to determine the contribution of TAMs to growth and survival of these tumors.

Authors : Hegab Ahmed E, Ozaki Mari, Kagawa Shizuko, Hamamoto Junko, Yasuda Hiroyuki, Naoki Katsuhiko, Soejima Kenzo, Yin Yongjun, Kinoshita Tomonari, Yaguchi Tomonori, Kawakami Yutaka, Ornitz David M, Betsuyaku Tomoko,



(3) Transcriptome profiling of bovine ovarian theca cells treated with fibroblast growth factor 9.[TOP]

Pubmed ID :29413902
Publication Date : //
We reported previously that fibroblast growth factor 9 (FGF9) acts as an antidifferentiation factor, stimulating proliferation of granulosa cells (GCs) and theca cells (TCs) while suppressing hormone-induced steroidogenesis of these cells. How FGF9 acts to simultaneously suppress steroidogenesis and stimulate proliferation remains to be fully elucidated. Thus, this study was undertaken to clarify the effects of FGF9 on the TC transcriptome. Ovaries were obtained from beef heifers at a local abattoir, TCs were isolated from large antral follicles, and cultured with or without 30 ng/mL of FGF9 for 24 h in the presence of LH and IGF-1. After treatment, total RNA was extracted from TC and processed for microarray using Affymetrix GeneChip Bovine Genome Arrays (n = 4/group). Transcriptome analysis comparing FGF9-treated TC with control TC using 1.3-fold cutoff, and a P < 0.05 significance level identified 355 differentially expressed transcripts, with 164 elements upregulated and 191 elements downregulated by FGF9. The ingenuity pathway analysis (IPA) was used to investigate how FGF9 treatment affects molecular pathways, biological functions, and the connection between molecules in bovine TC. The IPA software identified 346 pathways in response to FGF9 in TC involved in several biological functions and unveiled interesting relationships among genes related to cell proliferation (eg, CCND1, FZD5, and MYB), antioxidation/cytoprotection (eg, HMOX1 and NQO1), and steroidogenesis (eg, CYP11A1 and STAR). Overall, genes, pathways, and networks identified in this study painted a picture of how FGF9 may regulate folliculogenesis, providing novel candidate genes for further investigation of FGF9 functions in ovarian follicular development.

Authors : Schütz L F, Hurst R E, Schreiber N B, Spicer L J,



(4) MicroRNA 221 expression in theca and granulosa cells: hormonal regulation and function.[TOP]

Pubmed ID :29385487
Publication Date : //
Small noncoding RNA molecules (miRNA) regulate protein levels in a post-transcriptional manner by partial base pairing to the 3'-UTR of target genes thus mediating degradation or translational repression. Previous studies indicate that numerous miRNA regulate the biosynthesis of intraovarian hormones, and emerging evidence indicates that one of these, miRNA-221 (MIR221), may be a modulator of ovarian function. However, the hormonal control of ovarian MIR221 is not known. The objectives of this study were to investigate the developmental and hormonal regulation of MIR221 expression in granulosa (GC) and theca cell (TC) and its possible role in regulating follicular function. Bovine ovaries were collected from a local abattoir and GC and TC were obtained from small (<6 mm) and large (≥8 mm) follicles. In Exp. 1, GCs of small follicles had 9.7-fold greater (P < 0.001) levels of MIR221 than those of large follicles, and TCs of large follicles had 3.7-fold greater (P < 0.001) levels of MIR221 than those of small follicles. In large follicles, abundance of MIR221 was 66.6-fold greater (P < 0.001) in TCs than in GCs. In small follicles, MIR221 abundance did not differ (P = 0.14) between GC and TCs. In vitro Exp. 2, 3, and 4 revealed that treatment of bovine TCs with various steroids, phytoestrogens, IGF1, forskolin, and dibutyryl cyclic adenosine monophosphate had no effect (P > 0.35) on MIR221 expression, whereas treatment with fibroblast growth factor 9 (FGF9) and FGF2 increased (P < 0.001) TC MIR221 abundance 1.7- to 2.5-fold. In Exp. 5, FGF9 increased (P < 0.05) GC MIR221 abundance by 1.7- and 2.0-fold in small and large follicles, respectively. The role of MIR221 in GC steroidogenesis was investigated in Exp. 6 and it was found that transfection with a MIR221 mimic reduced (P < 0.01) GC estradiol and progesterone production induced by FSH and IGF1, whereas transfection with MIR221 inhibitor had little or no effect. We conclude that thecal MIR221 expression is increased by FGF9 and increased MIR221 may act to inhibit GC steroidogenesis in cattle.

Authors : Robinson Cheyenne L, Zhang Lingna, Schütz Luis F, Totty Morgan L, Spicer Leon J,



(5) The role of tight junction proteins in ovarian follicular development and ovarian cancer.[TOP]

Pubmed ID :29374086
Publication Date : //
Tight junctions (TJ) are protein structures that control the transport of water, ions and macromolecules across cell layers. Functions of the transmembrane TJ protein, occluding (OCLN) and the cytoplasmic TJ proteins, tight junction protein 1 (TJP1; also known as zona occludens protein-1), cingulin (CGN) and claudins (CLDN) are reviewed, and current evidence of their role in the ovarian function is reviewed. Abundance of , and mRNA changed during follicular growth. treatment with various growth factors known to affect ovarian folliculogenesis indicated that , and are hormonally regulated. The summarized studies indicate that expression of TJ proteins (i.e., , , and ) changes with follicle size in a variety of vertebrate species but whether these changes in TJ proteins are increased or decreased depends on species and cell type. Evidence indicates that autocrine, paracrine and endocrine regulators, such as fibroblast growth factor-9, epidermal growth factor, androgens, tumor necrosis factor-α and glucocorticoids may modulate these TJ proteins. Additional evidence presented indicates that TJ proteins may be involved in ovarian cancer development in addition to normal follicular and luteal development. A model is proposed suggesting that hormonal downregulation of TJ proteins during ovarian follicular development could reduce barrier function (i.e., selective permeability of molecules between theca and granulosa cells) and allow for an increase in the volume of follicular fluid as well as allow additional serum factors into the follicle that may directly impact granulosa cell functions.

Authors : Zhang Lingna, Feng Tao, Spicer Leon J,



(6) RNA sequencing identifies gene regulatory networks controlling extracellular matrix synthesis in intervertebral disk tissues.[TOP]

Pubmed ID :29227558
Publication Date : //
Degenerative disk disease of the spine is a major cause of back pain and disability. Optimization of regenerative medical therapies for degenerative disk disease requires a deep mechanistic understanding of the factors controlling the structural integrity of spinal tissues. In this investigation, we sought to identify candidate regulatory genes controlling extracellular matrix synthesis in spinal tissues. To achieve this goal we performed high throughput next generation RNA sequencing on 39 annulus fibrosus and 21 nucleus pulposus human tissue samples. Specimens were collected from patients undergoing surgical discectomy for the treatment of degenerative disk disease. Our studies identified associations between extracellular matrix genes, growth factors, and other important regulatory molecules. The fibrous matrix characteristic of annulus fibrosus was associated with expression of the growth factors platelet derived growth factor beta (PDGFB), vascular endothelial growth factor C (VEGFC), and fibroblast growth factor 9 (FGF9). Additionally we observed high expression of multiple signaling proteins involved in the NOTCH and WNT signaling cascades. Nucleus pulposus extracellular matrix related genes were associated with the expression of numerous diffusible growth factors largely associated with the transforming growth signaling cascade, including transforming factor alpha (TGFA), inhibin alpha (INHA), inhibin beta A (INHBA), bone morphogenetic proteins (BMP2, BMP6), and others.

Authors : Riester Scott M, Lin Yang, Wang Wei, Cong Lin, Mohamed Ali Abdel-Moneim, Peck Sun H, Smith Lachlan J, Currier Bradford L, Clark Michelle, Huddleston Paul, Krauss William, Yaszemski Michael J, Morrey Mark E, Abdel Matthew P, Bydon Mohamad, Qu Wenchun, Larson Annalise N, van Wijnen Andre J, Nassr Ahmad,



(7) Fibroblast growth factor 9 subfamily and the heart.[TOP]

Pubmed ID :29198068
Publication Date : //
The fibroblast growth factor (FGF) 9 subfamily is a member of the FGF family, including FGF9, 16, and 20, potentially sharing similar biochemical functions due to their high degree of sequence homology. Unlike other secreted proteins which have a cleavable N-terminal secreted signal peptide, FGF9/16/20 have non-cleaved N-terminal signal peptides. As an intercellular signaling molecule, they are involved in a variety of complex responses in animal development. Cardiogenesis is controlled by many members of the transcription factor family. Evidence suggests that FGF signaling, including the FGF9 subfamily, has a pretty close association with these cardiac-specific genes. In addition, recent studies have shown that the FGF9 subfamily maintains functional adaptation and survival after myocardial infarction in adult myocardium. Since FGF9/16/20 are secreted proteins, their function characterization in cardiac regeneration can promote their potential to be developed for the treatment of cardioprotection and revascularization. Here, we conclude that the FGF9 subfamily roles in cardiac development and maintenance of postnatal cardiac homeostasis, especially cardiac function maturation and functional maintenance of the heart after injury.

Authors : Wang Shen, Li Yong, Jiang Chao, Tian Haishan,



(8) MiR-665 regulates VSMCs proliferation via targeting FGF9 and MEF2D and modulating activities of Wnt/β-catenin signaling.[TOP]

Pubmed ID :29118903
Publication Date : //
Abnormal proliferation of vascular smooth muscle cells (VSMCs) contributes to the development of cardiovascular diseases. Studies have showed the great impact of microRNAs (miRNAs) on the cell proliferation in VSMCs. This study examined the functional roles of miR-665 in the VSMCs and explored the underlying molecular mechanisms. The mRNA and protein expression levels were determined by qRT-PCR and western blot assays, respectively. CCK-8, transwell invasion and wound healing assays were performed to measure VSMCs proliferation, invasion and migration, respectively. The miR-665 targeted-3'UTR of fibroblast growth factor 9 (FGF9) and myocyte enhancer factor 2D (MEF2D) was confirmed by luciferase reporter assay. Platelet-derived growth factor-bb (PDGF-bb) and 20% serum promoted cell proliferation and suppressed the expression of miR-665 in VSMCs. functional assays demonstrated that miR-665 inhibited VSMCs proliferation, invasion and migration. Bioinformatics analysis showed that FGF9 and MEF2D were found to be downstream targets of miR-665. Luciferase report assay confirmed that FGF9 and MEF2D 3'UTRs are direct targets of miR-665, and miR-665 overexpression suppressed both the mRNA and protein expression levels of FGF9 and MEF2D. Furthermore, rescue experiments showed that enforced expression of FGF9 or MEF2D attenuated the inhibitory effects of miR-665 on VSMCs proliferation. More importantly, overexpression of miR-665 also suppressed the mRNA and protein expression levels of β-catenin, c-myc and cyclin D1. In summary, miR-665 suppressed the VSMCs proliferation, invasion and migration via targeting FGF9 and MEF2D, and the effects of miR-665 on VSMCs may be associated with modulation of Wnt/β-catenin signaling activities.

Authors : Li Kai, Pan Jin, Wang Jianjun, Liu Fengrui, Wang Li,



(9) CXCR4/CXCR7/CXCL12 axis promotes an invasive phenotype in medullary thyroid carcinoma.[TOP]

Pubmed ID :29112684
Publication Date : //
Medullary thyroid carcinoma (MTC) is a rare and challenging endocrine malignancy. Once spread, the therapeutic options are limited and the outcome poor. For these patients, the identification of new druggable biological markers is of great importance. Here, we investigated the prognostic and biological role of the C-X-C chemokine receptors type 4 and 7 (CXCR4/7) in MTC.

Authors : Werner Thomas A, Forster Christina M, Dizdar Levent, Verde Pablo E, Raba Katharina, Schott Matthias, Knoefel Wolfram T, Krieg Andreas,



(10) miR-187 inhibits the growth of cervical cancer cells by targeting FGF9.[TOP]

Pubmed ID :28849071
Publication Date : //
MicroRNAs (miRNAs) are a cluster of short non-coding RNAs playing critical roles in human cancers. miR-187 was recently found to be a novel cancer-related microRNA. However, the expression and function of miR-187 in cervical cancer have not been investigated. In this study, we found that miR-187 level was decreased in cervical cancer tissues and cell lines. Patients with low level of miR-187 had significantly decreased rate of overall survival (OS) and progression-free survival (DFS). miR-187 overexpression inhibited proliferation and promoted apoptosis of cervical cancer cells, whereas miR-187 knockdown promoted proliferation and inhibited apoptosis of cervical cancer cells. Forced expression of miR-187 inhibited the subcutaneous growth of cervical cancer cells in nude mice. Furthermore, FGF9 was found to be the downstream target of miR-187 in cervical cancer cells. Importantly, targeting FGF9 was required for miR-187 exerting its tumor suppressive roles in cervical cancer cells.

Authors : Liang Hua, Luo Ruoyu, Chen Xiaoqi, Zhao Yuzi, Tan Aili,