Fibroblast growth factor stimulates the gene expression and production of tissue inhibitor of metalloproteinase-1 in bovine granulosa cells

1995 ◽  
Vol 31 (7) ◽  
pp. 559-563 ◽  
Author(s):  
Hiroyoshi Hoshi ◽  
Seiko Konno ◽  
Makoto Kikuchi ◽  
Yutaka Sendai ◽  
Takeshi Satoh
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Granulosa Cells ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Fibroblast Growth ◽  
Tissue Inhibitor

scholarly journals Effects of Fibroblast Growth Factor 9 (FGF9) on Steroidogenesis and Gene Expression and Control of FGF9 mRNA in Bovine Granulosa Cells

Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4491-4501 ◽  
Author(s):  
Nicole B. Schreiber ◽  
Leon J. Spicer
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Granulosa Cells ◽  
Hormonal Control ◽  
Mrna Abundance ◽  
Fibroblast Growth ◽  
Steroid Synthesis ◽  
Large Follicle ◽  
Igf I

Gene expression of fibroblast growth factor-9 (FGF9) is decreased in granulosa cells (GC) of cystic follicles compared with normal dominant follicles in cattle. The objectives of this study were to investigate the effects of FGF9 on GC steroidogenesis, gene expression, and cell proliferation and to determine the hormonal control of GC FGF9 production. GC were collected from small (1–5 mm) and large (8–22 mm) bovine follicles and treated in vitro with various hormones in serum-free medium for 24 or 48 h. In small- and large-follicle GC, FGF9 inhibited (P < 0.05) IGF-I-, dibutyryl cAMP-, and forskolin-induced progesterone and estradiol production. In contrast, FGF9 increased (P < 0.05) GC numbers induced by IGF-I and 10% fetal calf serum. FGF9 inhibited (P < 0.05) FSHR and CYP11A1 mRNA abundance in small- and large-follicle GC but had no effect (P > 0.10) on CYP19A1 or StAR mRNA. In the presence of a 3β-hydroxysteroid dehydrogenase inhibitor, trilostane, FGF9 also decreased (P < 0.05) pregnenolone production. IGF-I inhibited (P < 0.05) whereas estradiol and FSH had no effect (P > 0.10) on FGF9 mRNA abundance. TNFα and wingless-type mouse mammary tumor virus integration site family member-3A decreased (P < 0.05) whereas T4 and sonic hedgehog increased (P < 0.05) FGF9 mRNA abundance in control and IGF-I-treated GC. Thus, GC FGF9 gene expression is hormonally regulated, and FGF9 may act as an autocrine regulator of ovarian function by slowing follicular differentiation via inhibiting IGF-I action, gonadotropin receptors, the cAMP signaling cascade, and steroid synthesis while stimulating GC proliferation in cattle.

scholarly journals Sorsby Fundus Dystrophy Mutation in Tissue Inhibitor of Metalloproteinase 3 (TIMP3) promotes Choroidal Neovascularization via a Fibroblast Growth Factor-dependent Mechanism

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jian Hua Qi ◽  
Brent Bell ◽  
Rupesh Singh ◽  
Julia Batoki ◽  
Alyson Wolk ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Choroidal Neovascularization ◽  
Molecular Mechanisms ◽  
Retinal Pigment ◽  
Western Hemisphere ◽  
Age Related Macular Degeneration ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Fibroblast Growth ◽  
Tissue Inhibitor

AbstractChoroidal neovascularization (CNV) leads to loss of vision in patients with Sorsby Fundus Dystrophy (SFD), an inherited, macular degenerative disorder, caused by mutations in the Tissue Inhibitor of Metalloproteinase-3 (TIMP3) gene. SFD closely resembles age-related macular degeneration (AMD), which is the leading cause of blindness in the elderly population of the Western hemisphere. Variants in TIMP3 gene have recently been identified in patients with AMD. A majority of patients with AMD also lose vision as a consequence of choroidal neovascularization (CNV). Thus, understanding the molecular mechanisms that contribute to CNV as a consequence of TIMP-3 mutations will provide insight into the pathophysiology in SFD and likely the neovascular component of the more commonly seen AMD. While the role of VEGF in CNV has been studied extensively, it is becoming increasingly clear that other factors likely play a significant role. The objective of this study was to test the hypothesis that basic Fibroblast Growth Factor (bFGF) regulates SFD-related CNV. In this study we demonstrate that mice expressing mutant TIMP3 (Timp3S179C/S179C) showed reduced MMP inhibitory activity with an increase in MMP2 activity and bFGF levels, as well as accentuated CNV leakage when subjected to laser injury. S179C mutant-TIMP3 in retinal pigment epithelial (RPE) cells showed increased secretion of bFGF and conditioned medium from these cells induced increased angiogenesis in endothelial cells. These studies suggest that S179C-TIMP3 may promote angiogenesis and CNV via a FGFR-1-dependent pathway by increasing bFGF release and activity.

scholarly journals The Orphan Nuclear Receptor ERRγ Regulates Hepatic CB1 Receptor-Mediated Fibroblast Growth Factor 21 Gene Expression

PLoS ONE ◽  
2016 ◽  
Vol 11 (7) ◽  
pp. e0159425 ◽  
Author(s):  
Yoon Seok Jung ◽  
Ji-Min Lee ◽  
Don-Kyu Kim ◽  
Yong-Soo Lee ◽  
Ki-Sun Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Nuclear Receptor ◽  
Cb1 Receptor ◽  
Fibroblast Growth Factor 21 ◽  
Orphan Nuclear Receptor ◽  
Fibroblast Growth

scholarly journals Basic fibroblast growth factor inhibits type I collagen gene expression in osteoblastic MC3T3-E1 cells.

1993 ◽  
Vol 268 (8) ◽  
pp. 5588-5593
Author(s):  
M.M. Hurley ◽  
C. Abreu ◽  
J.R. Harrison ◽  
A.C. Lichtler ◽  
L.G. Raisz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Type I Collagen ◽  
Type I ◽  
Collagen Gene ◽  
Fibroblast Growth ◽  
Collagen Gene Expression

scholarly journals MicroRNA-Regulated Rickettsial Invasion into Host Endothelium via Fibroblast Growth Factor 2 and Its Receptor FGFR1

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 240 ◽  
Author(s):  
Abha Sahni ◽  
Hema Narra ◽  
Jignesh Patel ◽  
Sanjeev Sahni
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Host Cells ◽  
Microvascular Endothelial Cells ◽  
Target Cells ◽  
Fibroblast Growth ◽  
Wide Range ◽  
Microvascular Endothelial

Microvascular endothelial cells (ECs) represent the primary target cells during human rickettsioses and respond to infection via the activation of immediate–early signaling cascades and the resultant induction of gene expression. As small noncoding RNAs dispersed throughout the genome, microRNAs (miRNAs) regulate gene expression post-transcriptionally to govern a wide range of biological processes. Based on our recent findings demonstrating the involvement of fibroblast growth factor receptor 1 (FGFR1) in facilitating rickettsial invasion into host cells and published reports suggesting miR-424 and miR-503 as regulators of FGF2/FGFR1, we measured the expression of miR-424 and miR-503 during R. conorii infection of human dermal microvascular endothelial cells (HMECs). Our results revealed a significant decrease in miR-424 and miR-503 expression in apparent correlation with increased expression of FGF2 and FGFR1. Considering the established phenomenon of endothelial heterogeneity and pulmonary and cerebral edema as the prominent pathogenic features of rickettsial infections, and significant pathogen burden in the lungs and brain in established mouse models of disease, we next quantified miR-424 and miR-503 expression in pulmonary and cerebral microvascular ECs. Again, R. conorii infection dramatically downregulated both miRNAs in these tissue-specific ECs as early as 30 min post-infection in correlation with higher FGF2/FGFR1 expression. Changes in the expression of both miRNAs and FGF2/FGFR1 were next confirmed in a mouse model of R. conorii infection. Furthermore, miR-424 overexpression via transfection of a mimic into host ECs reduced the expression of FGF2/FGFR1 and gave a corresponding decrease in R. conorii invasion, while an inhibitor of miR-424 had the expected opposite effect. Together, these findings implicate the rickettsial manipulation of host gene expression via regulatory miRNAs to ensure efficient cellular entry as the critical requirement to establish intracellular infection.

scholarly journals Adenosine Stimulates Fibroblast Growth Factor-7 Gene Expression Via Adenosine A2b Receptor Signaling in Dermal Papilla Cells

2007 ◽  
Vol 127 (6) ◽  
pp. 1318-1325 ◽  
Author(s):  
Masato Iino ◽  
Ritsuko Ehama ◽  
Yosuke Nakazawa ◽  
Tokuro Iwabuchi ◽  
Masashi Ogo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Dermal Papilla ◽  
Fibroblast Growth ◽  
Receptor Signaling ◽  
Dermal Papilla Cells ◽  
Adenosine A2b Receptor ◽  
A2b Receptor ◽  
Adenosine A2b

scholarly journals Differential induction of gene expression by basic fibroblast growth factor and neuroD in cultured retinal pigment epithelial cells

2000 ◽  
Vol 17 (2) ◽  
pp. 157-164 ◽  
Author(s):  
RUN-TAO YAN ◽  
SHU-ZHEN WANG
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Retinal Pigment Epithelial ◽  
Retinal Pigment ◽  
Fibroblast Growth ◽  
Rpe Cells ◽  
Pigment Epithelial ◽  
Two Factors

Embryonic chick retinal pigment epithelial (RPE) cells can undergo transdifferentiation upon appropriate stimulation. For example, basic fibroblast growth factor (bFGF) induces intact RPE tissue younger than embryonic day 4.5 (E4.5) to transdifferentiate into a neural retina. NeuroD, a gene encoding a basic helix-loop–helix transcription factor, triggers de novo production of cells that resemble young photoreceptor cells morphologically and express general neuron markers (HNK-1/N-CAM and MAP2) and a photoreceptor-specific marker (visinin) from cell cultures of dissociated E6 RPE (Yan & Wang, 1998). The present study examined whether bFGF will lead to the same transdifferentiation phenomenon as neuroD when applied to dissociated, cultured E6 RPE cells, and whether interplay exists between the two factors under the culture conditions. Dissociated E6 RPE cells were cultured in the presence or absence of bFGF, and with or without the addition of retrovirus expressing neuroD. Gene expression was analyzed with immunocytochemistry and in situ hybridization. Unlike neuroD, bFGF did not induce the expression of visinin, or HNK-1/N-CAM and MAP2. However, bFGF elicited the expression of RA4 immunogenicity; yet, many of these RA4-positive cells lacked a neuronal morphology. Addition of bFGF to neuroD-expressing cultures did not alter the number of visinin-expressing cells; misexpression of neuroD in bFGF-treated cultures did not change the number of RA4-positive cells, suggesting the absence of interference or synergistic interaction between the two factors. Our data indicated that bFGF and neuroD induced the expression of different genes in cultured RPE cells.

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