Last update 01 Nov 2024

FGF8

Last update 01 Nov 2024

Basic Info

Synonyms

AIGF, Androgen-induced growth factor, FGF-8

+ [4]

Introduction

Plays an important role in the regulation of embryonic development, cell proliferation, cell differentiation and cell migration. Required for normal brain, eye, ear and limb development during embryogenesis. Required for normal development of the gonadotropin-releasing hormone (GnRH) neuronal system (PubMed:16384934, PubMed:16597617, PubMed:8663044). Plays a role in neurite outgrowth in hippocampal cells (PubMed:21576111).

Drugs associated with FGF8

KM-1334

Target

FGF8

Mechanism

FGF8 inhibitors

Active Org.-

Originator Org.

Kyowa Hakko Kogyo Co., Ltd.

Active Indication-

Inactive Indication

Arthritis [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with FGF8

100 Translational Medicine associated with FGF8

0 Patents (Medical) associated with FGF8

1,791

Literatures (Medical) associated with FGF8

01 Nov 2024·International Journal of Biological Macromolecules

Fgf8 contributes to the pathogenesis of Nager syndrome

Article

Author: Takada, Shinji ; Ogino, Yukiko ; Chen, Jen-Kun ; Jiang, Yun-Jin ; Yabe, Taijiro ; Tse, William Ka Fai ; You, May-Su ; Ulhaq, Zulvikar Syambani

Nager syndrome (NS, OMIM 154400) is a rare disease characterized by craniofacial and limb malformations due to variants in the gene encoding splicing factor 3B subunit 4 (SF3B4). Although various noncanonical functions of SF3B4 unrelated to splicing have been previously described, limited studies elucidate molecular mechanisms underlying NS pathogenesis. Here we showed that sf3b4-deficient fish displayed craniofacial and segmentation defects associated with suppression of fgf8 levels, which perturbed FGF signaling and neural crest cell (NCC) expression. Our finding also pointed out that oxidative stress-induced apoptosis was prominently detected in sf3b4-deficient fish and may further exaggerate the bone remodeling process. Notably, injection of exogenous FGF8 significantly rescued the demonstrated defects in sf3b4-deficient fish, which further supported the participation of Fgf8 in NS pathogenesis. Overall, our study provides valuable insights into the molecular mechanism underlying developmental abnormalities observed in NS and suggests future therapeutic strategies to protect against the pathogenesis of NS and possibilities for preventing severe outcomes.

01 Oct 2024·Annals of Anatomy - Anatomischer Anzeiger

Fibroblast growth factor 8 promotes in vitro neurite outgrowth of placode-derived petrosal and nodose ganglia to varying degrees

Article

Author: Kuerten, Stefanie ; Zhou, Peng ; Cheng, Longfei ; Hintze, Maik ; Qi, Xufeng ; Huang, Ruijin ; Tao, Hengxun ; Pu, Qin ; Cai, Dongqing ; Wang, Yajun ; Wang, Jianlin

Fibroblast growth factors (FGFs) are required for the specification and formation of the epibranchial placodes, which give rise to the distal part of the cranial sensory ganglia. However, it remains unclear whether FGFs play a role in regulating the neurite outgrowth of the epibranchial placode-derived ganglia during further development. Previous studies have shown that Fibroblast growth factor 8 (FGF8) promotes neurite outgrowth from the statoacoustic ganglion in vitro. However, these studies did not distinguish between the neural crest- and placode-derived components of the sensory ganglia. In this study, we focused on the petrosal and nodose ganglia as representatives of the epibranchial ganglia and investigated their axonal outgrowth under the influence of FGF8 signaling protein in vitro. To precisely isolate the placode-derived ganglion part, we labeled the placode and its derivatives with enhanced green fluorescent protein (EGFP) through electroporation. The isolated ganglia were then collected for qRT-PCR assay and cultured in a collagen gel with and without FGF8 protein. Our findings revealed that both placode-derived petrosal and nodose ganglia expressed FGFR1 and FGFR2. In culture, FGF8 exerted a neural trophic effect on the axon outgrowth of both ganglia. While the expression levels of FGFR1/2 were similar between the two ganglia, the petrosal ganglion exhibited greater sensitivity to FGF8 compared to the nodose ganglion. This indicates that the placode-derived ganglia have differential responsiveness to FGF8 signaling during axonal extension. Thus, FGF8 is not only required for the early development of the epibranchial placode, as shown in previous studies, but also promotes neurite outgrowth of placode-derived ganglia.

01 Oct 2024·Journal of Pediatric Urology

The possible role of epigenetics in the etiology of hypospadias

Article

Author: D, Avlan ; S, Yıldız ; I, Inanç ; E, Atlı ; D, Zhuri

INTRODUCTIONHypospadias is a common malformation of the genitourinary system and is thought with a complex interplay between genetics and environmental factors likely contributing to its pathogenesis. This study aimed to investigate the receptor gene expressions of sex hormones, FGFR2, FGF8 and BMP7 and DNA methylations in these genes as an epigenetic mark, which may play a role in the etiology of hypospadias.MATERIAL AND METHODSThe samples from the foreskin of 20 patients with hypospadias and 20 healthy children who underwent circumcision operations were collected. AR, ESR1, FGF8, FGFR2 and BMP7 gene expressions and DNA methylation rates of these genes were investigated in tissues.RESULTSWhile ESR1, FGFR2 and BMP7 gene expressions were found to be significantly higher in the hypospadias group, AR gene expression was found to be lower. In the hypospadias group, DNA methylation rates were found to be significantly higher in the ESR1, FGF8 and FGFR2 genes, but lower in the AR gene (Table).DISCUSSIONRecent clinical studies suggest that epigenetic modifications may play a significant role in genital development, potentially contributing to the etiology of hypospadias. Our recent study demonstrated significant differences in foreskin AR, ESR1, and FGFR2 gene expression between patients with hypospadias and controls. To address this, the present study investigated DNA methylation levels of these same genes in hypospadias patients, hypothesizing that epigenetic modifications might be responsible for the observed gene expression changes. We again observed abnormalities in AR, ESR1, and FGFR2 gene expression in hypospadias patients. Furthermore, we found that DNA methylation patterns associated with these genes differed significantly between hypospadias and control groups.CONCLUSIONSOur study demonstrates significant alterations in DNA methylation of sex hormone receptor genes (ESR1 and AR), FGFR2, and FGF8, which correlate with abnormal expression of these genes in hypospadias cases. These findings suggest a potential role for epigenetic modifications in hypospadias etiology.

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FGF8

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