scholarly journals CRISPR/Cas9-mediated Disruption of Fibroblast Growth Factor 5 in Rabbits Results in a Systemic Long Hair Phenotype by Prolonging Anagen

Genes ◽  
2020 ◽  
Vol 11 (3) ◽  
pp. 297 ◽  
Author(s):  
Yuxin Xu ◽  
Hongmei Liu ◽  
Huilin Pan ◽  
Xinyue Wang ◽  
Yuxin Zhang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Hair Growth ◽  
Negative Regulator ◽  
Fibroblast Growth ◽  
Hair Cycle ◽  
Ideal Model ◽  
Anagen Phase ◽  
Hematoxylin And Eosin ◽  
Scanning Electron

Hair growth and morphology are generally regulated by the hair cycle in mammals. Fibroblast Growth Factor 5 (FGF5), which is a hair cycle regulator, has a role in regulating the hair cycle during the transition from the anagen phase to the catagen phase, and a hereditary long hair phenotype has been widely reported when FGF5 is mutated in humans and other species. However, there has been no such report in rabbits. Thus, the first exon of rabbit FGF5 was disrupted by the CRISPR/Cas9 system, and the phenotype of FGF5-/- rabbits was characterized while using hematoxylin and eosin (H&E) staining, immunohistochemistry, quantitative PCR, scanning electron microscopy, and western blotting. The results showed a significant and systemic long hair phenotype in the FGF5-/- rabbits, which indicated that FGF5 is a negative regulator of hair growth. In addition, a decreased diameter of the fiber and a higher area proportion of hair follicle clusters were determined in FGF5-/- rabbits as compared with the WT rabbits. Further investigation verified that prolonging the anagen phase in rabbits, with decreased BMP2/4 pathway signaling and increased VERSICAN pathway signaling, caused the systemic long hair phenotype. Taken together, these results indicate a systemic long hair phenotype by prolonging anagen in FGF5-/- rabbits, which could be widely used for Fur production and an ideal model for studying the mechanism of long hair in the future.

scholarly journals Fibroblast Growth Factors Stimulate Hair Growth throughβ-Catenin and Shh Expression in C57BL/6 Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Wei-hong Lin ◽  
Li-Jun Xiang ◽  
Hong-Xue Shi ◽  
Jian Zhang ◽  
Li-ping Jiang ◽  
...  
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Hair Growth ◽  
Hair Follicles ◽  
Control Group ◽  
Fibroblast Growth ◽  
Acidic Fibroblast Growth Factor ◽  
Anagen Phase ◽  
Growth Promoting

Growth factors are involved in the regulation of hair morphogenesis and cycle hair growth. The present study sought to investigate the hair growth promoting activities of three approved growth factor drugs, fibroblast growth factor 10 (FGF-10), acidic fibroblast growth factor (FGF-1), and basic fibroblast growth factor (FGF-2), and the mechanism of action. We observed that FGFs promoted hair growth by inducing the anagen phase in telogenic C57BL/6 mice. Specifically, the histomorphometric analysis data indicates that topical application of FGFs induced an earlier anagen phase and prolonged the mature anagen phase, in contrast to the control group. Moreover, the immunohistochemical analysis reveals earlier induction ofβ-catenin and Sonic hedgehog (Shh) in hair follicles of the FGFs-treated group. These results suggest that FGFs promote hair growth by inducing the anagen phase in resting hair follicles and might be a potential hair growth-promoting agent.

Decapeptide with fibroblast growth factor (FGF)-5 partial sequence inhibits hair growth suppressing activity of FGF-5

2003 ◽  
Vol 197 (2) ◽  
pp. 272-283 ◽  
Author(s):  
Chikako Ito ◽  
Yuko Saitoh ◽  
Yasuko Fujita ◽  
Yoshimitsu Yamazaki ◽  
Toru Imamura ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Hair Growth ◽  
Partial Sequence ◽  
Fibroblast Growth

scholarly journals Dual effects of fibroblast growth factor 21 on hepatic energy metabolism

2015 ◽  
Vol 227 (1) ◽  
pp. 37-47 ◽  
Author(s):  
Ricardo J Samms ◽  
Michelle Murphy ◽  
Maxine J Fowler ◽  
Scott Cooper ◽  
Paul Emmerson ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Lipid Content ◽  
Negative Regulator ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Hepatic Lipid ◽  
Siberian Hamsters ◽  
Hepatic Lipid Content

The aim of this study was to investigate the mechanisms by which fibroblast growth factor 21 (FGF21) affects hepatic integration of carbohydrate and fat metabolism in Siberian hamsters, a natural model of adiposity. Twelve aged matched adult male Siberian hamsters maintained in their long-day fat state since birth were randomly assigned to one of two treatment groups and were continuously infused with either vehicle (saline;n=6) or recombinant human FGF21 protein (1 mg/kg per day;n=6) for 14 days. FGF21 administration caused a 40% suppression (P<0.05) of hepatic pyruvate dehydrogenase complex (PDC), the rate-limiting step in glucose oxidation, a 34% decrease (P<0.05) in hepatic acetylcarnitine accumulation, an index of reduced PDC flux, a 35% increase (P<0.05) in long-chain acylcarnitine content (an index of flux through β-oxidation) and a 47% reduction (P<0.05) in hepatic lipid content. These effects were underpinned by increased protein abundance of PD kinase-4 (PDK4, a negative regulator of PDC), the phosphorylated (inhibited) form of acetyl-CoA carboxylase (ACC, a negative regulator of delivery of fatty acids into the mitochondria) and the transcriptional co-regulators of energy metabolism peroxisome proliferator activated receptor gamma co-activator alpha (PGC1α) and sirtuin-1. These findings provide novel mechanistic basis to support the notion that FGF21 exerts profound metabolic benefits in the liver by modulating nutrient flux through both carbohydrate (mediated by a PDK4-mediated suppression of PDC activity) and fat (mediated by deactivation of ACC) metabolism, and therefore may be an attractive target for protection from increased hepatic lipid content and insulin resistance that frequently accompany obesity and diabetes.

scholarly journals Bone Formation Regulates Circulating Concentrations of Fibroblast Growth Factor 23

Endocrinology ◽  
2009 ◽  
Vol 150 (11) ◽  
pp. 4835-4845 ◽  
Author(s):  
Rana Samadfam ◽  
Christian Richard ◽  
Loan Nguyen-Yamamoto ◽  
Isabel Bolivar ◽  
David Goltzman
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Bone Formation ◽  
Bone Turnover ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Negative Regulator ◽  
Fibroblast Growth ◽  
Osteoblastic Cell Line ◽  
High Calcium

We examined the role of bone remodeling in the regulation of circulating concentrations of FGF23 using mouse models manifesting differing degrees of coupled and uncoupled bone turnover. Administration of the antiresorptive agent osteoprotegerin produced a profound reduction in bone resorption and formation in male and oophorectomized female mice, accompanied by an increase in serum levels of fibroblast growth factor 23 (FGF23) and a reduction in circulating 1,25-dihydroxyvitamin D [1,25(OH)2D]. In contrast, exogenous PTH(1-34) administration increased bone turnover and reduced circulating FGF23. In 1,25(OH)2D-deficient, 25-hydroxyvitamin D 1α-hydroxylase null mice on a high-calcium diet, endogenous PTH was elevated, bone formation but not resorption was increased, and serum FGF23 was virtually undetectable; on a rescue diet, serum calcium was normalized, PTH levels were reduced, bone formation was reduced, and serum FGF23 levels increased. After PTH treatment of wild-type mice, gene expression of dentin matrix protein 1 (DMP1) in bone was increased, whereas gene expression of FGF23 was reduced. In vitro studies in the osteoblastic cell line UMR-106 showed that externally added DMP1 could inhibit FGF23 gene expression and production stimulated by 1,25(OH)2D3. The results show that osteoblastic bone formation is a potent modulator of FGF23 production and release into the circulation, suggest that the biological consequences on mineral homeostasis of circulating FGF23 may also be dependent on the prevailing rate of bone turnover, and provide evidence that DMP1 may be a direct negative regulator of FGF23 production in osteoblastic cells.

Fibroblast Growth Factor 5 Inhibits Hair Growth by Blocking Dermal Papilla Cell Activation

2002 ◽  
Vol 290 (1) ◽  
pp. 169-176 ◽  
Author(s):  
Yutaka Ota ◽  
Yuko Saitoh ◽  
Satoshi Suzuki ◽  
Kazuo Ozawa ◽  
Mitsuko Kawano ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Hair Growth ◽  
Cell Activation ◽  
Dermal Papilla ◽  
Fibroblast Growth ◽  
Dermal Papilla Cell
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