scholarly journals Gene targeted ablation of high molecular weight fibroblast growth factor-2

2008 ◽  
Vol 238 (2) ◽  
pp. 351-357 ◽  
Author(s):  
Mohamad Azhar ◽  
Moying Yin ◽  
Ming Zhou ◽  
Hongqi Li ◽  
Marwan Mustafa ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
High Molecular Weight ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth

scholarly journals Biochemical Analysis of the Arginine Methylation of High Molecular Weight Fibroblast Growth Factor-2

2000 ◽  
Vol 275 (5) ◽  
pp. 3150-3157 ◽  
Author(s):  
Sharon Klein ◽  
James A. Carroll ◽  
Yan Chen ◽  
Michael F. Henry ◽  
Pamela A. Henry ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
High Molecular Weight ◽  
Biochemical Analysis ◽  
Arginine Methylation ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth

scholarly journals Methylation of high molecular weight fibroblast growth factor-2 determines post-translational increases in molecular weight and affects its intracellular distribution.

1996 ◽  
Vol 7 (8) ◽  
pp. 1249-1258 ◽  
Author(s):  
G Pintucci ◽  
N Quarto ◽  
D B Rifkin
Keyword(s):  
Molecular Weight ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
High Molecular Weight ◽  
Nuclear Protein ◽  
Intracellular Distribution ◽  
Nuclear Accumulation ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Post Translational Modification

The high molecular weight (HMW) forms (24, 22.5, and 22 kDa) of basic fibroblast growth factor-2 (FGF-2) contain an N-terminal extension responsible for their predominantly nuclear localization. These forms of FGF-2 are post-translationally modified, resulting in a 1- to 2-kDa increase in apparent molecular mass. Here we show that this post-translational modification is inhibited by methionine starvation and by the methyltransferase inhibitors 5'-deoxy-5'-methylthioadenosine (MTA) and 3-deaza-adenosine. Inhibition of the methylation-dependent modification results in a significant decrease in HMW FGF-2 nuclear accumulation, suggesting that methylation is relevant to the intracellular distribution of these forms of FGF-2. Treatment with MTA does not affect either the synthesis or the intracellular fate of another nuclear protein, the SV40 large T antigen, demonstrating that this drug does not have a generalized effect on nuclear protein accumulation. These results link HMW FGF-2 post-translational modification to its intracellular distribution.

Fibroblast Growth Factor 2 High Molecular Weight Isoforms in Dentoalveolar Mineralization

2021 ◽  
Author(s):  
Grethel Millington ◽  
Johnny Joseph ◽  
Liping Xiao ◽  
Anushree Vijaykumar ◽  
Mina Mina ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
High Molecular Weight ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth

scholarly journals Elimination or neutralization of endogenous high-molecular-weight FGF2 mitigates doxorubicin-induced cardiotoxicity

2019 ◽  
Vol 316 (2) ◽  
pp. H279-H288 ◽  
Author(s):  
Navid Koleini ◽  
Jon-Jon Santiago ◽  
Barbara E. Nickel ◽  
Glen Lester Sequiera ◽  
Jie Wang ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
High Molecular Weight ◽  
Cardiac Response ◽  
Neonatal Rat ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Cardiac Damage

Cardiac fibroblast growth factor 2 (FGF2) exerts multiple paracrine activities related to cardiac response to injury. Endogenous FGF2 is composed of a mixture of 70% high- and 30% low-molecular-weight isoforms (Hi-FGF2 and Lo-FGF2, respectivley); although exogenously added Lo-FGF2 is cardioprotective, the roles of endogenous Hi-FGF2 or Lo-FGF2 have not been well defined. Therefore, we investigated the effect of elimination of Hi-FGF2 expression on susceptibility to acute cardiac damage in vivo caused by an injection of the genotoxic drug doxorubicin (Dox). Mice genetically depleted of endogenous Hi-FGF2 and expressing only Lo-FGF2 [FGF2(Lo) mice] were protected from the Dox-induced decline in ejection fraction displayed by their wild-type FGF2 [FGF2(WT)] mouse counterparts, regardless of sex, as assessed by echocardiography for up to 10 days post-Dox treatment. Because cardiac FGF2 is produced mainly by nonmyocytes, we next addressed potential contribution of fibroblast-produced FGF2 on myocyte vulnerability to Dox. In cocultures of neonatal rat cardiomyocytes (r-cardiomyocytes) with mouse fibroblasts from FGF2(WT) or FGF2(Lo) mice, only the FGF2(Lo)-fibroblast cocultures protected r-cardiomyocytes from Dox-induced mitochondrial and cellular damage. When r-cardiomyocytes were cocultured with or exposed to conditioned medium from human fibroblasts, neutralizing antibodies for human Hi-FGF-2, but not total FGF2, mitigated Dox-induced injury of cardiomyocytes. We conclude that endogenous Hi-FGF2 reduces cardioprotection by endogenous Lo-FGF2. Antibody-based neutralization of endogenous Hi-FGF2 may offer a prophylactic treatment against agents causing acute cardiac damage. NEW & NOTEWORTHY Cardiomyocytes, in vivo and in vitro, were protected from the deleterious effects of the anticancer drug doxorubicin by the genetic elimination or antibody-based neutralization of endogenous paracrine high-molecular-weight fibroblast growth factor 2 isoforms. These findings have a translational potential for mitigating doxorubicin-induced cardiac damage in patients with cancer by an antibody-based treatment.

scholarly journals High Molecular Weight Fibroblast Growth Factor-2 in the Human Heart Is a Potential Target for Prevention of Cardiac Remodeling

PLoS ONE ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. e97281 ◽  
Author(s):  
Jon-Jon Santiago ◽  
Leslie J. McNaughton ◽  
Navid Koleini ◽  
Xin Ma ◽  
Brian Bestvater ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
High Molecular Weight ◽  
Cardiac Remodeling ◽  
Human Heart ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Potential Target
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