FGF-16 is required for embryonic heart development

Lu, Shun; Sheikh, Farah; Sheppard, Patricia; Fresnoza, Agnes; Duckworth, Mary Lynn; Detillieux, Karen A.; Cattini, Peter A.

doi:10.1016/j.bbrc.2008.06.029

Cited by 57 publications

(63 citation statements)

References 19 publications

(25 reference statements)

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“…There are both in vivo and in vitro data showing that the activated epicardium produces VEGFA and FGF2, factors that promote angiogenesis in the remodeling tissue (18). Throughout embryonic development, the epicardium stimulates myocardial proliferation through the secretion of mitogenic factors including FGF9/16/20 (53)(54)(55). Therefore, epicardial activation following MI injury in the adult heart may recapitulate developmental mechanisms to serve as a source of signaling molecules directing myocardial repair in the post-MI setting.…”

Section: Discussionmentioning

confidence: 99%

Epicardial YAP/TAZ orchestrate an immunosuppressive response following myocardial infarction

Ramjee¹,

Li²,

Manderfield³

et al. 2017

Journal of Clinical Investigation

134

106

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Section: Discussionmentioning

confidence: 99%

Epicardial YAP/TAZ orchestrate an immunosuppressive response following myocardial infarction

Ramjee¹,

Li²,

Manderfield³

et al. 2017

Journal of Clinical Investigation

134

106

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“…Mutation of either gene caused a thin myocardium phenotype and, similarly, conditional mutation of Fgfr1 and Fgfr2 (genes encoding FGF receptors) together in the myocardium resulted in a thin-walled ventricle (Lavine et al, 2005;Lu et al, 2008). FGF2 is prominently expressed in the embryonic heart, although mutation of Fgf2 alone has no impact on heart development, and does not further enhance the heart phenotype when combined with Fgf9 deficiency (Lavine et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

IGF signaling directs ventricular cardiomyocyte proliferation during embryonic heart development

et al. 2011

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SUMMARYSecreted factors from the epicardium are believed to be important in directing heart ventricular cardiomyocyte proliferation and morphogenesis, although the specific factors involved have not been identified or characterized adequately. We found that IGF2 is the most prominent mitogen made by primary mouse embryonic epicardial cells and by a newly derived immortalized mouse embryonic epicardial cell line called MEC1. In vivo, Igf2 is expressed in the embryonic mouse epicardium during midgestation heart development. Using a whole embryo culture assay in the presence of inhibitors, we confirmed that IGF signaling is required to activate the ERK proliferation pathway in the developing heart, and that the epicardium is required for this response. Global disruption of the Igf2 gene, or conditional disruption of the two IGF receptor genes Igf1r and Insr together in the myocardium, each resulted in a significant decrease in ventricular wall proliferation and in ventricular wall hypoplasia. Ventricular cardiomyocyte proliferation in mutant embryos was restored to normal at E14.5, concurrent with the establishment of coronary circulation. Our results define IGF2 as a previously unexplored epicardial mitogen that is required for normal ventricular chamber development.

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“…Other FGFs in contrast regulate important developmental processes in mammalians, such as blastocyst formation (FGF4), gastrulation (FGF8), epithelial-mesenchymal interactions necessary for development of epithelial (FGF10) or mesenchymal (FGF9, FGF18) components of multiple organs, and heart and brain morphogenesis (FGF15, FGF16, FGF17) [15][16][17][18][19][20][21]. These processes rely on FGF-mediated communication between distant cell populations within the embryo, and therefore demand the FGF structure to be stable enough to fulfill the required spatiotemporal signaling needs.…”

Section: Introductionmentioning

confidence: 99%

Instability restricts signaling of multiple fibroblast growth factors

Buchtová

Chaloupková

Zakrzewska

et al. 2015

Cell. Mol. Life Sci.

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Fibroblast growth factors (FGFs) deliver extracellular signals that govern many developmental and regenerative processes, but the mechanisms regulating FGF signaling remain incompletely understood. Here, we explored the relationship between intrinsic stability of FGF proteins and their biological activity for all 18 members of the FGF family. We report that FGF1, FGF3, FGF4, FGF6, FGF8, FGF9, FGF10, FGF16, FGF17, FGF18, FGF20, and FGF22 exist as unstable proteins, which are rapidly degraded in cell cultivation media. Biological activity of FGF1, FGF3, FGF4, FGF6, FGF8, FGF10, FGF16, FGF17, and FGF20 is limited by their instability, manifesting as failure to activate FGF receptor signal transduction over long periods of time, and influence specific cell behavior in vitro and in vivo. Stabilization via exogenous heparin binding, introduction of stabilizing mutations or lowering the cell cultivation temperature rescues signaling of unstable FGFs. Thus, the intrinsic ligand instability is an important elementary level of regulation in the FGF signaling system.

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FGF-16 is required for embryonic heart development

Cited by 57 publications

References 19 publications

Epicardial YAP/TAZ orchestrate an immunosuppressive response following myocardial infarction

Epicardial YAP/TAZ orchestrate an immunosuppressive response following myocardial infarction

IGF signaling directs ventricular cardiomyocyte proliferation during embryonic heart development

Instability restricts signaling of multiple fibroblast growth factors

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