Divergence of intracellular signaling pathways and early response genes of two closely related fibroblast growth factors, FGF8 and FGF18, in bovine ovarian granulosa cells

Jiang, Zhongliang; Guerrero-Netro, Hilda M; Juengel, Jennifer L.; Price, Christopher A.

doi:10.1016/j.mce.2013.05.017

Cited by 40 publications

(25 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a comparison of FGF8 and FGF18 signaling pathways in bovine granulosa cells, we demonstrated that FGF8 activates the typical FGF responses including phosphorylation of MAPK3/1 and rapid and transient expression of SPRY2 and NR4A2, whereas FGF18 altered none of these targets (Jiang et al 2013). Using a microarray approach, we identified additional early immediate response genes that were upregulated by FGF8 but not by FGF18, including FOS and XIRP1, and others that were stimulated by both FGF8 and FGF18, including FOSL1 (Jiang et al 2013).…”

Section: Intracellular Fgf Signaling In Granulosa Cellsmentioning

confidence: 95%

“…In human granulosa lutein cells, FGF2 but not FGF4 or FGF10 increased SPRY2 mRNA levels (Haimov-Kochman et al 2005), whereas in bovine granulosa cells FGF2 and FGF4 stimulated SPRY2 mRNA abundance (Jiang et al 2011, Jiang & Price 2012. Several studies have demonstrated that FGF8 stimulates MAPK3/1 phosphorylation and SPRY2 mRNA levels in rat, human and mouse granulosa/ cumulus cells (Sugiura et al 2009, Miyoshi et al 2010, Jiang et al 2013.…”

Section: Intracellular Fgf Signaling In Granulosa Cellsmentioning

confidence: 99%

“…Using a microarray approach, we identified additional early immediate response genes that were upregulated by FGF8 but not by FGF18, including FOS and XIRP1, and others that were stimulated by both FGF8 and FGF18, including FOSL1 (Jiang et al 2013). Perhaps the most interesting difference between FGF8 and FGF18 was the stimulation by FGF8 and marked inhibition by FGF18 of abundance of mRNA encoding the DNA damage response gene GADD45B.…”

Section: Intracellular Fgf Signaling In Granulosa Cellsmentioning

confidence: 99%

“…Horizontal lines indicate no effect; NA, data not available. Data from Miyoshi et al (2010), Jiang et al (2011Jiang et al ( , 2013 and Portela et al (2015). intracellular signaling and/or ii) interactions between FGFs, FGFRs, and HSPGs.…”

Section: The Basis For Divergent Signaling Of Related Fgfsmentioning

confidence: 99%

“…FGF8b provokes a strong activation of MAPK3/1 in the midbrain, whereas FGF8a results in a lower level of MAPK3/1 phosphorylation (Sato & Nakamura 2004). Data from studies with bovine granulosa cells show that FGF8 results in a strong and transient phosphorylation of MAPK3/1 while addition of FGF18 provokes a very weak response (Jiang et al 2013). The difference in the activities of FGF8a and FGF8b has been attributed to a single phenylalanine residue (F32) present in the N-terminus of FGF8b that allows strong binding with the receptor, and which is absent in FGF8a leading to a weak receptor binding complex .…”

Section: Differential Intracellular Signalingmentioning

confidence: 99%

See 4 more Smart Citations

Mechanisms of fibroblast growth factor signaling in the ovarian follicle

Price

2015

Journal of Endocrinology

View full text Add to dashboard Cite

Fibroblast growth factors (FGFs) have been shown to alter growth and differentiation of reproductive tissues in a variety of species. Within the female reproductive tract, the effects of FGFs have been focused on the ovary, and the most studied one is FGF2, which stimulates granulosa cell proliferation and decreases differentiation (decreased steroidogenesis). Other FGFs have also been implicated in ovarian function, and this review summarizes the effects of members of two subfamilies on ovarian function; the FGF7 subfamily that also contains FGF10, and the FGF8 subfamily that also contains FGF18. There are data to suggest that FGF8 and FGF18 have distinct actions on granulosa cells, despite their apparent similar receptor binding properties. Studies of non-reproductive developmental biology also indicate that FGF8 is distinct from FGF18, and that FGF7 is also distinct from FGF10 despite similar receptor binding properties. In this review, the potential mechanisms of differential action of FGF7/FGF10 and FGF8/FGF18 during organogenesis will be reviewed and placed in the context of follicle development. A model is proposed in which FGF8 and FGF18 differentially activate receptors depending on the properties of the extracellular matrix in the follicle.

show abstract

Section: Intracellular Fgf Signaling In Granulosa Cellsmentioning

confidence: 95%

Section: Intracellular Fgf Signaling In Granulosa Cellsmentioning

confidence: 99%

Section: Intracellular Fgf Signaling In Granulosa Cellsmentioning

confidence: 99%

Section: The Basis For Divergent Signaling Of Related Fgfsmentioning

confidence: 99%

Section: Differential Intracellular Signalingmentioning

confidence: 99%

See 3 more Smart Citations

Mechanisms of fibroblast growth factor signaling in the ovarian follicle

Price

2015

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

Nkx6.1‐mediated insulin secretion and β‐cell proliferation is dependent on upregulation of c‐Fos

et al. 2016

View full text Add to dashboard Cite

Edited by L aszl o NagyUnderstanding the molecular pathways that enhance b-cell proliferation, survival, and insulin secretion may be useful to improve treatments for diabetes. Nkx6.1 induces proliferation through the Nr4a nuclear receptors, and improves insulin secretion and survival through the peptide hormone VGF. Here we demonstrate that Nkx6.1-mediated upregulation of Nr4a1, Nr4a3, and VGF is dependent on c-Fos expression. c-Fos overexpression results in activation of Nkx6.1 responsive genes and increases b-cell proliferation, insulin secretion, and cellular survival. c-Fos knockdown impedes Nkx6.1-mediated b-cell proliferation and insulin secretion. These data demonstrate that c-Fos is critical for Nkx6.1-mediated expansion of functional b-cell mass.

show abstract

The developing story of Sprouty and cancer

Masoumi-Moghaddam

Amini

Morris

2014

Cancer Metastasis Rev

140

181

View full text Add to dashboard Cite

Sprouty proteins are evolutionarily conserved modulators of MAPK/ERK pathway. Through interacting with an increasing number of effectors, mediators, and regulators with ultimate influence on multiple targets within or beyond ERK, Sprouty orchestrates a complex, multilayered regulatory system and mediates a crosstalk among different signaling pathways for a coordinated cellular response. As such, Sprouty has been implicated in various developmental and physiological processes. Evidence shows that ERK is aberrantly activated in malignant conditions. Accordingly, Sprouty deregulation has been reported in different cancer types and shown to impact cancer development, progression, and metastasis. In this article, we have tried to provide an overview of the current knowledge about the Sprouty physiology and its regulatory functions in health, as well as an updated review of the Sprouty status in cancer. Putative implications of Sprouty in cancer biology, their clinical relevance, and their proposed applications are also revisited. As a developing story, however, role of Sprouty in cancer remains to be further elucidated.

show abstract

Divergence of intracellular signaling pathways and early response genes of two closely related fibroblast growth factors, FGF8 and FGF18, in bovine ovarian granulosa cells

Cited by 40 publications

References 57 publications

Mechanisms of fibroblast growth factor signaling in the ovarian follicle

Mechanisms of fibroblast growth factor signaling in the ovarian follicle

Nkx6.1‐mediated insulin secretion and β‐cell proliferation is dependent on upregulation of c‐Fos

The developing story of Sprouty and cancer

Contact Info

Product

Resources

About