Role of fibroblast growth factor receptor signaling in kidney development

Bates, Carlton M.

doi:10.1007/s00467-006-0239-7

Cited by 41 publications

(14 citation statements)

References 38 publications

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“…FGF10 is a multifunctional growth factor playing crucial roles in the development of many organs and tissues including the kidney ( Beenken and Mohammadi, 2009 ; Itoh, 2015 ). Deletion of either Fgf10 or its receptor Fgfr2-IIIb in mice led to kidney dysgenesis characterized by fewer collecting ducts and nephrons ( Bates, 2007 ). Overexpression of a dominant negative receptor isoform in transgenic mice has revealed more striking defects including renal aplasia or severe dysplasia ( Bates, 2007 ).…”

Section: Introductionmentioning

confidence: 99%

FGF10 Protects Against Renal Ischemia/Reperfusion Injury by Regulating Autophagy and Inflammatory Signaling

et al. 2018

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Ischemia-reperfusion (I/R) is a common cause of acute kidney injury (AKI), which is associated with high mortality and poor outcomes. Autophagy plays important roles in the homeostasis of renal tubular cells (RTCs) and is implicated in the pathogenesis of AKI, although its role in the process is complex and controversial. Fibroblast growth factor 10 (FGF10), a multifunctional FGF family member, was reported to exert protective effect against cerebral ischemia injury and myocardial damage. Whether FGF10 has similar beneficial effect, and if so whether autophagy is associated with the potential protective activity against AKI has not been investigated. Herein, we report that FGF10 treatment improved renal function and histological integrity in a rat model of renal I/R injury. We observed that FGF10 efficiently reduced I/R-induced elevation in blood urea nitrogen, serum creatinine as well as apoptosis induction of RTCs. Interestingly, autophagy activation following I/R was suppressed by FGF10 treatment based on the immunohistochemistry staining and immunoblot analyses of LC3, Beclin-1 and SQSTM1/p62. Moreover, combined treatment of FGF10 with Rapamycin partially reversed the renoprotective effect of FGF10 suggesting the involvement of mTOR pathway in the process. Interestingly, FGF10 also inhibited the release of HMGB1 from the nucleus to the extracellular domain and regulated the expression of inflammatory cytokines such as TNF-α, IL-1β and IL-6. Together, these results indicate that FGF10 could alleviate kidney I/R injury by suppressing excessive autophagy and inhibiting inflammatory response and may therefore have the potential to be used for the prevention and perhaps treatment of I/R-associated AKI.

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Section: Introductionmentioning

confidence: 99%

FGF10 Protects Against Renal Ischemia/Reperfusion Injury by Regulating Autophagy and Inflammatory Signaling

et al. 2018

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“…Since then, this locus has been successfully validated in various populations throughout the world including those of European ancestry, Asian, Ashkenazi Jewish and Israeli populations [18], [37]–[39]. FGFR2 encodes fibroblast growth factor receptor type 2, which is a receptor tyrosine kinase playing a critical role in the growth signaling pathway that is involved in growth and differentiation of cells in various tissues including the breast and kidney [40], [41]. All the SNPs that were found to be associated with breast cancer are located in intron 2 of the gene; the risk allele of rs2981578, a SNP that was identified in this study, created a putative binding site for Oct-1/Runx2, which gives rise to a strong protein-DNA complex that alters binding of the transcription factor and causes differential expression between the common and minor haplotypes of FGFR2 [42].…”

Section: Discussionmentioning

confidence: 99%

Genome-Wide Association Study of Breast Cancer in the Japanese Population

et al. 2013

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Breast cancer is the most common malignancy among women in worldwide including Japan. Several studies have identified common genetic variants to be associated with the risk of breast cancer. Due to the complex linkage disequilibrium structure and various environmental exposures in different populations, it is essential to identify variants associated with breast cancer in each population, which subsequently facilitate the better understanding of mammary carcinogenesis. In this study, we conducted a genome-wide association study (GWAS) as well as whole-genome imputation with 2,642 cases and 2,099 unaffected female controls. We further examined 13 suggestive loci (P<1.0×10−5) using an independent sample set of 2,885 cases and 3,395 controls and successfully validated two previously-reported loci, rs2981578 (combined P-value of 1.31×10−12, OR = 1.23; 95% CI = 1.16–.30) on chromosome 10q26 (FGFR2), rs3803662 (combined P-value of 2.79×10−11, OR = 1.21; 95% CI = 1.15–.28) and rs12922061 (combined P-value of 3.97×10−10, OR = 1.23; 95% CI = 1.15–.31) on chromosome 16q12 (TOX3-LOC643714). Weighted genetic risk score on the basis of three significantly associated variants and two previously reported breast cancer associated loci in East Asian population revealed that individuals who carry the most risk alleles in category 5 have 2.2 times higher risk of developing breast cancer in the Japanese population than those who carry the least risk alleles in reference category 1. Although we could not identify additional loci associated with breast cancer, our study utilized one of the largest sample sizes reported to date, and provided genetic status that represent the Japanese population. Further local and international collaborative study is essential to identify additional genetic variants that could lead to a better, accurate prediction for breast cancer.

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“…Clearly, ear neurosensory development depends on several Fgfs (3,8,10) and Fgfr2 for overall neurosensory and Fgfr3 for supporting cell development (Pirvola et al, 2000; Puligilla et al, 2007). Kidney development also depends on Fgf 7/10 ligands signaling mostly via the Fgfr1 receptor (Bates, 2007; Rossini et al, 2005), but also Fgfr2 (McMahon, 2016). BMP4 downregulation combined with Fgf expression is an essential early step in neural induction (Fritzsch et al, 2006a; Meinhardt, 2015) that results in an unclear proportion of BMP4/Fgf signaling (Singh and Groves, 2016).…”

Section: Introductionmentioning

confidence: 99%

Gene, cell, and organ multiplication drives inner ear evolution

Fritzsch

Elliott

2017

Developmental Biology

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We review the development and evolution of the ear neurosensory cells, the aggregation of neurosensory cells into an otic placode, the evolution of novel neurosensory structures dedicated to hearing and the evolution of novel nuclei and their input dedicated to processing those novel auditory stimuli. The evolution of the apparently novel auditory system lies in duplication and diversification of cell fate transcription regulation that allows variation at the cellular level [transforming a single neurosensory cell into a sensory cell connected to its targets by a sensory neuron as well as diversifying hair cells], organ level [duplication of organ development followed by diversification and novel stimulus acquisition] and brain nuclear level [multiplication of transcription factors to regulate various neuron and neuron aggregate fate to transform the spinal cord into the unique hindbrain organization]. Tying cell fate changes driven by bHLH and other transcription factors into cell and organ changes is at the moment tentative as not all relevant factors are known and their gene regulatory network is only rudimentary understood. Future research can use the blueprint proposed here to provide both the deeper molecular evolutionary understanding as well as a more detailed appreciation of developmental networks. This understanding can reveal how an auditory system evolved through transformation of existing cell fate determining networks and thus how neurosensory evolution occurred through molecular changes affecting cell fate decision processes. Appreciating the evolutionary cascade of developmental program changes could allow identifying essential steps needed to restore cells and organs in the future.

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Role of fibroblast growth factor receptor signaling in kidney development

Cited by 41 publications

References 38 publications

FGF10 Protects Against Renal Ischemia/Reperfusion Injury by Regulating Autophagy and Inflammatory Signaling

FGF10 Protects Against Renal Ischemia/Reperfusion Injury by Regulating Autophagy and Inflammatory Signaling

Genome-Wide Association Study of Breast Cancer in the Japanese Population

Gene, cell, and organ multiplication drives inner ear evolution

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