Role of FGF signalling in neural crest cell migration during early chick embryo development

Zhang, Xiao-Tan; Wang, Guang; Li, Yán; Chuai, Manli; Lee, Kenneth K.; Yang, Xuesong

doi:10.1017/s096719941800045x

Cited by 5 publications

(2 citation statements)

References 42 publications

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“…Notably, 2 additional members of the FGF family, FGF1 and FGF23, have also been observed as DE genes upon miR-149 overexpression in our data set. Previous research has demonstrated that FGFs and their receptors (FGFR) are involved in general craniofacial development and orofacial clefting (Stanier and Pauws 2012) and are modulators of hNCC development (Zhang et al 2018). Finally, we also identified TGFB2 among our DE genes, which is noteworthy as it was recently revealed as a target of miR-193a-3p during craniofacial development in mice (Fu et al 2021).…”

Section: Discussionsupporting

confidence: 53%

MiRNA-149 as a Candidate for Facial Clefting and Neural Crest Cell Migration

et al. 2021

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Nonsyndromic cleft lip with or without palate (nsCL/P) ranks among the most common human birth defects and has a multifactorial etiology. Human neural crest cells (hNCC) make a substantial contribution to the formation of facial bone and cartilage and are a key cell type in terms of nsCL/P etiology. Based on increasing evidence for the role of noncoding regulatory mechanisms in nsCL/P, we investigated the role of hNCC-expressed microRNAs (miRNA) in cleft development. First, we conducted a systematic analysis of miRNAs expressed in human-induced pluripotent stem cell–derived hNCC using Affymetrix microarrays on cell lines established from 4 unaffected donors. These analyses identified 152 candidate miRNAs. Based on the hypothesis that candidate miRNA loci harbor genetic variation associated with nsCL/P risk, the genomic locations of these candidates were cross-referenced with data from a previous genome-wide association study of nsCL/P. Associated variants were reanalyzed in independent nsCL/P study populations. Jointly, the results suggest that miR-149 is implicated in nsCL/P etiology. Second, functional follow-up included in vitro overexpression and inhibition of miR-149 in hNCC and subsequent analyses at the molecular and phenotypic level. Using 3′RNA-Seq, we identified 604 differentially expressed (DE) genes in hNCC overexpressing miR-149 compared with untreated cells. These included TLR4 and JUNB, which are established targets of miR-149, and NOG, BMP4, and PAX6, which are reported nsCL/P candidate genes. Pathway analyses revealed that DE genes were enriched in pathways including regulation of cartilage development and NCC differentiation. At the cellular level, distinct hNCC migration patterns were observed in response to miR-149 overexpression. Our data suggest that miR-149 is involved in the etiology of nsCL/P via its role in hNCC migration.

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Section: Discussionsupporting

confidence: 53%

MiRNA-149 as a Candidate for Facial Clefting and Neural Crest Cell Migration

et al. 2021

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“…[ 10 ] Moreover, FGF plays a key role in neural crest cell migration and development. [ 11 ] It has been shown that the addition of FGFs to blastocyst increased the number of trophoblastic cells. Furthermore, FGF signalling induces cell division in the pre-implantation embryo.…”

Section: Introductionmentioning

confidence: 99%

Association of Fibroblast Growth Factor-1 Promoter Polymorphism and its Serum Concentrations with Repeated Implantation Failure after In vitro Fertilisation: A Cross-sectional Study

Kharamani,

Mashayekhi,

Salehi

2024

Journal of Human Reproductive Sciences

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Background: Fibroblast growth factors (FGFs) play a key role in embryo implantation and support endometrial trophoblastic interaction. Aim: The aim of the study was to evaluate the association between FGF-1 (rs34011) gene variety and its serum concentration with repeated implantation failure (RIF). Setting and Design: The design of the study was a cross-sectional study. Materials and Methods: Four hundred infertile women with a history of RIF and 400 healthy women undergoing the first in vitro fertilisation-embryo transfer attempt with successful delivery (controls) were enrolled in the study. Genomic DNA was extracted from peripheral blood leucocytes and genotyped by Tetra-Primer Amplification Refractory Mutation System-Polymerase Chain Reaction. Serum FGF-1 concentration was evaluated with enzyme-linked immunosorbent assay. Statistical Analysis Used: The ANOVA test was used to analyse the difference between the means of the groups. Results: In RIF group, the genotype frequencies of the GG, GA and AA were 59%, 33.5% and 7.5%, respectively, whereas in controls were 72.5%, 24% and 3.5%, respectively. The G and A allele frequencies in the RIF group were 75.75% and 24.25%, while in controls were 84.5% and 15.5%, respectively (P < 0.0001). We have also shown that serum FGF-1 concentration in RIF and control groups was 17 ± 3.55 and 23.62 ± 4.91 pg/mL, respectively (P = 0.008). We have also shown that AA genotype is significantly associated with decreased serum FGF-1 concentration in RIF (AA, GA and GG serum levels were 9.55 ± 2.65, 14 ± 3.35 and 22.55 ± 7.26 pg/mL, and in controls were 12.22 ± 2.27, 18.44 ± 5.98 and 26.66 ± 8.29 pg/mL, respectively). Conclusion: The current study suggests that a significant association between FGF-1 (rs34011) promoter polymorphism and its serum concentration with RIF. The study also suggests that AA genotype is linked to lower FGF-1 serum levels and may play a risk factor for RIF.

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Neural Tube Disorders

Bhandari

Thada

2011

Encyclopedia of Child Behavior and Development

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Role of FGF signalling in neural crest cell migration during early chick embryo development

Cited by 5 publications

References 42 publications

MiRNA-149 as a Candidate for Facial Clefting and Neural Crest Cell Migration

MiRNA-149 as a Candidate for Facial Clefting and Neural Crest Cell Migration

Association of Fibroblast Growth Factor-1 Promoter Polymorphism and its Serum Concentrations with Repeated Implantation Failure after In vitro Fertilisation: A Cross-sectional Study

Neural Tube Disorders

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