Mutation of the mouse hepatocyte nuclear factor/forkhead homologue 4 gene results in an absence of cilia and random left-right asymmetry.

Chen, Shiguo; Knowles, Heather; Hebert, Jennifer; Hackett, Brian P.

doi:10.1172/jci4786

Cited by 373 publications

(312 citation statements)

References 35 publications

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“…In mouse lung, the expression of HFH-4 protein is restricted to subsets of the epithelial cells in the conducting airways from E17 and maintained postnatally. HFH-4 has been implicated in ciliated cell differentiation since mice homozygous null mutant for HFH-4 gene lacked ciliated cells in all tissues (Chen et al, 1998). In lung, HFH-4 expression colocalized with ␤-tubulin IV in ciliated epithelial cells, but not with CCSP, a marker for Clara cells (Tichelaar et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

TGF‐β1 perturbs vascular development and inhibits epithelial differentiation in fetal lung in vivo

Zeng

Gray

Stahlman

et al. 2001

Developmental Dynamics

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Members of the transforming growth factor ␤ (TGF-␤) family of polypeptides have been implicated in morphogenesis and differentiation in numerous tissues, including the lung. In order to further define effects of TGF-␤ signaling in lung morphogenesis, a constitutively active form of TGF-␤1 was expressed in respiratory epithelial cells of the fetal mouse lung in vivo. Expression of TGF-␤1 arrested lung morphogenesis in the pseudoglandular stage of development, inhibiting synthesis of differentiation-dependent proteins, SP-B, SP-C, and CCSP, and maintaining embryonic patterns of staining for thyroid transcription factor-1 (TTF-1) and hepatocyte nuclear factor-3␤ (HNF-3␤). The pulmonary mesenchyme was thickened and vascular density was increased by TGF-␤1. TGF-␤1 decreased expression of vascular endothelial growth factor-A (VEGF-A) mRNA and protein, and the abundance of Flk-1 mRNA in the lung mesenchyme. Distribution of platelet-endothelial cell adhesion molecule (PECAM)-1, a marker of pulmonary blood vessels, was altered, and ultrastructural studies demonstrated that TGF-␤1 inhibited vascular development in the fetal lung. TGF-␤1 perturbed both epithelial cell differentiation and formation of the pulmonary vasculature, supporting the concept that precise control of signaling via the TGF-␤ receptor pathway is critical for normal lung morphogenesis.

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Section: Discussionmentioning

confidence: 99%

TGF‐β1 perturbs vascular development and inhibits epithelial differentiation in fetal lung in vivo

Zeng

Gray

Stahlman

et al. 2001

Developmental Dynamics

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“…The embryonic expression of Foxj3 is strikingly different from that of Foxj1, which is specific for ciliated cells, e.g., in the airways and the node (Chen et al, 1998;Blatt et al, 1999;Brody et al, 2000), further emphasizing the evolutionary distance between these two genes. The closest relative, Foxj2, is expressed in gonads and preimplantation embryos , but nothing has been published on its postimplantation embryonic expression.…”

Section: Embryonic Foxj3 Expressionmentioning

confidence: 92%

Foxj3, a novel mammalian forkhead gene expressed in neuroectoderm, neural crest, and myotome

Landgren

Carlsson

2004

Developmental Dynamics

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“…Foxo proteins are important in the maintaining of quiescence and tolerance of T and B cells, and Foxp3 plays a critical role in regulatory T cell development (Coffer and Burgering 2004). Foxj1, a member of the forkhead family also known as HFH-4 and FKHL-13, is expressed mainly in the ciliated cells of lung, choroids plexus, and oviduct, and is linked with developmental regulation in ciliated epithelial cells and the determination of the left-right axis (Chen et al 1998;Blatt et al 1999;Brody et al 2000;Okada et al 2004;Lim et al 1997). Recently, Lin et al (2004) found that Foxj1-deficient mice suffered multi-organ systemic inflammation, exaggerated Th1 cytokine production, and T cell proliferation in autologous mixed lymphocyte reactions.…”

Section: Introductionmentioning

confidence: 99%

Identification of single nucleotide polymorphisms in FOXJ1 and their association with allergic rhinitis

Chae

Lee

et al. 2006

J Hum Genet

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Forkhead-box J1 (FOXJ1) is a presumed transcription factor that can suppress T cell activity, at least partially, through the repression of NFjB activity. Thus, dysregulation of FOXJ1 is thought to be associated with autoimmune diseases and/or other inflammatory diseases. To investigate the association between single nucleotide polymorphisms (SNPs) of human FOXJ1 and allergic rhinitis, we scanned the whole human FOXJ1 gene, including the promoter region, by direct sequencing of DNA from 32 individuals. We identified seven SNPs, three of which (g.-460C>T, g.1805G>T, and g.3375G>C) were chosen for large sample size genotyping (n=713), and to assess the genotype frequencies of these SNPs between controls and allergic rhinitis patients. We also investigated the relationships of each genotype with serum total IgE levels in allergic rhinitis patients, and compared the frequencies of haplotypes constructed by these SNPs between the two groups. Our results suggest that the SNPs g.-460C>T, g.1805G>T and g.3375G>C in the human FOXJ1 gene might be associated with susceptibility to allergic rhinitis (P=0.0184, 0.0076, and 0.0143, respectively). The main haplotype, CGG, also revealed a significant association with allergic rhinitis (P=0.000018). However, no significant association was found between serum total IgE levels and the genotypes of these polymorphisms.

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Mutation of the mouse hepatocyte nuclear factor/forkhead homologue 4 gene results in an absence of cilia and random left-right asymmetry.

Cited by 373 publications

References 35 publications

TGF‐β1 perturbs vascular development and inhibits epithelial differentiation in fetal lung in vivo

TGF‐β1 perturbs vascular development and inhibits epithelial differentiation in fetal lung in vivo

Foxj3, a novel mammalian forkhead gene expressed in neuroectoderm, neural crest, and myotome

Identification of single nucleotide polymorphisms in FOXJ1 and their association with allergic rhinitis

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