Zinc-finger transcriptional factor Sall1 induces angiogenesis by activation of the gene for VEGF-A

Yamamoto, Chii; Fukuda, Noboru; Matsumoto, Tarô; Higuchi, Terumi; Ueno, Takayoshi; Matsumoto, Koichí

doi:10.1038/hr.2009.195

Cited by 11 publications

(8 citation statements)

References 26 publications

(27 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus Sall1 and Sall4 can assist Nanog (52) and other pluripotency factors in the silencing of differentiation genes. Despite the ability of Sall1 to activate gene expression observed in this and previous reports (12, 20, 21), it does not contain a transcription activation domain. Thus it is likely that activation or repression by Sall1 is determined by signal-regulated switches and/or by the presence of distinct promoter-specific factors.…”

Section: Discussioncontrasting

confidence: 93%

“…It has been reported that Sall1 acts as a transcriptional repressor by localizing in the heterochromatin and interacting with components of the nucleosome remodeling and deacetylase complex (NuRD) (18, 19). Conversely, Sall1 was found to cooperatively activate the Wnt pathway with β-catenin (20) to activate kidney mesenchymal markers (12) and induce angiogenesis by activating VEGF-A (21). The molecular mechanism whereby Sall1 directly targets genes for repression or activation remains unknown.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Sall1 Regulates Embryonic Stem Cell Differentiation in Association with Nanog

Karantzali

Lekakis

Ioannou

et al. 2011

Journal of Biological Chemistry

View full text Add to dashboard Cite

Sall1 is a multi-zinc finger transcription factor that regulates kidney organogenesis. It is considered to be a transcriptional repressor, preferentially localized on heterochromatin. Mutations or deletions of the human SALL1 gene are associated with the Townes-Brocks syndrome. Despite its high expression, no function was yet assigned for Sall1 in embryonic stem (ES) cells. In the present study, we show that Sall1 is expressed in a differentiation-dependent manner and physically interacts with Nanog and Sox2, two components of the core pluripotency network. Genome-wide mapping of Sall1-binding loci has identified 591 genes, 80% of which are also targeted by Nanog. A large proportion of these genes are related to self-renewal and differentiation. Sall1 positively regulates and synergizes with Nanog for gene transcriptional regulation. In addition, our data show that Sall1 suppresses the ectodermal and mesodermal differentiation. Specifically, the induction of the gastrulation markers T brachyury, Goosecoid, and Dkk1 and the neuroectodermal markers Otx2 and Hand1 was inhibited by Sall1 overexpression during embryoid body differentiation. These data demonstrate a novel role for Sall1 as a member of the transcriptional network that regulates stem cell pluripotency.

show abstract

Section: Discussioncontrasting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Sall1 Regulates Embryonic Stem Cell Differentiation in Association with Nanog

Karantzali

Lekakis

Ioannou

et al. 2011

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…MECOM encodes a zinc finger transcription factor that may be involved in hematopoiesis, cell cycle regulation, differentiation, proliferation, and embryogenesis, overexpression may be a predisposing factor of leukemia and osteoporotic fracture (Hwang et al, 2013; Wieser, 2007). The protein encoded by SALL1, also a zinc finger transcription factor, may regulate angiogenesis, vascularization, embryonic stem cell differentiation, and organogenesis, especially kidney development (Nishinakamura et al, 2001; Nishinakamura and Takasato, 2005; Yamamoto et al, 2010). ARL9 encodes a GTP binding member of the small GTPase protein family with a high degree of similarity to ARF proteins of the RAS superfamily.…”

Section: Discussionmentioning

confidence: 99%

Infant sex-specific placental cadmium and DNA methylation associations

Mohanty

Farin

Bammler

et al. 2015

Environmental Research

View full text Add to dashboard Cite

Background Recent evidence suggests that maternal cadmium (Cd) burden and fetal growth associations may vary by fetal sex. However, mechanisms contributing to these differences are unknown. Objectives Among 24 maternal-infant pairs, we investigated infant sex-specific associations between placental Cd and placental genome-wide DNA methylation. Methods We used ANOVA models to examine sex-stratified associations of placental Cd (dichotomized into high/low Cd using sex-specific Cd median cutoffs) with DNA methylation at each cytosine-phosphate-guanine site or region. Statistical significance was defined using a false discovery rate cutoff (<0.10). Results Medians of placental Cd among females and males were 5 and 2 ng/g, respectively. Among females, three sites (near ADP-ribosylation factor-like 9 (ARL9), siah E3 ubiquitin protein ligase family member 3 (SIAH3), and heparin sulfate (glucosamine) 3-O-sulfotransferase 4 (HS3ST4) and one region on chromosome 7 (including carnitine O-octanoyltransferase (CROT) and TP5S target 1 (TP53TG1)) were hypomethylated in high Cd placentas. Among males, high placental Cd was associated with methylation of three sites, two (hypomethylated) near MDS1 and EVI1 complex locus (MECOM) and one (hypermethylated) near spalt-like transcription factor 1 (SALL1), and two regions (both hypomethylated, one on chromosome 3 including MECOM and another on chromosome 8 including rho guanine nucleotide exchange factor (GEF) 10 (ARHGEF10). Differentially methylated sites were at or close to transcription start sites of genes involved in cell damage response (SIAH3, HS3ST4, TP53TG1) in females and cell differentiation, angiogenesis and organ development (MECOM, SALL1) in males. Conclusions Our preliminary study supports infant sex-specific placental Cd-DNA methylation associations, possibly accounting for previously reported differences in Cd-fetal growth associations across fetal sex. Larger studies are needed to replicate and extend these findings. Such investigations may further our understanding of epigenetic mechanisms underlying maternal Cd burden with suboptimal fetal growth associations.

show abstract

“…Recently, it has been shown that the subacute administration of zinc before an ischemic process provides significant neuroprotection to hippocampal CA1 layer, thus reducing cell death [22]. This neuroprotection might be mediated by CCL2 and its receptor CCR2 [23] and IGF-1, FGF2, and vascular endothelial growth factor (VEGF) [23–25]. Interestingly, all these growth factors are involved in cell survival, proliferation, migration, and maturity of neuronal cells after a brain lesion [26].…”

Section: Introductionmentioning

confidence: 99%

Prophylactic Chronic Zinc Administration Increases Neuroinflammation in a Hypoxia-Ischemia Model

Tomás-Sanchez

Blanco-Álvarez

González-Barrios

et al. 2016

Journal of Immunology Research

View full text Add to dashboard Cite

Acute and subacute administration of zinc exert neuroprotective effects in hypoxia-ischemia animal models; yet the effect of chronic administration of zinc still remains unknown. We addressed this issue by injecting zinc at a tolerable dose (0.5 mg/kg weight, i.p.) for 14 days before common carotid artery occlusion (CCAO) in a rat. After CCAO, the level of zinc was measured by atomic absorption spectrophotometry, nitrites were determined by Griess method, lipoperoxidation was measured by Gerard-Monnier assay, and mRNA expression of 84 genes coding for cytokines, chemokines, and their receptors was measured by qRT-PCR, whereas nitrotyrosine, chemokines, and their receptors were assessed by ELISA and histopathological changes in the temporoparietal cortex-hippocampus at different time points. Long-term memory was evaluated using Morris water maze. Following CCAO, a significant increase in nitrosative stress, inflammatory chemokines/receptors, and cell death was observed after 8 h, and a 2.5-fold increase in zinc levels was detected after 7 days. Although CXCL12 and FGF2 protein levels were significantly increased, the long-term memory was impaired 12 days after reperfusion in the Zn+CCAO group. Our data suggest that the chronic administration of zinc at tolerable doses causes nitrosative stress, toxic zinc accumulation, and neuroinflammation, which might account for the neuronal death and cerebral dysfunction after CCAO.

show abstract

Zinc-finger transcriptional factor Sall1 induces angiogenesis by activation of the gene for VEGF-A

Cited by 11 publications

References 26 publications

Sall1 Regulates Embryonic Stem Cell Differentiation in Association with Nanog

Sall1 Regulates Embryonic Stem Cell Differentiation in Association with Nanog

Infant sex-specific placental cadmium and DNA methylation associations

Prophylactic Chronic Zinc Administration Increases Neuroinflammation in a Hypoxia-Ischemia Model

Contact Info

Product

Resources

About