DNA-binding motif and target genes of the imprinted transcription factor PEG3

Thiaville, Michelle M.; Huang, Jennifer M.; Kim, Hana; Ekram, Muhammad B.; Roh, Tae-Young; Kim, Joomyeong

doi:10.1016/j.gene.2012.10.005

Cited by 56 publications

(96 citation statements)

References 34 publications

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“…6I). We note that a recent study has identified a Peg3-specific DNAbinding motif (42), and indeed we found a single minimal consensus sequence for Peg3 (TGGCT) at −604 bp relative to the transcription start site. Collectively, these results support the notion that decorin signals through VEGFR2 in endothelial cells and corroborate the binding studies discussed above.…”

Section: Decorin Requires Vegfr2 For Its Downstream Signaling Andsupporting

confidence: 75%

Decorin causes autophagy in endothelial cells via Peg3

Buraschi

Neill

Goyal

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

175

239

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Significance We identified a function for a member of the extracellular matrix in the regulation of autophagy. Decorin, a member of the small leucine-rich proteoglycan family and an established pan-receptor tyrosine kinase inhibitor, evokes endothelial cell autophagy and inhibits angiogenesis. This process is mediated by a high-affinity interaction with VEGFR2 which leads to increased levels of Peg3, a tumor-suppressor gene. We provide mechanistic evidence that Peg3 is required to maintain basal levels of Beclin 1, a major autophagic marker. These data provide a paradigmatic shift for other soluble matrix constituents to regulate autophagy.

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Section: Decorin Requires Vegfr2 For Its Downstream Signaling Andsupporting

confidence: 75%

Decorin causes autophagy in endothelial cells via Peg3

Buraschi

Neill

Goyal

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

175

239

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“…18 PW1 has also been shown to function as a transcription factor with a DNA-binding motif regulating a large array of genes involved in metabolic homeostasis. 19 Moreover, PW1 expression is required for the myogenic and migratory capacities of both mouse and human mesoangioblasts, reinforcing the relevance of PW1 to identify competent mesoangioblasts before their use in stem cell-mediated therapeutic applications. 20 Given the distribution of PW1 expression in a wide array of adult somatic stem cells and the role of PW1 in cell stress responses, we investigated whether PW1…”

mentioning

confidence: 93%

Resident PW1 ⁺ Progenitor Cells Participate in Vascular Remodeling During Pulmonary Arterial Hypertension

Dierick

Héry

Hoareau

et al. 2016

Circulation Research

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Rationale: Pulmonary arterial hypertension is characterized by vascular remodeling and neomuscularization. PW1 + progenitor cells can differentiate into smooth muscle cells (SMCs) in vitro. Objective: To determine the role of pulmonary PW1 + progenitor cells in vascular remodeling characteristic of pulmonary arterial hypertension. Methods and Results: We investigated their contribution during chronic hypoxia–induced vascular remodeling in Pw1 nLacZ+/− mouse expressing β-galactosidase in PW1 + cells and in differentiated cells derived from PW1 + cells. PW1 + progenitor cells are present in the perivascular zone in rodent and human control lungs. Using progenitor markers, 3 distinct myogenic PW1 + cell populations were isolated from the mouse lung of which 2 were significantly increased after 4 days of chronic hypoxia. The number of proliferating pulmonary PW1 + cells and the proportion of β-gal + vascular SMC were increased, indicating a recruitment of PW1 + cells and their differentiation into vascular SMC during early chronic hypoxia–induced neomuscularization. CXCR4 inhibition using AMD3100 prevented PW1 + cells differentiation into SMC but did not inhibit their proliferation. Bone marrow transplantation experiments showed that the newly formed β-gal + SMC were not derived from circulating bone marrow–derived PW1 + progenitor cells, confirming a resident origin of the recruited PW1 + cells. The number of pulmonary PW1 + cells was also increased in rats after monocrotaline injection. In lung from pulmonary arterial hypertension patients, PW1-expressing cells were observed in large numbers in remodeled vascular structures. Conclusions: These results demonstrate the existence of a novel population of resident SMC progenitor cells expressing PW1 and participating in pulmonary hypertension–associated vascular remodeling.

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“…9,10 Recent studies confirmed that PEG3 indeed binds to a large number of genomic targets as a DNA-binding protein. 7 According to the results, PEG3 functions as a transcriptional repressor for these downstream genes. 7 In particular, PEG3 binds to its adjacent imprinted gene, maternally expressed Zim1.…”

Section: Introductionmentioning

confidence: 98%

“…5,6 Some imprinted genes are also known to encode DNA-binding proteins, such as Zac1 and Peg3. 7,8 The DNA-binding protein encoded by Zac1 binds to the 3 0 enhancer of H19 as a transcriptional activator, suggesting a functional connection between the 2 imprinted genes, paternally expressed Zac1 and maternally expressed H19. 8 Detailed surveys further revealed that many imprinted genes behave coordinately in response to environmental and developmental cues.…”

Section: Introductionmentioning

confidence: 99%

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PEG3 binds to H19-ICR as a transcriptional repressor

Kim

2016

Epigenetics

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Paternally expressed gene 3 (Peg3) encodes a DNA-binding protein with 12 C2H2 zinc finger motifs. In the current study, we performed ChIP-seq using mouse embryonic fibroblast (MEF) cells. This experiment identified a set of 16 PEG3 genomic targets, the majority of which overlapped with the promoter regions of genes with oocyte expression. These potential downstream genes were upregulated in MEF cells lacking PEG3 protein, suggesting a potential repressor role for PEG3. Our study also identified the imprinting control region (ICR) of H19 as a genomic target. According to the results, PEG3 binds to a specific sequence motif located between the 3 rd and 4 th CTCF binding sites of the H19-ICR. PEG3 also binds to the active maternal allele of the H19-ICR. The expression levels of H19 were upregulated in MEF cells lacking PEG3, and this upregulation was mainly derived from the maternal allele. This suggests that PEG3 may function as a transcriptional repressor for the maternal allele of H19. Overall, the current study uncovers a potential functional relationship between Peg3 and H19, and also confirms PEG3 as a transcriptional repressor for the identified downstream genes.

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DNA-binding motif and target genes of the imprinted transcription factor PEG3

Cited by 56 publications

References 34 publications

Decorin causes autophagy in endothelial cells via Peg3

Decorin causes autophagy in endothelial cells via Peg3

Resident PW1 ⁺ Progenitor Cells Participate in Vascular Remodeling During Pulmonary Arterial Hypertension

PEG3 binds to H19-ICR as a transcriptional repressor

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DNA-binding motif and target genes of the imprinted transcription factor PEG3

Cited by 56 publications

References 34 publications

Decorin causes autophagy in endothelial cells via Peg3

Decorin causes autophagy in endothelial cells via Peg3

Resident PW1 + Progenitor Cells Participate in Vascular Remodeling During Pulmonary Arterial Hypertension

PEG3 binds to H19-ICR as a transcriptional repressor

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Resident PW1 ⁺ Progenitor Cells Participate in Vascular Remodeling During Pulmonary Arterial Hypertension