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Olfactomedin 2, a novel regulator for transforming growth factor-β-induced smooth muscle differentiation of human embryonic stem cell-derived mesenchymal cells.

Shi N, Guo X, Chen SY - Mol. Biol. Cell (2014)

Bottom Line: Olfm2 also inhibited HERP1 expression.Moreover, blockade of Olfm2 expression inhibited TGF-β-induced SRF binding to SM gene promoters in a chromatin setting, whereas overexpression of Olfm2 dose dependently enhanced SRF binding.These results demonstrate that Olfm2 mediates TGF-β-induced SM gene transcription by empowering SRF binding to CArG box in SM gene promoters.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pharmacology, University of Georgia, Athens, GA 30602.

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TGF-β–induced Olfm2 expression while promoting SM differentiation in hES-MCs. (A) TGF-β–induced Olfm2 expression along with the differentiation of hES-MCs. Serum-starved hES-MCs were treated with vehicle (−) or TGF-β (+; 1 ng/ml) for the time indicated. Western blotting was performed to examine the expression of Olfm2 and SM marker proteins. (B–E) Quantification of Olfm2 and SM marker expression by normalizing to α-tubulin shown in A. *p < 0.01 compared with vehicle-treated group (0 h; n = 3). (F) Olfm2 was expressed in human aortic smooth muscle. Human aorta was paraffin embedded and sectioned and stained with IgG or Olfm2 antibody as indicated. Olfm2 was shown to predominantly express in the nuclei of vascular smooth muscles.
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Figure 1: TGF-β–induced Olfm2 expression while promoting SM differentiation in hES-MCs. (A) TGF-β–induced Olfm2 expression along with the differentiation of hES-MCs. Serum-starved hES-MCs were treated with vehicle (−) or TGF-β (+; 1 ng/ml) for the time indicated. Western blotting was performed to examine the expression of Olfm2 and SM marker proteins. (B–E) Quantification of Olfm2 and SM marker expression by normalizing to α-tubulin shown in A. *p < 0.01 compared with vehicle-treated group (0 h; n = 3). (F) Olfm2 was expressed in human aortic smooth muscle. Human aorta was paraffin embedded and sectioned and stained with IgG or Olfm2 antibody as indicated. Olfm2 was shown to predominantly express in the nuclei of vascular smooth muscles.

Mentions: TGF-β is an important determinant for SM lineage. To determine the role of Olfm2 in TGF-β–induced SM differentiation, we examined the expression of Olfm2 and SM markers in TGF-β–treated hES-MCs. As shown in Figure 1, Olfm2 expression markedly increased soon after TGF-β induction, and TGF-β induced Olfm2 expression in a time-dependent manner, with an 8.4-fold increase after 48-h treatment (Figure 1, A and B). Of importance, Olfm2 induction occurred earlier than expression of SM markers α-SMA, SM22α, and SMMHC (Figure 1, A–E, and Supplemental Figure S1). Moreover, Olfm2 expression was observed in smooth muscle of human aorta tissue (Figure 1F). These data suggest that Olfm2 is involved in TGF-β–induced SM differentiation.


Olfactomedin 2, a novel regulator for transforming growth factor-β-induced smooth muscle differentiation of human embryonic stem cell-derived mesenchymal cells.

Shi N, Guo X, Chen SY - Mol. Biol. Cell (2014)

TGF-β–induced Olfm2 expression while promoting SM differentiation in hES-MCs. (A) TGF-β–induced Olfm2 expression along with the differentiation of hES-MCs. Serum-starved hES-MCs were treated with vehicle (−) or TGF-β (+; 1 ng/ml) for the time indicated. Western blotting was performed to examine the expression of Olfm2 and SM marker proteins. (B–E) Quantification of Olfm2 and SM marker expression by normalizing to α-tubulin shown in A. *p < 0.01 compared with vehicle-treated group (0 h; n = 3). (F) Olfm2 was expressed in human aortic smooth muscle. Human aorta was paraffin embedded and sectioned and stained with IgG or Olfm2 antibody as indicated. Olfm2 was shown to predominantly express in the nuclei of vascular smooth muscles.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4263453&req=5

Figure 1: TGF-β–induced Olfm2 expression while promoting SM differentiation in hES-MCs. (A) TGF-β–induced Olfm2 expression along with the differentiation of hES-MCs. Serum-starved hES-MCs were treated with vehicle (−) or TGF-β (+; 1 ng/ml) for the time indicated. Western blotting was performed to examine the expression of Olfm2 and SM marker proteins. (B–E) Quantification of Olfm2 and SM marker expression by normalizing to α-tubulin shown in A. *p < 0.01 compared with vehicle-treated group (0 h; n = 3). (F) Olfm2 was expressed in human aortic smooth muscle. Human aorta was paraffin embedded and sectioned and stained with IgG or Olfm2 antibody as indicated. Olfm2 was shown to predominantly express in the nuclei of vascular smooth muscles.
Mentions: TGF-β is an important determinant for SM lineage. To determine the role of Olfm2 in TGF-β–induced SM differentiation, we examined the expression of Olfm2 and SM markers in TGF-β–treated hES-MCs. As shown in Figure 1, Olfm2 expression markedly increased soon after TGF-β induction, and TGF-β induced Olfm2 expression in a time-dependent manner, with an 8.4-fold increase after 48-h treatment (Figure 1, A and B). Of importance, Olfm2 induction occurred earlier than expression of SM markers α-SMA, SM22α, and SMMHC (Figure 1, A–E, and Supplemental Figure S1). Moreover, Olfm2 expression was observed in smooth muscle of human aorta tissue (Figure 1F). These data suggest that Olfm2 is involved in TGF-β–induced SM differentiation.

Bottom Line: Olfm2 also inhibited HERP1 expression.Moreover, blockade of Olfm2 expression inhibited TGF-β-induced SRF binding to SM gene promoters in a chromatin setting, whereas overexpression of Olfm2 dose dependently enhanced SRF binding.These results demonstrate that Olfm2 mediates TGF-β-induced SM gene transcription by empowering SRF binding to CArG box in SM gene promoters.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pharmacology, University of Georgia, Athens, GA 30602.

Show MeSH
Related in: MedlinePlus