Journal: Stem Cells and Development

Article Title: Hypoxic Conditioning Enhances the Angiogenic Paracrine Activity of Human Adipose-Derived Stem Cells

doi: 10.1089/scd.2012.0602

Figure Lengend Snippet: Degree of hypoxia differentially regulated the adipose derived stem cell (ASC) paracrine factor profile. Expression levels of the vascular endothelial growth factor-A (VEGF-A) (A) , VEGF-C (B) , angiogenin (ANG) (D) , and interleukin-8 (IL-8) (E) were upregulated

Article Snippet: To determine the contribution of VEGF-A and ANG in ASCCM -induced angiogenesis in vivo, neutralizing antibodies against the VEGF-A (30 μg/mL; Santa Cruz) and/or ANG (10 μg/mL; R & D Systems) were incubated with the hypoxic ASCCM for 2 h at 4°C with constant agitation.

Techniques: Derivative Assay, Expressing

Journal: Stem Cells and Development

Article Title: Hypoxic Conditioning Enhances the Angiogenic Paracrine Activity of Human Adipose-Derived Stem Cells

doi: 10.1089/scd.2012.0602

Figure Lengend Snippet: The hypoxic ASC CM promoted angiogenesis in vivo in a VEGF-A- and ANG-dependent manner. (A) The hypoxic ASC CM increased CD31-positive vessels grown into the sponges at 2 weeks postimplantation. Removal of the VEGF-A and/or ANG from the hypoxic ASC CM significantly

Article Snippet: To determine the contribution of VEGF-A and ANG in ASCCM -induced angiogenesis in vivo, neutralizing antibodies against the VEGF-A (30 μg/mL; Santa Cruz) and/or ANG (10 μg/mL; R & D Systems) were incubated with the hypoxic ASCCM for 2 h at 4°C with constant agitation.

Techniques: In Vivo

Journal: Stem Cells and Development

Article Title: Hypoxic Conditioning Enhances the Angiogenic Paracrine Activity of Human Adipose-Derived Stem Cells

doi: 10.1089/scd.2012.0602

Figure Lengend Snippet: Hypoxia increased VEGF-A, VEGF-C, and ANG secretion from ASCs. Treatment of ASCs with

Article Snippet: To determine the contribution of VEGF-A and ANG in ASCCM -induced angiogenesis in vivo, neutralizing antibodies against the VEGF-A (30 μg/mL; Santa Cruz) and/or ANG (10 μg/mL; R & D Systems) were incubated with the hypoxic ASCCM for 2 h at 4°C with constant agitation.

Techniques:

Journal: International Journal of Molecular Medicine

Article Title: Lack of endogenous parathyroid hormone delays fracture healing by inhibiting vascular endothelial growth factor-mediated angiogenesis

doi: 10.3892/ijmm.2018.3614

Figure Lengend Snippet: (A) Immunohistochemical staining of VEGF-A (magnification, ×400) in fractures. (a) In PTHKO and (b) WT mice 1 week after fracture, VEGF-A expression was significantly reduced in PTHKO mice compared with in WT mice. (c) In PTHKO and (d) WT mice 2 weeks after fracture, VEGF-A expression was increased in PTHKO mice, but remained significantly lower than that in WT mice. (B) Immunohistochemical staining of pVEGFR2 (magnification, ×400) in fractures. (a) In PTHKO and (b) WT mice 1 week after fracture, a significantly smaller number of pVEGFR2-positive cells was detected in the cartilaginous callus in PTHKO mice compared with in WT mice. (c) In PTHKO and (d) WT mice 2 weeks after fracture, a large number of pVEGFR2-positive cells was observed in the cartilaginous callus in WT mice, whereas a much lower level of angiogenesis was detected in PTHKO mice. (C) Immunohistochemical staining for HIF1α (magnification, ×400) in fractures. (a) In PTHKO and (b) WT mice 1 week after fracture, the expression levels of cytoplasmic HIF1α were significantly lower in PTHKO mice. (c) In PTHKO and (d) WT mice 2 weeks after fracture, HIF1α expression was increased in both groups; however, the expression remained lower in PTHKO mice compared with in WT mice. Black arrows indicate positive areas. (D) Protein expression levels of VEGF, pVEGFR2 and HIF1α were detected by western blot analysis. HIF1α, hypoxia inducible factor-1α; PTH, parathroid hormone; PTHKO, PTH knockout; pVEGFR, phosphorylated-VEGF receptor 2; VEGF, vascular endothelial growth factor; WT, wild-type.

Article Snippet: RUNX2 (ab76956; 1:600), HIF1α (ab8366; 1:600), pVEGF receptor 2 (pVEGFR2; ab131241; 1:200), proliferating cell nuclear antigen (PCNA; ab92552; 1:400), VEGF (ab46154; 1:200), PKA (ab75991) and pAKT monoclonal antibodies (ab81283) were purchased from Abcam (Cambridge, MA, USA).

Techniques: Immunohistochemistry, Staining, Mouse Assay, Expressing, Western Blot, Knock-Out

Journal: Cell Death & Disease

Article Title: FLI1 and PKC co-activation promote highly efficient differentiation of human embryonic stem cells into endothelial-like cells

doi: 10.1038/s41419-017-0162-9

Figure Lengend Snippet: FLI1 and PKC co-activation mediated hESCs differentiation into iECs a Schematic illustration of the EC differentiation strategy from hESCs. b Typical morphological images of hESC-EC differentiation on days of 0, 1, 2, and 3. Scale bar, 100 μm. c The ratio of CD31+/CD144+ cells gradually increased during induction. Columns represent the mean ± SD; n = 5 independent differentiation experiments. d Representative results of the percentage of CD31+/CD144+ cells during the induction process detected by FCM. e Overexpression of FLI1 and activation of PKC in different hESC lines (hESC-254 or hESC-137) induced iECs. f Overexpressing FLI1 with different PKC activators (PMA or prostratin) yielded iECs. g Expression levels of VEGF , GATA2 , CD31 and CD144 genes in hESCs, human fibroblasts (HFs), iECs and EPCs. Columns represent the mean ± SD; n = 5 independent differentiation experiments

Article Snippet: After 3 days, supplements were changed with 50 ng ml−1 VEGF-A (96-100-20-10, PEPROTECH).

Techniques: Activation Assay, Over Expression, Expressing