Fetal bovine serum enhances expression of PEDF in epidermal keratinocytes and dermal fibroblasts / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the effect of fetal bovine serum (FBS) on expression of pigment epithelium-derived factor (PEDF) in normal epidermal keratinocytes and dermal fibroblasts.</p><p><b>METHODS</b>Keratinocytes and fibroblasts were incubated with 10% FBS. PEDF protein level in the cells was determined by immunofluorescence and Western blot.</p><p><b>RESULTS</b>PEDF was localized mostly in the cytoplasm,while some in the nuclei. The distribution of PEDF in cytoplasm was in a granular pattern. 10% FBS increased the expression of PEDF both in keratinocytes and fibroblasts,but histamine and Phorbol 12-myristate 13-acetate (PMA) did not interfere the distribution of PEDF in cells.</p><p><b>CONCLUSION</b>10% FBS can upregulate expression of PEDF in epidermal keratinocytes and dermal fibroblasts.</p>

Autocrine effect of vascular endothelial growth factor on the proliferation of HaCaT cells / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To determine the autocrine effect of vascular endothelial growth factor (VEGF) on epidermal keratinocytes HaCaT cells.</p><p><b>METHODS</b>Cultured HaCaT cells were treated with various concentrations of VEGF(165) (0,1,5,10,25,50,100 ng/ml) or Avastin (0,0.063,0.125,0.25,0.50,1.0,2.0 mg/ml) in vitro. HaCaT cell proliferation was determined by MTT assay and the cell migration was measured by migration assay. The effect of VEGF(165) (10 ng/ml) on phosphorylation of ERK1/2 was detected in HaCaT cells pretreated or not pretreated with Avastin (0.5 mg/ml).</p><p><b>RESULTS</b>VEGF enhanced the proliferation and migration of HaCaT cells in a dose-dependent manner, while Avastin inhibited the effects of VEGF also in a dose-dependent manner. VEGF(165) (10 ng/ml) induced the phosphorylation of ERK1/2 in HaCaT cells,but which was blocked by Avastin (0.5 mg/ml).</p><p><b>CONCLUSION</b>VEGF enhanced the proliferation and migration of HaCaT cells in a dose-dependent manner, while Avastin inhibited the effects of VEGF also in a dose-dependent manner. VEGF(165) (10 ng/ml) induced the phosphorylation of ERK1/2 in HaCaT cells,but which was blocked by Avastin (0.5 mg/ml).</p>

Advancements in expression of vascular endothelial growth factor receptors in skin diseases / 中国医学科学院学报

Vascular endothelial growth factor (VEGF) exerts its biological functions by its specific VEGF receptors (VEGFR), which includes VEGFR-1, VEGFR-2, VEGFR-3, neuropilin-1, and neuropilin-2. These VEGFR distributes in endothelial cells, and are also expressed in normal skin, inflammatory skin diseases, and skin cancers. The VEGF-VEGFR signaling pathway may be a new key target in the management of the skin diseases.

Advances in pathogenesis of psoriasis / 浙江大学学报·医学版

The pathogenesis of psoriasis recently made great advancement due to the introduction of transgenic mouse model. K14-VEGF transgenic mouse showed many of the cellular and molecular features of psoriasis, including angiogenesis in dermis, altered epidermal proliferation and differentiation. Psoriasis of early onset and severe disease showed significantly increased frequency of the +405CC genotype and the C allele. Transgenic mice with keratinocytes expressing active Stat3 (K5. Stat3C mice) developed a skin phenotype closely resembling psoriasis. Stat 3 may link activated keratinocytes and immunocytes required for development of psoriasis. More recently, a novel mouse model with epidermal specific double-knockout of the c-Jun and JunB genes showed developments of psoriasis-like skin phenotype and arthritic lesions. All these data provided more profound understanding in pathogenesis and therapy of psoriasis.