Recombinant human endostatin is beneficial to endothelial cell growth exposed to mildly oxidized low-density lipoproteins
| Autor: | Rabasseda X, Wang Y, Wang Yz, Ren B |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
medicine.medical_specialty
Cell division Arteriosclerosis Angiogenesis Inhibitors Biology law.invention law Internal medicine medicine Animals Humans Aorta Cells Cultured Vascular disease Biological activity medicine.disease In vitro Peptide Fragments Recombinant Proteins Endostatins Endothelial stem cell Lipoproteins LDL Endocrinology Apoptosis Recombinant DNA lipids (amino acids peptides and proteins) Collagen Endothelium Vascular Rabbits Endostatin Oxidation-Reduction Cell Division |
| Zdroj: | Methods and findings in experimental and clinical pharmacology. 24(4) |
| ISSN: | 0379-0355 |
| Popis: | Endostatin significantly reduced atherosclerosis in genetically susceptible mice. One of the main factors associated with atherogenesis is oxidized low-density lipoproteins (LDL), which also causes apoptosis of endothelial cells. Therefore, we proposed that the antiatherogenic effect of endostatin was partly associated with its protective effect on the endothelial injury induced by oxidized LDL. To confirm such a hypothesis, we studied the effects of recombinant human endostatin (rhEndo) on the proliferation of cultured endothelial cells exposed to mildly oxidized LDL (mox-LDL), rhEndo did not show an obvious inhibitory effect on the proliferation of rabbit aorta endothelial cells (RAEC) (p > 0.05), while mox-LDL inhibited their proliferation (p < 0.01 or p < 0.05). Interestingly, rhEndo seemed to antagonize the role of mox-LDL in inhibiting the proliferation of RAEC. rhEndo seemed, thus, to be beneficial to the proliferating endothelial cells, suggesting that it protects RAECs from the injury caused by mox-LDL. The activity of rhEndo in endothelial cells may possibly result from the interaction of different factors in cell signaling, which remains to be further elucidated. |
| Databáze: | OpenAIRE |
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