精氨酸加压素对内皮型一氧化氮合酶基因敲除小鼠及其野生型对照小鼠成骨样细胞的影响。
The effects of arg-vasopressin on osteoblast-like cells in endothelial nitric oxide synthase-knockout mice and their wild type counterparts.
作者信息
Lagumdzija A, Pernow Y, Bucht E, Gonon A, Petersson M
机构信息
Department of Molecular Medicine, Endocrine and Diabetes Unit, Karolinska Institutet and Karolinska University Hospital, S-17176 Stockholm, Sweden.
出版信息
Peptides. 2005 Sep;26(9):1661-6. doi: 10.1016/j.peptides.2005.02.007. Epub 2005 Mar 2.
In the present study, we investigated whether nitric oxide (NO) could be involved in the effects of arg-vasopressin (AVP) on osteoblast-like cells. Cells derived from endothelial nitric oxide synthase (eNOS)-knockout mice and their wild type (WT) counterparts, and an osteosarcoma cell line (SaOS-2) were used. AVP (10-100 pmol/l) increased proliferation of osteoblast-like cells from WT mice. The effect was abolished by an AVP V1-receptor antagonist. AVP increased proliferation of cells from eNOSKO mice only when a NO donor, SNAP, was added. A nitric oxide synthase-inhibitor, L-NAME, antagonized the increase in cell proliferation in response to AVP in SaOS-2 cells. In conclusion, this study indicates that NO is involved in the effects of AVP on cell proliferation in osteoblast-like cells.
在本研究中，我们调查了一氧化氮（NO）是否参与精氨酸加压素（AVP）对成骨样细胞的作用。使用了源自内皮型一氧化氮合酶（eNOS）基因敲除小鼠及其野生型（WT）对照的细胞，以及一种骨肉瘤细胞系（SaOS-2）。AVP（10 - 100 pmol/l）增加了野生型小鼠成骨样细胞的增殖。AVP V1受体拮抗剂消除了该作用。仅当添加NO供体SNAP时，AVP才增加eNOS基因敲除小鼠细胞的增殖。一氧化氮合酶抑制剂L-NAME拮抗了SaOS-2细胞中AVP诱导的细胞增殖增加。总之，本研究表明NO参与了AVP对成骨样细胞增殖的作用。
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