Human immunodeficiency virus envelope protein Gp120 induces proliferation but not apoptosis in osteoblasts at physiologic concentrations.
Human immunodeficiency virus envelope protein Gp120 induces proliferation but not apoptosis in osteoblasts at physiologic concentrations.
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DOI：
10.1371/journal.pone.0024876
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发表时间：
2011
期刊：
影响因子：
3.7
通讯作者：
Badley AD
中科院分区：
文献类型：
--
作者：
Cummins NW;Klicpera A;Sainski AM;Bren GD;Khosla S;Westendorf JJ;Badley AD
与未感染的患者相比，HIV感染患者的成骨细胞数量减少，骨密度降低，骨折风险增加;然而，这些相关性背后的分子机制仍不清楚。我们质疑是否Gp 120，HIV包膜蛋白的一个组成部分，能够在许多细胞类型中诱导凋亡，是能够诱导成骨细胞的细胞死亡。我们发现，在体外用生理浓度的外源性Gp 120处理永生化成骨细胞样细胞和原代人成骨细胞不会导致细胞凋亡。相反，在成骨细胞样U2 OS细胞系中，表达CXCR 4（Gp 120的受体）的细胞在用Gp 120处理时与对照相比具有增加的增殖（P<0.05），其被CXCR 4抑制剂和G蛋白抑制剂预处理抑制。这表明Gp 120不是人成骨细胞凋亡的诱导剂，并且可能不会通过这种机制直接导致感染患者的骨质疏松症。
Patients with HIV infection have decreased numbers of osteoblasts, decreased bone mineral density and increased risk of fracture compared to uninfected patients; however, the molecular mechanisms behind these associations remain unclear. We questioned whether Gp120, a component of the envelope protein of HIV capable of inducing apoptosis in many cell types, is able to induce cell death in bone-forming osteoblasts. We show that treatment of immortalized osteoblast-like cells and primary human osteoblasts with exogenous Gp120 in vitro at physiologic concentrations does not result in apoptosis. Instead, in the osteoblast-like U2OS cell line, cells expressing CXCR4, a receptor for Gp120, had increased proliferation when treated with Gp120 compared to control (P<0.05), which was inhibited by pretreatment with a CXCR4 inhibitor and a G-protein inhibitor. This suggests that Gp120 is not an inducer of apoptosis in human osteoblasts and likely does not directly contribute to osteoporosis in infected patients by this mechanism.
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