Corisdeo S, Gyda M, Zaidi M, Moonga B S, Troen B R
Geriatric Research Education and Clinical Center, Bronx VA Medical Center, 130 West Kingsbridge Road, Bronx, NY 10468, USA.
Biochem Biophys Res Commun. 2001 Jul 13;285(2):335-9. doi: 10.1006/bbrc.2001.5127.
Cathepsin K plays a key role in bone resorption. We provide the first evidence that osteoprotegerin ligand (OPGL), a critical pro-resorptive cytokine, acutely stimulates the expression of cathepsin K in osteoclasts. We used in situ RT-PCR and real time quantitative RT-PCR to analyze cathepsin K gene expression. OPGL enhanced cathepsin K mRNA levels in mature osteoclasts isolated from rat neonatal long bones. OPGL together with macrophage colony-stimulating factor (M-CSF) also stimulated cathepsin K gene expression in monocytic cells and multinucleate osteoclasts in bone marrow cultures. Real time quantitative RT-PCR demonstrated high levels of cathepsin K mRNA in bone marrow cultures, paralleling the degree of osteoclastogenesis. We therefore suggest that OPGL enhances bone resorption, at least in part, by inducing cathepsin K gene expression.
组织蛋白酶K在骨吸收过程中起关键作用。我们首次提供证据表明，破骨细胞生成素配体（OPGL），一种关键的促吸收细胞因子，可急性刺激破骨细胞中组织蛋白酶K的表达。我们使用原位逆转录聚合酶链反应（RT-PCR）和实时定量RT-PCR分析组织蛋白酶K基因的表达。OPGL可提高从大鼠新生长骨分离的成熟破骨细胞中组织蛋白酶K的mRNA水平。OPGL与巨噬细胞集落刺激因子（M-CSF）共同作用，也能刺激骨髓培养物中单核细胞和多核破骨细胞的组织蛋白酶K基因表达。实时定量RT-PCR显示骨髓培养物中组织蛋白酶K的mRNA水平较高，这与破骨细胞生成的程度平行。因此，我们认为OPGL至少部分地通过诱导组织蛋白酶K基因表达来增强骨吸收。
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