Zini Nicoletta, Lisignoli Gina, Solimando Liliana, Bavelloni Alberto, Grassi Francesco, Guidotti Lia, Trimarchi Carmela, Facchini Andrea, Maraldi Nadir Mario
Sezioni di Bologna c/o IOR, ITOI-CNR, via di Barbiano 1/10, 40136 Bologna, Italy.
Histochem Cell Biol. 2003 Sep;120(3):243-50. doi: 10.1007/s00418-003-0563-y. Epub 2003 Aug 12.
Osteoarthritis (OA) and rheumatoid arthritis (RA) are common joint diseases that can lead to destruction of cartilage and structural changes in the subchondral bone. In this study we show by western blot and quantitative immunocytochemistry that nuclear phospholipase C beta(1) (PLC beta(1)) and phosphatidylinositol 4,5-bisphosphate (PIP(2)), two key elements of the polyphosphoinositide signal transduction system that regulate different cellular processes, increase in primary osteoblast cultures of RA patients when compared with post-traumatic after fall (PT) patients, whilst those of OA are not significantly affected. Moreover, we demonstrate that these alterations could be induced in PT osteoblasts by proinflammatory cytokines IL-1 beta and TNF-alpha. This suggests that proinflammatory cytokines, highly produced by RA infiltrating mononuclear cells, can modulate the nuclear polyphosphoinositide signalling pathway of the osteoblasts involved in bone remodelling.
骨关节炎（OA）和类风湿性关节炎（RA）是常见的关节疾病，可导致软骨破坏和软骨下骨的结构改变。在本研究中，我们通过蛋白质免疫印迹法和定量免疫细胞化学表明，核磷脂酶Cβ(1)（PLCβ(1)）和磷脂酰肌醇4,5-二磷酸（PIP(2)）是多磷酸肌醇信号转导系统的两个关键元件，可调节不同的细胞过程，与跌倒后创伤后（PT）患者相比，RA患者原代成骨细胞培养物中的这两个元件增加，而OA患者的这两个元件未受到显著影响。此外，我们证明促炎细胞因子IL-1β和TNF-α可在PT成骨细胞中诱导这些改变。这表明，由RA浸润单核细胞大量产生的促炎细胞因子可调节参与骨重塑的成骨细胞核多磷酸肌醇信号通路。
