Department of Oral Sciences and Translational Research, College of Dental Medicine, Nova Southeastern University, Davie, Florida, USA.
Department of Biomedical Sciences and Comprehensive Care, Indiana University School of Dentistry, Indianapolis, Indiana, USA.
J Cell Mol Med. 2022 May;26(10):2841-2851. doi: 10.1111/jcmm.17299. Epub 2022 Apr 16.
Emerging studies indicate that intracellular eukaryotic ceramide species directly activate cathepsin B (CatB), a lysosomal-cysteine-protease, in the cytoplasm of osteoclast precursors (OCPs) leading to elevated RANKL-mediated osteoclastogenesis and inflammatory osteolysis. However, the possible impact of CatB on osteoclastogenesis elevated by non-eukaryotic ceramides is largely unknown. It was reported that a novel class of phosphoglycerol dihydroceramide (PGDHC), produced by the key periodontal pathogen Porphyromonas gingivalis upregulated RANKL-mediated osteoclastogenesis in vitro and in vivo. Therefore, the aim of this study was to evaluate a crosstalk between host CatB and non-eukaryotic PGDHC on the promotion of osteoclastogenesis. According to a pulldown assay, high affinity between PGDHC and CatB was observed in RANKL-stimulated RAW264.7 cells in vitro. It was also demonstrated that PGDHC promotes enzymatic activity of recombinant CatB protein ex vivo and in RANKL-stimulated osteoclast precursors in vitro. Furthermore, no or little effect of PGDHC on the RANKL-primed osteoclastogenesis was observed in male and female CatB-knock out mice compared with their wild type counterparts. Altogether, these findings demonstrate that bacterial dihydroceramides produced by P. gingivalis elevate RANKL-primed osteoclastogenesis via direct activation of intracellular CatB in OCPs.
新兴研究表明,细胞内真核神经酰胺直接激活溶酶体半胱氨酸蛋白酶 cathepsin B (CatB),从而导致破骨细胞前体 (OCPs) 细胞质中 RANKL 介导的破骨细胞生成和炎症性骨溶解增加。然而,CatB 对非真核神经酰胺引起的破骨细胞生成的可能影响在很大程度上是未知的。据报道,一种新型的磷酸甘油二氢神经酰胺 (PGDHC),由关键的牙周病原体牙龈卟啉单胞菌产生,可在上调体外和体内 RANKL 介导的破骨细胞生成。因此,本研究旨在评估宿主 CatB 与非真核 PGDHC 之间的相互作用对破骨细胞生成的促进作用。根据下拉实验,在体外 RANKL 刺激的 RAW264.7 细胞中观察到 PGDHC 与 CatB 之间具有高亲和力。还证明 PGDHC 可促进重组 CatB 蛋白的体外酶活性以及体外 RANKL 刺激的破骨细胞前体中的酶活性。此外,与野生型相比,在 CatB 敲除雄性和雌性小鼠中,PGDHC 对 RANKL 引发的破骨细胞生成几乎没有影响或没有影响。总之,这些发现表明,牙龈卟啉单胞菌产生的细菌二氢神经酰胺通过直接激活 OCPs 中的细胞内 CatB 来增加 RANKL 引发的破骨细胞生成。