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骨细胞暴露于钛颗粒中，通过直接的细胞间接触，增加骨钙素蛋白的表达并抑制成骨细胞的分化。

Osteocytic cells exposed to titanium particles increase sclerostin expression and inhibit osteoblastic cell differentiation mostly via direct cell-to-cell contact.

机构信息

Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China.

The Experiment Center, The Medical College of Soochow University, Suzhou, Jiangsu Province, China.

出版信息

J Cell Mol Med. 2022 Aug;26(15):4371-4385. doi: 10.1111/jcmm.17460. Epub 2022 Jun 28.

DOI:10.1111/jcmm.17460
PMID:35762300
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9345295/
Abstract

The mechanism underlying induction of periprosthetic osteolysis by wear particles remains unclear. In this study, cultured MLO-Y4 osteocytic cells were exposed to different concentrations of titanium (Ti) particles. The results showed that Ti particles increased expression of the osteocytic marker SOST/sclerostin in a dose-dependent manner, accelerated apoptosis of MLO-Y4 cells, increased the expression of IL-6, TNF-α and connexin 43. SOST silence alleviated the increase of MLO-Y4 cells apoptosis, decreased the expression of IL-6, TNF-α and connexin 43 caused by Ti particles. The different co-culture systems of MLO-Y4 cells with MC3T3-E1 osteoblastic cells were further used to observe the effects of osteocytic cells' changes induced by Ti particles on osteoblastic cells. MLO-Y4 cells treated with Ti particles inhibited dramatically differentiation of MC3T3-E1 cells mostly through direct cell-to-cell contact. SOST silence attenuated the inhibition effects of Ti-induced MLO-Y4 on MC3T3-E1 osteoblastic differentiation, which ALP level and mineralization of MC3T3-E1 cells increased and the expression of ALP, OCN and Runx2 increased compared to the Ti-treated group. Taken together, Ti particles had negative effects on MLO-Y4 cells and the impact of Ti particles on osteocytic cells was extensive, which may further inhibit osteoblastic differentiation mostly through intercellular contact directly. SOST/sclerostin plays an important role in the process of mutual cell interaction. These findings may help to understand the effect of osteocytes in wear particle-induced osteolysis.

摘要

磨损颗粒引起假体周围骨溶解的机制尚不清楚。在这项研究中，培养的 MLO-Y4 破骨细胞被暴露于不同浓度的钛（Ti）颗粒中。结果表明，Ti 颗粒以剂量依赖性方式增加破骨细胞标志物 SOST/骨硬化蛋白的表达，加速 MLO-Y4 细胞凋亡，并增加 IL-6、TNF-α 和连接蛋白 43 的表达。SOST 沉默减轻了 Ti 颗粒引起的 MLO-Y4 细胞凋亡的增加，并降低了 IL-6、TNF-α 和连接蛋白 43 的表达。进一步使用 MLO-Y4 细胞与 MC3T3-E1 成骨细胞的不同共培养系统来观察 Ti 颗粒诱导的破骨细胞变化对成骨细胞的影响。Ti 颗粒处理的 MLO-Y4 细胞通过直接细胞间接触显著抑制 MC3T3-E1 细胞的分化。SOST 沉默减弱了 Ti 诱导的 MLO-Y4 对 MC3T3-E1 成骨分化的抑制作用，与 Ti 处理组相比，MC3T3-E1 细胞的 ALP 水平和矿化增加，ALP、OCN 和 Runx2 的表达增加。总之，Ti 颗粒对 MLO-Y4 细胞有负面影响，Ti 颗粒对破骨细胞的影响广泛，可能主要通过直接细胞间接触进一步抑制成骨细胞分化。SOST/骨硬化蛋白在细胞间相互作用过程中起着重要作用。这些发现可能有助于理解破骨细胞在磨损颗粒诱导的骨溶解中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/5d57509f7c70/JCMM-26-4371-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/6638314949d2/JCMM-26-4371-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/c4db6943bf2c/JCMM-26-4371-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/ec05610a65f7/JCMM-26-4371-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/753b56972027/JCMM-26-4371-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/51cf95d38312/JCMM-26-4371-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/608d9a0549ad/JCMM-26-4371-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/0a57fe7c3cb3/JCMM-26-4371-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/5d57509f7c70/JCMM-26-4371-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/6638314949d2/JCMM-26-4371-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/c4db6943bf2c/JCMM-26-4371-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/ec05610a65f7/JCMM-26-4371-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/753b56972027/JCMM-26-4371-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/51cf95d38312/JCMM-26-4371-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/608d9a0549ad/JCMM-26-4371-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/0a57fe7c3cb3/JCMM-26-4371-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a9/9345295/5d57509f7c70/JCMM-26-4371-g003.jpg

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