
Porphyromonas gingivalis ‐derived outer membrane vesicles promote calcification of vascular smooth muscle cells through ERK 1/2‐ RUNX 2
Author(s) -
Yang Wen Wei,
Guo Bin,
Jia Wen Yuan,
Jia Yue
Publication year - 2016
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12151
Subject(s) - runx2 , vascular smooth muscle , porphyromonas gingivalis , calcification , microbiology and biotechnology , mapk/erk pathway , transcription factor , biology , gene silencing , signal transduction , chemistry , osteoblast , in vitro , medicine , endocrinology , biochemistry , smooth muscle , bacteria , gene , genetics
The outer membrane vesicle ( OMV ) derived from Porphyromonas gingivalis plays an essential role in causing inflammation which, in turn, plays an important part in the pathogenesis of cardiovascular diseases such as atherosclerosis and thromboembolism. However, the contribution of oral bacteria to vascular calcification is yet to be determined. Here, we evaluated the effect of OMV on vascular smooth muscle cell ( VSMC ) calcification both in vitro and ex vivo . We established a reproducible P. gingivalis OMV ‐induced differentiation and calcification model of VSMC s in vitro . The results indicate that OMV promotes VSMC calcification in a concentration‐dependent manner, modulating the expression of bone markers and SMC markers both on genes and proteins that are important for osteoblastic differentiation and mineralization of VSMC s. We also showed that the key osteogenic transcription factor, runt‐related transcription factor 2 (Runx2), which is affected by upstream extracellular‐regulated kinase ( ERK ) signaling, is a key regulator of OMV ‐induced VSMC differentiation and calcification. Taken together, our research demonstrates that Runx2 is a crucial component of OMV ‐induced calcification of VSMC s, and ERK signaling plays a vital role in mediating Runx2 up‐regulation and VSMC calcification.