Monocytic cell junction proteins serve important roles in atherosclerosis via the endoglin pathway

Chen,Lina; Chen,Zhongliang; Ge,Menghua; Tang,Oushan; Cheng,Yinhong; Zhou,Haoliang; Shen,Yu; Qin,Fengming

doi:10.3892/mmr.2017.7444

Monocytic cell junction proteins serve important roles in atherosclerosis via the endoglin pathway

Authors:
- Lina Chen
- Zhongliang Chen
- Menghua Ge
- Oushan Tang
- Yinhong Cheng
- Haoliang Zhou
- Yu Shen
- Fengming Qin
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Affiliations: Department of Cardiology, Shaoxing Second Hospital, Shaoxing, Zhejiang 312000, P.R. China
Published online on: September 8, 2017 https://doi.org/10.3892/mmr.2017.7444
Pages: 6750-6756
Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The formation of atherosclerosis is recognized to be caused by multiple factors including pathogenesis in monocytes during inflammation. The current study provided evidence that monocytic junctions were significantly altered in patients with atherosclerosis, which suggested an association between cell junctions and atherosclerosis. Claudin‑1, occludin‑1 and ZO‑1 were significantly enhanced in atherosclerosis, indicating that the tight junction pathway was activated during the pathogenesis of atherosclerosis. In addition, the gene expression of 5 connexin members involved in the gap junction pathway were quantified, indicating that connexin 43 and 46 were significantly up‑regulated in atherosclerosis. Furthermore, inflammatory factors including endoglin and SMAD were observed, suggesting that immune regulative factors were down‑regulated in this pathway. Silicon‑based analysis additionally identified that connexins and tight junctions were altered in association with monocytic inflammation regulations, endoglin pathway. The results imply that reduced expression of the immune regulation pathway in monocytes is correlated with the generation of gap junctions and tight junctions which serve important roles in atherosclerosis.

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