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Zip1 在 MLT 调节 NPY 表达促进大鼠骨折愈合中的作用。

Role of Zip1 in the regulation of NPY expression by MLT to promote fracture healing in rats.

机构信息

Graduate Training Base of Jinzhou Medical University, Air Force Hospital of the Northern Theater of Chinese People's Liberation Army (PLA), Shenyang, Liaoning.

Division of Spine Surgery, Department of Orthopaedics, Tongji Hospital, Tongji University School of Medicine, Shanghai.

出版信息

Eur J Histochem. 2020 Dec 2;64(s2):3183. doi: 10.4081/ejh.2020.3183.

DOI:10.4081/ejh.2020.3183
PMID:33334091
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7731576/
Abstract

Our previous study documented that melatonin (MLT) induced the osteogenic differentiation of mesenchymal stem cells (MSCs) and promoted the healing of femoral fractures in rats via the neuropeptide Y (NPY)/neuropeptide Y1 receptor (NPY1R) signaling pathway. MLT treatment upregulated the expression of the zinc uptake transporter zinc transporter 1 (Zip1) in nerve cells. Prior research demonstrated that oral zinc upregulated NPY expression. MSCs were isolated from rat bone marrow and identified using flow cytometry in our study. The results showed that MLT treatment upregulated NPY and NPY1R levels in MSCs with osteogenic differentiation, which was accompanied by upregulated Zip1 expression. However, the MLT-induced osteogenic differentiation of MSCs was reversed after interference of Zip1 expression. It was confirmed by the decreased alkaline phosphatase (ALP) level; downregulated activities of type I collagen α1 chain (COL1A1), osteocalcin (OCN), runt-related transcription factor 2 (Runx2) and ALP; and reduced mineralized nodule formation. MLT promoted fracture healing in rats with femoral fracture, which was accompanied by increased expression of NPY and NPY1R and significantly increased expression of Zip1. In contrast, the silencing of Zip1 expression reversed MLT-mediated fracture healing. In summary, Zip1 participated in the regulation of the NPY/NPY1R signaling pathway via MLT to promote the osteogenic differentiation of MSCs and fracture healing.

摘要

我们之前的研究表明，褪黑素（MLT）通过神经肽 Y（NPY）/神经肽 Y1 受体（NPY1R）信号通路诱导间充质干细胞（MSCs）的成骨分化，并促进大鼠股骨骨折的愈合。MLT 治疗上调了神经细胞中锌转运体 1（Zip1）的表达。先前的研究表明，口服锌上调了 NPY 的表达。在我们的研究中，从大鼠骨髓中分离出 MSCs 并通过流式细胞术进行鉴定。结果表明，MLT 处理上调了具有成骨分化的 MSCs 中的 NPY 和 NPY1R 水平，同时上调了 Zip1 的表达。然而，Zip1 表达的干扰逆转了 MLT 诱导的 MSCs 成骨分化。碱性磷酸酶（ALP）水平降低；Ⅰ型胶原α1 链（COL1A1）、骨钙素（OCN）、 runt 相关转录因子 2（Runx2）和 ALP 活性下调；以及矿化结节形成减少证实了这一点。MLT 促进了股骨骨折大鼠的骨折愈合，同时伴随着 NPY 和 NPY1R 的表达增加，以及 Zip1 的表达显著增加。相比之下，Zip1 表达的沉默逆转了 MLT 介导的骨折愈合。总之，Zip1 通过 MLT 参与 NPY/NPY1R 信号通路的调节，促进 MSCs 的成骨分化和骨折愈合。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e2c/7731576/2683282e42f9/ejh-64-s2-3183-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e2c/7731576/c04c7bcd8793/ejh-64-s2-3183-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e2c/7731576/dd4d7acda10f/ejh-64-s2-3183-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e2c/7731576/8f1f8d01a5e8/ejh-64-s2-3183-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e2c/7731576/b9615cba0f31/ejh-64-s2-3183-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e2c/7731576/2683282e42f9/ejh-64-s2-3183-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e2c/7731576/c04c7bcd8793/ejh-64-s2-3183-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e2c/7731576/dd4d7acda10f/ejh-64-s2-3183-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e2c/7731576/8f1f8d01a5e8/ejh-64-s2-3183-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e2c/7731576/b9615cba0f31/ejh-64-s2-3183-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e2c/7731576/2683282e42f9/ejh-64-s2-3183-g005.jpg

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