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细胞因子受体样因子 1（CRLF1）及其在骨软骨修复中的作用。

Cytokine Receptor-like Factor 1 (CRLF1) and Its Role in Osteochondral Repair.

机构信息

Department of Urology, New York University Grossman School of Medicine, New York, NY 10010, USA.

Rothman Orthopedic Institute, Orlando, FL 32803, USA.

出版信息

Cells. 2024 Apr 28;13(9):757. doi: 10.3390/cells13090757.

DOI:10.3390/cells13090757
PMID:38727293
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11083199/
Abstract

BACKGROUND

Since cytokine receptor-like factor 1 (CRLF1) has been implicated in tissue regeneration, we hypothesized that CRLF1 released by mesenchymal stem cells can promote the repair of osteochondral defects.

METHODS

The degree of a femoral osteochondral defect repair in rabbits after intra-articular injections of bone marrow-derived mesenchymal stem cells (BMSCs) that were transduced with empty adeno-associated virus (AAV) or AAV containing CRLF1 was determined by morphological, histological, and micro computer tomography (CT) analyses. The effects of CRLF1 on chondrogenic differentiation of BMSCs or catabolic events of interleukin-1beta-treated chondrocyte cell line TC28a2 were determined by alcian blue staining, gene expression levels of cartilage and catabolic marker genes using real-time PCR analysis, and immunoblot analysis of Smad2/3 and STAT3 signaling.

RESULTS

Intra-articular injections of BMSCs overexpressing CRLF1 markedly improved repair of a rabbit femoral osteochondral defect. Overexpression of CRLF1 in BMSCs resulted in the release of a homodimeric CRLF1 complex that stimulated chondrogenic differentiation of BMSCs via enhancing Smad2/3 signaling, whereas the suppression of CRLF1 expression inhibited chondrogenic differentiation. In addition, CRLF1 inhibited catabolic events in TC28a2 cells cultured in an inflammatory environment, while a heterodimeric complex of CRLF1 and cardiotrophin-like Cytokine (CLC) stimulated catabolic events via STAT3 activation.

CONCLUSION

A homodimeric CRLF1 complex released by BMSCs enhanced the repair of osteochondral defects via the inhibition of catabolic events in chondrocytes and the stimulation of chondrogenic differentiation of precursor cells.

摘要

背景

细胞因子受体样因子 1（CRLF1）已被牵涉到组织再生中，我们假设骨髓间充质干细胞（BMSCs）分泌的 CRLF1 可以促进骨软骨缺损的修复。

方法

通过形态学、组织学和微计算机断层扫描（CT）分析，确定经空腺相关病毒（AAV）或含 CRLF1 的 AAV 转导的骨髓间充质干细胞（BMSCs）关节内注射后，兔股骨骨软骨缺损的修复程度。通过阿利新蓝染色、实时 PCR 分析软骨和成代谢标志物基因的表达水平，以及 Smad2/3 和 STAT3 信号的免疫印迹分析，来确定 CRLF1 对 BMSCs 软骨分化或白细胞介素-1β处理的软骨细胞系 TC28a2 中分解代谢事件的影响。

结果

BMSCs 过表达 CRLF1 的关节内注射显著改善了兔股骨骨软骨缺损的修复。BMSCs 中 CRLF1 的过表达导致同源二聚体 CRLF1 复合物的释放，通过增强 Smad2/3 信号刺激 BMSCs 的软骨分化，而 CRLF1 表达的抑制抑制了软骨分化。此外，CRLF1 抑制了在炎症环境中培养的 TC28a2 细胞中的分解代谢事件，而 CRLF1 和心肌营养素样细胞因子（CLC）的异源二聚体复合物通过激活 STAT3 刺激分解代谢事件。

结论

BMSCs 释放的同源二聚体 CRLF1 复合物通过抑制软骨细胞的分解代谢事件和刺激前体细胞的软骨分化来增强骨软骨缺损的修复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0056/11083199/6d4a15ec1b05/cells-13-00757-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0056/11083199/9519a129a0f8/cells-13-00757-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0056/11083199/73f1e468cbf9/cells-13-00757-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0056/11083199/3c7c503d35bf/cells-13-00757-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0056/11083199/9254d6f98c95/cells-13-00757-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0056/11083199/77b9b2dfae2e/cells-13-00757-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0056/11083199/6d4a15ec1b05/cells-13-00757-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0056/11083199/9519a129a0f8/cells-13-00757-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0056/11083199/73f1e468cbf9/cells-13-00757-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0056/11083199/3c7c503d35bf/cells-13-00757-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0056/11083199/9254d6f98c95/cells-13-00757-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0056/11083199/77b9b2dfae2e/cells-13-00757-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0056/11083199/6d4a15ec1b05/cells-13-00757-g006.jpg

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