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骨髓间充质基质细胞通过分泌肿瘤坏死因子诱导基因6蛋白减轻大鼠缺血/再灌注损伤诱导的急性肾损伤。

Bone Marrow Derived Mesenchymal Stromal Cells Ameliorate Ischemia/Reperfusion Injury-Induced Acute Kidney Injury in Rats via Secreting Tumor Necrosis Factor-Inducible Gene 6 Protein.

作者信息

Chen Yue, Tang Xiaochen, Li Ping, Zhou Ying, Xue Ting, Liu Jie, Yu Chen

机构信息

Department of Nephrology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China.

Translational Center for Stem Cell Research, Tongji Hospital, Stem Cell Research Center, Tongji University School of Medicine, Shanghai 200065, China.

出版信息

Biomed Res Int. 2019 Mar 11;2019:9845709. doi: 10.1155/2019/9845709. eCollection 2019.

DOI:10.1155/2019/9845709
PMID:30984789
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6432703/
Abstract

AIMS

To investigate whether bone marrow derived mesenchymal stromal cells (BMSC) have ameliorated ischemia/reperfusion injury-induced acute kidney injury (IRI-AKI) via tumor necrosis factor-inducible gene 6 protein (TSG-6) and how TSG-6 exerted this effect.

METHODS

We used lentiviral vectors of short hairpin RNA (shRNA) targeting TSG-6 gene to silence TSG-6 in BMSC. And TSG-6-silenced BMSC were administrated into IRI-AKI rats. Then we analyzed serum creatinine (Scr) and renal histology of IRI-AKI rats treated with BMSC after different pretreatments. Furthermore, we explored the effect of TSG-6 on renal tubular epithelial cells proliferation and assays.

RESULTS

The Scr levels of IRI-AKI rats treated with BMSC (73.5±7.8 mol/L) significantly decreased compared to those of IRI-AKI rats treated without BMSC (392.5±24.8 mol/L, P<0.05) or with DMEM (314.0±19.8 mol/L, P<0.05). Meanwhile, the renal tissue injury in IRI-AKI rats treated with BMSC improved markedly. However, the Scr levels of IRI-AKI rats treated with TSG-6-silenced BMSC (265.1±21.2 mol/L) significantly increased compared to those with BMSC (74.0±8.5 mol/L, P<0.05). The proportion of Ki67-positive cells was reduced in IRI-AKI rats treated with TSG-6-silenced BMSC compared to that in IRI-AKI rats treated with BMSC (29.7±0.8% versus 43.4±3.0%, P<0.05). , the cell proliferation rate of TSG-6-stimulated NRK-52E cells under hypoxia (89.2±3.9%) increased significantly compared to that of NRK-52E cells alone under hypoxia (82.4±0.8%, P<0.05). Similarly, the proportion of Ki67-positive cells was significantly elevated in TSG-6-stimulated NRK-52E cells under hypoxia. Furthermore, TSG-6 could inhibit infiltration of neutrophils in kidney tissue of IRI-AKI.

CONCLUSIONS

TSG-6 plays a key role in the treatment of IRI-AKI with BMSC, which may be due to its effect on promoting renal tubular epithelial cells proliferation by modulating inflammation.

摘要

目的

研究骨髓间充质干细胞（BMSC）是否通过肿瘤坏死因子诱导基因6蛋白（TSG-6）改善缺血/再灌注损伤诱导的急性肾损伤（IRI-AKI），以及TSG-6如何发挥这种作用。

方法

我们使用靶向TSG-6基因的短发夹RNA（shRNA）慢病毒载体使BMSC中的TSG-6沉默。然后将TSG-6沉默的BMSC注入IRI-AKI大鼠体内。接着我们分析了不同预处理后接受BMSC治疗的IRI-AKI大鼠的血清肌酐（Scr）水平和肾脏组织学情况。此外，我们还探究了TSG-6对肾小管上皮细胞增殖的影响及相关检测。

结果

与未接受BMSC治疗的IRI-AKI大鼠（392.5±24.8 μmol/L，P<0.05）或接受DMEM治疗的IRI-AKI大鼠（314.0±19.8 μmol/L，P<0.05）相比，接受BMSC治疗的IRI-AKI大鼠的Scr水平（73.5±7.8 μmol/L）显著降低。同时，接受BMSC治疗的IRI-AKI大鼠的肾组织损伤明显改善。然而，与接受BMSC治疗的IRI-AKI大鼠（74.0±8.5 μmol/L，P<0.05）相比，接受TSG-6沉默的BMSC治疗的IRI-AKI大鼠的Scr水平（265.1±21.2 μmol/L）显著升高。与接受BMSC治疗的IRI-AKI大鼠相比，接受TSG-6沉默的BMSC治疗的IRI-AKI大鼠中Ki67阳性细胞的比例降低（29.7±0.8%对43.4±3.0%，P<0.05）。此外，与单纯缺氧条件下的NRK-52E细胞相比，缺氧条件下TSG-6刺激的NRK-52E细胞的细胞增殖率显著增加（89.2±3.9%对82.4±0.8%，P<0.05）。同样，缺氧条件下TSG-6刺激的NRK-52E细胞中Ki67阳性细胞的比例显著升高。此外，TSG-6可抑制IRI-AKI大鼠肾组织中中性粒细胞的浸润。

结论

TSG-6在BMSC治疗IRI-AKI中起关键作用，这可能是由于其通过调节炎症促进肾小管上皮细胞增殖的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbc3/6432703/bb17d7f25a2f/BMRI2019-9845709.010.jpg
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