Soluble receptor for advanced glycation end-products inhibits myocardial fibrosis of ischemia/reperfusion mice

CAO Xian-Xian; HAN Xue-Jie; WANG Hong-Xia; ZENG Xiang-Jun; GUO Cai-Xia

doi:10.16098/j.issn.0529-1356.2021.05.015

PDF(7078 KB)

Acta Anatomica Sinica ›› 2021, Vol. 52 ›› Issue (5) : 772-776. DOI: 10.16098/j.issn.0529-1356.2021.05.015

Histology,Embryology and Developmental Biology

Soluble receptor for advanced glycation end-products inhibits myocardial fibrosis of ischemia/reperfusion mice

CAO Xian-xian¹ HAN Xue-jie¹ WANG Hong-xia² ZENG Xiang-jun^2* GUO Cai-xia^1*

Author information +

History +

Abstract

Objective To investigate the effect of soluble receptor for advanced glycation end-products (sRAGE) on inflammation in myocardial ischemia/reperfusion(I/R) mice and its mechanism. Methods Myocardial I/R injury model was conducted by left anterior descending ligation for 30 minutes and reperfusion for 2 weeks in male C57BL/6 mice aged 6-8 weeks. The mice were randomly divided into four groups with five C57BL/6 mice in each group. The cardiac function was detected by echocardiography, the inflammatory cells infiltration was observed by HE staining, the myocardial fibrosis was detected by Masson and Sirius red staining, the expression of galectin-3 was detected by immunohistochemical staining. Results Compared with the sham group, the cardiac function decreased, the inflammatory cells infiltrated increased among the myocardial tissue, the percentage of myocardial fibrosis area increased, and the expression of galectin-3 increased in I/R groups. After exogenous sRAGE treatment, the cardiac function of mice was significantly improved, the inflammatory cells infiltration decreased, the myocardial fibrosis area decreased, and the expression of galectin-3 decreased as well. Conclusion sRAGE may reduce inflammatory cells infiltration in mice heart by inhibiting the expression of galectin-3, and then alleviating myocardial fibrosis during myocardial ischemia/reperfusion injury.

Key words

Soluble receptor for advanced glycation end-products / Ischemia/reperfusion / Fibrosis / Immunohistochemistry / Mouse

Cite this article

EndNote

Ris (Procite)

Bibtex

Download Citations

CAO Xian-xian HAN Xue-jie WANG Hong-xia ZENG Xiang-jun GUO Cai-xia. Soluble receptor for advanced glycation end-products inhibits myocardial fibrosis of ischemia/reperfusion mice[J]. Acta Anatomica Sinica. 2021, 52(5): 772-776 https://doi.org/10.16098/j.issn.0529-1356.2021.05.015

References

［1］ Ib á?ez B, Heusch G, Ovize M, et al. Evolving therapies for myocardial ischemia/reperfusion injury ［J］. J Am Coll Cardiol, 2015, 65(14):1454--1471.

［2］ Hausenloy DJ, Yellon DM. Myocardial ischemia-reperfusion injury: a neglected therapeutic target ［J］. J Clin Invest, 2013, 123(1):92-100.

［3］ Yellon DM, Hausenloy DJ. Myocardial reperfusion injury ［J］. N Engl J Med, 2007, 357(11):1121-1135.

［4］ Fujiwara M, Matoba T, Koga JI, et al. Nanoparticle incorporating Toll-like receptor 4 inhibitor attenuates myocardial ischaemia-reperfusion injury by inhibiting monocyte-mediated inflammation in mice ［J］. Cardiovasc Res, 2019, 115(7):1244-1255.

［5］ Wallert M, Ziegler M, Wang X, et al. α-Tocopherol preserves cardiac function by reducing oxidative stress and inflammation in ischemia/reperfusion injury ［J］. Redox Biol, 2019, 26:101292.

［6］ Maillard-Lefebvre H, Boulanger E, Daroux M, et al. Soluble receptor for advanced glycation end products: a new biomarker in diagnosis and prognosis of chronic inflammatory diseases ［J］. Rheumatology, 2009, 48(10):1190-1196.

［7］ Liu Y, Yu M, Zhang L, et al. Soluble receptor for advanced glycation end products mitigates vascular dysfunction in spontaneously hypertensive rats［J］. Mol Cell Biochem, 2016, 419(1-2):165-176.

［8］ Gao E, Koch WJ. A novel and efficient model of coronary artery ligation in the mouse ［J］. Methods Mol Biol, 2013, 1037:299-311.

［9］ Ku SH, Hong J, Moon HH, et al. Deoxycholic acid-modified polyethylenimine based nanocarriers for RAGE siRNA therapy in acute myocardial infarction ［J］. Arch Pharm Res, 2015, 38(7):1317-1324.

［10］ Arif M, Pandey R, Alam P, et al. MicroRNA-210-mediated proliferation, survival, and angiogenesis promote cardiac repair post myocardial infarction in rodents ［J］. J Mol Med, 2017, 95(12):1369-1385.

［11］ Paulik R, Micsik T, Kiszler G, et al. An optimized image analysis algorithm for detecting nuclear signals in digital whole slides for histopathology ［J］. Cytometry Part A, 2017, 91(6):595-608.

［12］ Yin J, Wang Y, Chang J, et al. Apelin inhibited epithelial-mesenchymal transition of podocytes in diabetic mice through downregulating immunoproteasome subunits β5i ［J］. Cell Death Dis, 2018, 9(10):1031.

［13］ Zhang J, Wang YJ, Zeng XJ. Attenuating effects and mechanisms of apelin-13 on aortic injuries in diabetic mice ［J］. Acta Anatomica Sinica, 2018, 49(1):81-86. (in Chinese)

张佳，王炀佳，曾翔俊. Apelin-13减轻糖尿病小鼠主动脉损伤［J］. 解剖学报，2018，49（1）：81-86.

［14］ Dang M, Zeng X, Chen B, et al. Interferon-γ mediates the protective effects of soluble receptor for advanced glycation end-product in myocardial ischemia/reperfusion ［J］. Lab Invest, 2019, 99(3):358-370.

［15］ Jiang X, Guo C, Zeng X, et al. A soluble receptor for advanced glycation end-products inhibits myocardial apoptosis induced by ischemia/reperfusion via the JAK2/STAT3 pathway ［J］. Apoptosis, 2015, 20(8):1033-1047.

［16］ Guo C, Jiang X, Zeng X, et al. Soluble receptor for advanced glycation end-products protects against ischemia/reperfusion-induced myocardial apoptosis via regulating the ubiquitin proteasome system ［J］. Free Radic Biol Med, 2016, 94:17-26.

［17］ Toba H, Cannon PL, Yabluchanskiy A, et al. Transgenic overexpression of macrophage matrix metalloproteinase-9 exacerbates age-related cardiac hypertrophy, vessel rarefaction, inflammation, and fibrosis ［J］. Am J Physiol-Heart C, 2017, 312(3):H375-H383.

［18］ Yu R, Wang YP, Cui L, et al. Pathogenesy and research advancement of myocardial fibrosis ［J］. China Modern Doctor, 2015, 53(13):157-159. (in Chinese)

于瑞，王幼平，崔琳，等. 心肌纤维化的发病机制及其研究进展［J］. 中国现代医生，2015，53（13）：157-159.

［19］ Nguyen JT, Evans DP, Galvan M, et al. CD45 modulates galectin-1-induced T cell death: regulation by expression of core 2 O-glycans ［J］. J Immunol, 2001, 167(10):5697-5707.

［20］ Mo D, Tian W, Zhang HN, et al. Cardioprotective effects of galectin-3 inhibition against ischemia/reperfusion injury ［J］. Eur J Pharmacol, 2019, 863:172701.

［21］ Gao P, Simpson JL, Zhang J, et al. Galectin-3: its role in asthma and potential as an anti-inflammatory target ［J］. Respir Res, 2013, 14(1):136.

［22］ Filer A, Bik M, Parsonage GN, et al. Galectin 3 induces a distinctive pattern of cytokine and chemokine production in rheumatoid synovial fibroblasts via selective signaling pathways ［J］. Arthritis Rheum, 2009, 60(6):1604-1614.