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Expression and clinical significance of microRNA-141 and HMGB1 pathway in different degrees of cardiorenal syndrome |
Qiao Lu-jun, Peng Jin, Hu Guo-xin, Liu Jian, Yang Guang-hu, Luo Huan |
Intensive Care Unit, Shengli Oilfield Central Hospital, Dongying 257034, China |
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Abstract Objective To study the expression of microRNA-141 (miR-141) and recombinant human high mobility group protein B1 (HMGB1) pathway in peripheral blood of patients with cardiorenal syndrome (CRS), and to explore the relationship between miR-141 and the occurrence and development of CRS. Methods The peripheral blood samples of 80 patients with CRS admitted to ICU in our hospital from January 2017 to December 2018 and 40 healthy volunteers in the physical examination center at the same time were collected. According to the 2010 KDIGO/ADQI consensus, the patients were divided into acute cardiorenal syndrome (CRSⅠ) and chronic cardiorenal syndrome (CRSⅡ). Serum B-type natriuretic peptide precursor (NT-proBNP), high sensitive C-reactive protein (hs-CRP), serum creatinine (SCr), left ventricular ejection fraction (LVEF), mitral orifice diastolic peak flow velocity (E peak) and late diastolic peak flow velocity (A peak) were measured, and the ratio of E≥A was calculated. The expression of miR-141, HMGB1, Beclin-1 and LC3 in peripheral blood samples were detected by RT-PCR and WB. Results The ratio of NT-proBNP, hs-CRP, SCr, LVEF, E/A ratio of CRSⅠ patients were higher than those of CRSⅡ patients and the difference was statistically significant (P<0.05). The results of RT-PCR showed that the expression of miR-141 in normal group, CRSⅠ group and CRSⅡ group were (1.64±0.17), (0.58±0.12) and (1.21±0.28), respectively, the expression of miR-141 in both CRS groups was lower than that in normal group, and the expression of miR-141 in CRSⅠ group was the lowest (P<0.05). The expression levels of HMGB1-mRNA in normal group, CRSⅠ group and CRSⅡ group were (0.81±0.31), (2.230.35) and (1.61±0.42), respectively, the expression levels in both CRS groups were higher than those in normal group, and the expression level in CRSⅠ group was the highest (P<0.05). The results of Western blot showed that the expression of HMGB1, Beclin-1 and LC3 in CRSⅠ type were(1.69±0.21), (1.89±0.35) and (1.94±0.28), respectively, which was higher than those in CRSⅡ type (1.31±0.29), (1.39±0.29), (1.34±0.31)(P<0.05), and the expressions in both CRS groups were significantly higher than those in normal group (0.61±0.23), (0.64±0.12), (0.51±0.22), the difference was statistically significant (P<0.05). Conclusion The expression of miR-141 in serum of CRSⅠ patients is decreased, which is related to the fact that miR-141 affects the level of autophagy by affecting the level of HMGB1, which leads to the occurrence and development of CRS, so miR-141 may be a potential therapeutic target for CRS.
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About author:: Luo Huan, E-mail: qihaian@163.com |
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[1]Forman DE, Butler J, Wang Y, et al. Incidence, predictors at admission, and impact of worsening renal function among patients hospitalized with heart failure[J]. J Am Coll Cardiol, 2004, 43(1):61-67.
[2]汪雁博,傅向华.1型心肾综合征病理生理学机制研究进展[J].中华临床医师杂志(电子版), 2016, 25(1):96-99.
[3]Gannon SA, Mukamal KJ, Chang JD, et al. Echocardiographic predictors of change in renal function with intravenous diuresis for decompensated heart failure[J]. ESC Heart Fail, 2018, 5(5): 858-863.
[4]Leskovar B, Furlan T, Pozni S, et al. Hemodialysis treatment of cardiorenal syndrome[J]. Clin Nephrol, 2017, 88(13): 57-60.
[5]Ronco C, Cicoira M, McCullough PA. Cardiorenal syndrome type 1:pathophysiological crosstalk leading to combined heart and kidney dysfunction in the setting of acutely decompensated heart failure[J]. J Am Coll Cardiol, 2012, 60(12): 1031-1042.
[6]Shah HR,Singh NP, Aggarwal NP, et al. Cardiorenal syndrome: clinical outcome study[J]. J Assoc Physicians India, 2016, 64 (12):41-46.
[7]Issad B,Rostoker G, Bagnis C, et al. Peritoneal dialysis for acute renal failure: rediscovery of an old modality of renal replacement therapy[J]. Nephrol Ther, 2016, 12( 4): 193-197.
[8]Zhu H, Huang L, Zhu S, et al. Regulation of autophagy by systemic admission of microRNA-141 to target HMGB1 in l-arginine-induced acute pancreatitis in vivo[J]. Pancreatology, 2016, 16(3):337-346.
[9]Ronco C, Mocullough P, Anker SD, et al. Cardiorenal syndromes: report from the consensus conference of the acute dialysis qualityinitiative[J]. Eur Heart J, 2010, 31(6):703-711.
[10]Atici A, Emet S, Cakmak R, et al. Type I cardiorenal syndrome in patients with acutely decompensated heart failure: the importance of new renal biomarkers[J]. Eur Rev Med Pharmacol Sci, 2018, 22(11):3534-3543.
[11]何群鹏,谢红浪.心肾综合征的发病机制及治疗[J].肾脏病与透析肾移植杂志, 2010, 19(3):256-62.
[12]Gukovskaya AS, Gukovsky I, Algül H, et al. Autophagy,inflammation,and immune dysfunction in the pathogenesis of pancreatitis[J]. Gastroenterology, 2017, 153(5):1212-1226.
[13]Gukovsky I, Pandol SJ, Mareninova OA, et al. Impaired autophagy and organellar dysfunction in pancreatitis[J]. Gastroenterol Hepatol, 2012, 27(2):27-32.
[14]Hamurcu Z, Deliba N, Ge ene S, et al. Targeting LC3 and Beclin-1 autophagy genes suppresses proliferation,survival,migration and invasion by inhibition of Cyclin-D1 and uPAR/Integrin β1/ Src signaling in triple negative breast cancer cells[J]. J Cancer Res Clin Oncol, 2018, 144(3):415-430.
[15]Kang R, Chen R, Zhang Q, et al. HMGB1 in health and disease[J]. Mol Aspects Med, 2014, 40:1-116.
[16]Yu C, Yu X, Zhu HW, et al. Expression pattern of HMGB1 and its association with autophagy in acute necrotizing pancreatitis[J]. Mol Med Rep, 2016, 14(6):5507-5513.
[17]Andrukonis K, Bell C, Bodine L, et al. Cardiorenal syndrome: understanding the connections between cardiac andrenal disease[J]. JAAPA, 2014, 27(2): 12-17.
[18]Hu LH, Ji JT, Li ZS. Potential application of miRNAs as diagnostic and therapeutic tools in chronic pancreatitis[J]. J Cell Mol Med, 2015, 19(9):2049-2057. |
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