scholarly journals Effects of apigenin on the expression levels of B‑cell lymphoma‑2, Fas and Fas ligand in renal ischemia‑reperfusion injury in rats

2017 ◽  
Author(s):  
Yang Liu ◽  
Xiuheng Liu ◽  
Lei Wang ◽  
Yang Du ◽  
Zhiyuan Chen ◽  
...  
Keyword(s):  
B Cell ◽  
Reperfusion Injury ◽  
Fas Ligand ◽  
Ischemia Reperfusion Injury ◽  
Cell Lymphoma ◽  
Ischemia Reperfusion ◽  
B Cell Lymphoma ◽  
Renal Ischemia ◽  
Expression Levels ◽  
Renal Ischemia Reperfusion Injury

Role of miR-139-5p in relieving renal allograft ischemia-reperfusion injury by inhibiting c-Jun NH-terminal kinase (JNK) signaling pathway

2020 ◽  
Vol 10 (2) ◽  
pp. 231-239
Author(s):  
Yan Zhang ◽  
Shu Wang ◽  
Ping Yang ◽  
Tao Wang
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Jnk Pathway ◽  
Jnk Signaling ◽  
Expression Levels ◽  
Renal Ischemia Reperfusion Injury ◽  
Related Proteins

Renal ischemia-reperfusion injury cannot be avoided in the process of kidney transplants. In this study, the role of miR-139-5p in renal ischemia-reperfusion injury in mice was investigated. Hyperuricemia cells were detected using qPCR. The results confirm that the expression levels of miR-139-5p, Jun, and c-Jun were detected, and miR-139-5p was down-regulated in the ischemia-reperfusion injury after renal transplantation, while CDK4 and Jun were up-regulated. The levels of [Ca++]i and ROO were measured in HK-2 cells, and it was determined that overexpression of miR-139-5p reduced these levels to approach a normal state. After cell silencing of miR139-5p, the levels of [Ca++]i and ROO of the hyperuricemia cells increased significantly. After down-regulation of miR-139-5p via CCK-8 and clonal cell formation assays, it was determined that the survival rate and viability of hyperuricemia cells were decreased significantly. However, the addition of the agent anisomycin (JNK activation) improved the survival rate of hyperuricemia cells and increased their viability. The detection of the cycle of the hyperuricemia cells revealed that the up-regulation of miR-139-5p blocked a large number of cells in the G1 phase; however, the number of these cells significantly decreased after the addition of anisomycin. The expression levels of c-Jun and JNK in hyperuricemia cells were detected via immunofluorescence. In the hyperuricemia cells, the fluorescence intensity in the miR-139-5p overexpression group was higher compared to that in the control group. Moreover, the fluorescence intensity decreased significantly after the addition of anisomycin. Nano-magnetic beads were fabricated and used to extract high purity RNA. Scanning electron microscopy was used to confirm the efficacy of the nanoparticles in the extraction of RNA. The detection of the JNK pathway-related proteins of hyperuricemia cells using qPCR and Western blot revealed that the downregulation of miR-139-5p promoted the expression of JNK pathway-related proteins while the up-regulation of miR-139-5p inhibited the expression levels of c-jun, JNK, JNK 1, and JNK 2. The experimental results indicate that miR-139-5p alleviates renal–renal ischemia-reperfusion injury by targeting Jun-mediated JNK signaling pathways.

scholarly journals MiR-155 is Involved in Renal Ischemia-Reperfusion Injury via Direct Targeting of FoxO3a and Regulating Renal Tubular Cell Pyroptosis

2016 ◽  
Vol 40 (6) ◽  
pp. 1692-1705 ◽  
Author(s):  
Haoyu Wu ◽  
Tao Huang ◽  
Liang Ying ◽  
Conghui Han ◽  
Dawei Li ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Tubular Cell ◽  
Luciferase Reporter ◽  
Expression Levels ◽  
Caspase 1 ◽  
Renal Ischemia Reperfusion Injury ◽  
Hk2 Cells

Background/Aims: Ischemia/reperfusion injury (IRI) plays a crucial role in renal transplantation and can cause renal failure associated with pyroptosis, a pro-inflammatory-induced programmed cell death. Small endogenous non-coding RNAs have been shown to be involved in renal ischemia/reperfusion injury. This study was performed to investigate which miRNAs regulate pyroptosis in response to renal ischemia/reperfusion injury and determine the mechanism underlying this regulation. Methods: An in vivo rat model of renal IRI was established, and the serum and kidneys were harvested 24 h after reperfusion to assess renal function and histological changes. For the in vitro study, the cultured human renal proximal tubular cell line HK-2 was subjected to 24 h of hypoxia (5% CO2, 1% O2, and 94% N2) followed by 12 h of reoxygenation (5% CO2, 21% O2, and 74% N2). The mRNA expression levels were analyzed by real-time PCR, and the protein expression levels were analyzed using Western blot, immunofluorescence staining and enzyme-linked immunosorbent assay (ELISA). Bioinformatics analyses were applied to predict miR-155 targets, which were then confirmed by a luciferase reporter assay. Results: We found that the levels of pyroptosis-related proteins, including caspase-1, caspase-11, IL-1β and IL-18, were significantly increased after renal ischemia/reperfusion injury. Similarly, hypoxia-reoxygenation injury (HRI) also induced pyroptosis in HK2 cells. Furthermore, our study revealed that miR-155 expression was substantially increased in the renal tissues of IRI rats and in HRI HK2 cells. Up-regulation of miR-155 promoted HK2 cell pyroptosis in HRI; conversely, knockdown of miR-155 attenuated this process. To understand the signaling mechanisms underlying the pro-pyroptotic activity of miR-155, we found that exogenous expression of miR-155 up-regulated the expression of caspase-1 as well as the pro-inflammatory cytokines IL-1β and IL-18. Moreover, miR-155 directly repressed FoxO3a expression and its downstream protein apoptosis repressor with caspase recruitment domain (ARC). Conclusions: Our study proposes a new signaling pathway of miR-155/FoxO3a/ARC leading to renal pyroptosis under ischemia/reperfusion injury conditions.

scholarly journals B Cell Deficiency Confers Protection from Renal Ischemia Reperfusion Injury

2003 ◽  
Vol 171 (6) ◽  
pp. 3210-3215 ◽  
Author(s):  
Melissa J. Burne-Taney ◽  
Dolores B. Ascon ◽  
Frank Daniels ◽  
Lorraine Racusen ◽  
William Baldwin ◽  
...  
Keyword(s):  
B Cell ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury ◽  
B Cell Deficiency

1843: Role of Cxcr2 in Renal Ischemia/Reperfusion Injury

2004 ◽  
Vol 171 (4S) ◽  
pp. 487-487
Author(s):  
Motoo Araki ◽  
Masayoshi Miura ◽  
Hiromi Kumon ◽  
John Belperio ◽  
Robert Strieter ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury
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