LncRNA136131 suppresses apoptosis of renal tubular epithelial cells in acute kidney injury by targeting the miR-378a-3p/Rab10 axis

Wu, Zhifen; Pan, Jian; Yang, Jurong; Zhang, Dongshan

doi:10.18632/aging.204036

Cited by 10 publications

(10 citation statements)

References 42 publications

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“…For example, the lncRNAs MEG3, XIST, and ENSMUST_147219 are apoptosis inducers [ 13 , 14 , 15 ]. However, H19, lncRNA136131, and lncRNA NONRATG019935.2 are apoptosis inhibitors [ 16 , 17 , 18 ]. The above studies suggest that the role of lncRNAs in apoptosis needs to be clarified during ischemic injury.…”

Section: Discussionmentioning

confidence: 99%

“…For example, lncRNAs MEG3, XIST, and ENSMUST_147219 mediated IAKI by facilitating the apoptosis of renal tubular cells [ 13 , 14 , 15 ]. By contrast, H19, lncRNA136131, and lncRNA NONRATG019935.2 mitigated IAKI via the suppression of renal tubular epithelial cell apoptosis [ 16 , 17 , 18 ]. LncRNA171502 is located at chr14:41307367-41307568.…”

Section: Introductionmentioning

confidence: 99%

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LncRNA ENSMUST00000171502 Induced by HIF-1α Ameliorates Ischemic Acute Kidney Injury via Targeting the miR-130b-3p/Mybl-1 Axis

Wang

Zhang

2022

Cells

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Background: Numerous studies have suggested that long non-coding RNA (lncRNA) affects the progression of ischemic acute kidney injury (IAKI). However, little information is currently available concerning the mechanisms of lncRNA171502 involved in IAKI. Methods: We applied an RT-qPCR assay for the expression of lncRNA171502 and miRNA-130b-3p, immunoblotting for the detection of Mybl-1-myeloblastosis oncogene-like 1 (Mybl-1) and cleaved caspase-3 (CC3) expression, and flow cytometry (FCM) for the evaluation of apoptosis. Result: Initially, lncRNA171502 was induced by HIF-1α in the mouse proximal tubular (BUMPT) cell line and C57BL/6J mice during ischemic injury. Secondly, ischemic injury-induced BUMPT cell apoptosis was markedly relieved following the overexpression of lncRNA171502. However, this effect was enhanced by the knockdown of lncRNA171502. Mechanistically, lncRNA171502 could sponge miRNA-130b-3p and would subsequently upregulate the expression of Mybl-1 to drive the apoptotic process. Lastly, the overexpression of lncRNA171502 alleviated the development of IAKI by targeting miRNA-130b-3p/Mybl-1 pathways. Conclusions: In summary, the HIF-1α/lncRNA171502/miRNA-130b-3p/Mybl-1 axis prevented the progression of IAKI and might serve as a potential therapeutic target.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

LncRNA ENSMUST00000171502 Induced by HIF-1α Ameliorates Ischemic Acute Kidney Injury via Targeting the miR-130b-3p/Mybl-1 Axis

Wang

Zhang

2022

Cells

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“…TECs undergo various types of programmed cell death (PCD) including apoptosis, pyroptosis, necroptosis, and ferroptosis (64)(65)(66)(67). Upon sensing local tissue injury, resident and infiltrating inflammatory cells in the kidney promote TEC PCD by producing and releasing large amounts of inflammatory cytokines and activating various pathway proteins, leading to TEC detachment, tubular occlusion, and tubular inactivation.…”

Section: Immune Cells Promote Various Types Of Programmed Cell Deaths...mentioning

confidence: 99%

Interaction Between Intrinsic Renal Cells and Immune Cells in the Progression of Acute Kidney Injury

Deng

et al. 2022

Front. Med.

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A growing number of studies have confirmed that immune cells play various key roles in the pathophysiology of acute kidney injury (AKI) development. After the resident immune cells and intrinsic renal cells are damaged by ischemia and hypoxia, drugs and toxins, more immune cells will be recruited to infiltrate through the release of chemokines, while the intrinsic cells promote macrophage polarity conversion, and the immune cells will promote various programmed deaths, phenotypic conversion and cycle arrest of the intrinsic cells, ultimately leading to renal impairment and fibrosis. In the complex and dynamic immune microenvironment of AKI, the bidirectional interaction between immune cells and intrinsic renal cells affects the prognosis of the kidney and the progression of fibrosis, and determines the ultimate fate of the kidney.

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“…Before the I/R injury model was established, the Rb1 (40mg/kg per injection) (18) or saline was injected intraperitoneally into male C57BL/6J mice once a day for three consecutive days. The renal blood supply was blocked for 28 min and then restored for 36 h (19). Renal tissue samples were collected after 36 h. All experimental processes were carried out in accordance with the animal care rules of Chongqing Medical University.…”

Section: Animals and Ischemic Aki Modelmentioning

confidence: 99%

“…Total protein samples were extracted from HK-2 cells or renal cortex for Western blotting. The method was performed as described previously (19). The membranes were incubated with primary antibodies against GPX4, SLC7A11, and 𝛽-actin followed by horseradish peroxidase-conjugated secondary antibody incubation.…”

Section: Immunoblot Analysismentioning

confidence: 99%

Ginsenoside Rb1 ameliorates renal tubular epithelial cells ferroptosis in AKI

Deng

Tao³

et al. 2022

Preprint

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Acute kidney injury (AKI) is mainly caused by ischemia-reperfusion (I/R), with high clinical mortality since there is a lack of definite and effective drug intervention except for renal replacement therapy. Previous research emphasized that ferroptosis is the pivotal process in I/R injury of renal. Ginsenoside Rb1 is a chemical compound belonging to the ginsenoside family and has been proved to have benefits for kidney diseases, but its specific mechanism in AKI is uncovered. Here we discovered Rb1 could mitigate ferroptosis in renal tubular epithelial cells of AKI animals. Mechanically, Rb1 significantly inhibited oxidative stress including promotion of GSH, reduction of malondialdehyde (MDA) and reactive oxygen species (ROS), also reduced inflammatory response, then relieved renal injury in I/R mice. RSL3, the inhibitor of GPX4, or Erastin, the inhibitor of SLC7A11, could induce ferroptosis and eliminate the protective effect of Rb1. Also, a ferroptosis inhibitor or ROS scavenger could simulate the protective effect of Rb1 on renal tubular epithelial cells. In conclusion, we confirmed that Rb1 promotes GSH synthesis by preventing oxidative stress, upregulating the expression of GPX4 and SLC7A11, and ultimately scavengers of ROS or MDA, and reduces the occurrence of ferroptosis in renal tubular epithelial cells. Rb1 has potential benefits for AKI patients.

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LncRNA136131 suppresses apoptosis of renal tubular epithelial cells in acute kidney injury by targeting the miR-378a-3p/Rab10 axis

Cited by 10 publications

References 42 publications

LncRNA ENSMUST00000171502 Induced by HIF-1α Ameliorates Ischemic Acute Kidney Injury via Targeting the miR-130b-3p/Mybl-1 Axis

LncRNA ENSMUST00000171502 Induced by HIF-1α Ameliorates Ischemic Acute Kidney Injury via Targeting the miR-130b-3p/Mybl-1 Axis

Interaction Between Intrinsic Renal Cells and Immune Cells in the Progression of Acute Kidney Injury

Ginsenoside Rb1 ameliorates renal tubular epithelial cells ferroptosis in AKI

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