Long Non-coding RNA Expression Profiling in Biopsy to Identify Renal Allograft at Risk of Chronic Damage and Future Graft Loss

Xu, Jing; Hu, Jinglei; Xu, Hong‐Xi; Zhou, Hong‐Hao; Liu, Zhao‐Qian; Zhou, Yong; Liu, Rong; Zhang, Wei

doi:10.1007/s12010-019-03082-2

Cited by 11 publications

(9 citation statements)

References 23 publications

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“…Biopsy is still the gold standard to differentiate allogeneic graft rejection from other injuries, but this invasive examination has notable risks and limitations. Recently, an obvious variation of the microRNA (miRNA) and long non-coding RNA (lncRNA) expression profiling based on the biopsies in allograft rejection was reported; however, it still required an invasive method, and the mechanism of miRNA and lncRNA modulating allogeneic graft rejection remains unknown [19,20].…”

Section: Discussionmentioning

confidence: 99%

IL-27Rα: A Novel Molecular Imaging Marker for Allograft Rejection

Zhao

Shi

et al. 2020

IJMS

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Non-invasively monitoring allogeneic graft rejection with a specific marker is of great importance for prognosis of patients. Recently, data revealed that IL-27Rα was up-regulated in alloreactive CD4+ T cells and participated in inflammatory diseases. Here, we evaluated whether IL-27Rα could be used in monitoring allogeneic graft rejection both in vitro and in vivo. Allogeneic (C57BL/6 donor to BALB/c recipient) and syngeneic (BALB/c both as donor and recipient) skin grafted mouse models were established. The expression of IL-27Rα in grafts was detected. The radio-probe, 125I-anti-IL-27Rα mAb, was prepared. Dynamic whole-body phosphor-autoradiography, ex vivo biodistribution and immunofluorescence staining were performed. The results showed that the highest expression of IL-27Rα was detected in allogeneic grafts on day 10 post transplantation (top period of allorejection). 125I-anti-IL-27Rα mAb was successfully prepared with higher specificity and affinity. Whole-body phosphor-autoradiography showed higher radioactivity accumulation in allogeneic grafts than syngeneic grafts on day 10. The uptake of 125I-anti-IL-27Rα mAb in allogeneic grafts could be almost totally blocked by pre-injection with excess unlabeled anti-IL-27Rα mAb. Interestingly, we found that 125I-anti-IL-27Rα mAb accumulated in allogeneic grafts, along with weaker inflammation earlier on day 6. The high uptake of 125I-anti-IL-27Rα mAb was correlated with the higher infiltrated IL-27Rα positive cells (CD3+/CD68+) in allogeneic grafts. In conclusion, IL-27Rα may be a novel molecular imaging marker to predict allorejection.

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Section: Discussionmentioning

confidence: 99%

IL-27Rα: A Novel Molecular Imaging Marker for Allograft Rejection

Zhao

Shi

et al. 2020

IJMS

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“…Moreover, in a rat study, the lncRNA PRINS was shown to be significantly up-regulated in kidneys of rats with cold ischemia-elicited allograft rejection, compared with rats without rejection [ 23 ]. In addition, lncRNAs may also be of value in predicting the development of chronic damage after kidney transplantation [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Circulating Long Noncoding RNA LNC-EPHA6 Associates with Acute Rejection after Kidney Transplantation

Groeneweg

Duijs

Florijn

et al. 2020

IJMS

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Acute rejection (AR) of a kidney graft in renal transplant recipients is associated with microvascular injury in graft dysfunction and, ultimately, graft failure. Circulating long noncoding RNAs (lncRNAs) may be suitable markers for vascular injury in the context of AR. Here, we first investigated the effect of AR after kidney transplantation on local vascular integrity and demonstrated that the capillary density markedly decreased in AR kidney biopsies compared to pre-transplant biopsies. Subsequently, we assessed the circulating levels of four lncRNAs (LNC-RPS24, LNC-EPHA6, MALAT1, and LIPCAR), that were previously demonstrated to associate with vascular injury in a cohort of kidney recipients with a stable kidney transplant function (n = 32) and recipients with AR (n = 15). The latter were followed longitudinally six and 12 months after rejection. We found higher levels of circulating LNC-EPHA6 during rejection, compared with renal recipients with a stable kidney function (p = 0.017), that normalized one year after AR. In addition, LNC-RPS24, LNC-EPHA6, and LIPCAR levels correlated significantly with the vascular injury marker soluble thrombomodulin. We conclude that AR and microvascular injury are associated with higher levels of circulating LNC-EPHA6, which emphasizes the potential role of lncRNAs as biomarker in the context of AR.

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“…The mode of action can be roughly divided into four categories: signal, decoy, guide and scaffold. 23 LncRNAs can regulate the expression of genes through epigenetic regulation, transcriptional regulation and post-transcriptional regulation, and thus participate in various biological processes such as cell proliferation, differentiation and apoptosis in cancer, the role of LncRNAs in signaling pathways has become an important part of the mechanism of cancer development. 24,25 Lnc TCF7 is highly expressed in liver cancer cells and plays an important role in the maintenance of liver cancer stem cell self-renewal ability.…”

Section: Discussionmentioning

confidence: 99%

<p>LncRNA RP11-422N16.3 Inhibits Cell Proliferation and EMT, and Induces Apoptosis in Hepatocellular Carcinoma Cells by Sponging miR-23b-3p</p>

Sun

Zhou

et al. 2019

OTT

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Objective: This study investigated the mechanism of RP11-422N16.3 sponging miR-23b-3p in cell proliferation, apoptosis and epithelial-mesenchymal transition (EMT) in liver cancer. Methods: Expressions of RP11-422N16.3, miR-23b-3p and dimethylglycine dehydrogenase (DMGDH) were determined in liver cancer tissues, adjacent normal tissues, hepatocellular carcinoma cell lines and normal liver epithelial cell line. Up-regulation of RP11-422N16.3 and downregulation of miR-23b-3p were conducted in hepatocellular carcinoma cells. Bioinformatics analysis, luciferase reporter assay and RNA-pull down assay were performed to verify the relationship among miR-23b-3p, DMGDH, as well as RP11-422N16.3. Cell proliferation and cell apoptosis were determined by CCK-8 and Flow Cytometry analysis, respectively. Results: Expressions of RP11-422N16.3 and DMGDH were down-regulated while that of miR-23b-3p were up-regulated in hepatocellular carcinoma cancer tissues and cells. RP11-422N16.3 localized in cytoplasm and competitively bound to miR-23b-3p. Up-regulation of RP11-422N16.3 and down-regulation of miR-23b-3p contributed to increased expressions of DMGDH and E-cadherin, and decreased expressions of miR-23b-3p, ZEB1, Snail and Vimentin, resulting in inhibiting cell proliferation and promoting cell apoptosis. Inhibition of RP11-422N16.3 or overexpression of miR-23b-3p accelerated cell proliferation and slowed down cell apoptosis. miR-23b-3p inhibited the expression of DMGDH. Conclusion: Our data suggested that LncRNA RP11-422N16.3, by competitively binding to miR-23b-3p, promoted DMGDH expression, contributing to inhibit cell proliferation and EMT, and induce cell apoptosis in hepatocellular carcinoma cells.

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Long Non-coding RNA Expression Profiling in Biopsy to Identify Renal Allograft at Risk of Chronic Damage and Future Graft Loss

Cited by 11 publications

References 23 publications

IL-27Rα: A Novel Molecular Imaging Marker for Allograft Rejection

IL-27Rα: A Novel Molecular Imaging Marker for Allograft Rejection

Circulating Long Noncoding RNA LNC-EPHA6 Associates with Acute Rejection after Kidney Transplantation

<p>LncRNA RP11-422N16.3 Inhibits Cell Proliferation and EMT, and Induces Apoptosis in Hepatocellular Carcinoma Cells by Sponging miR-23b-3p</p>

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