scholarly journals Identification of TIMP2 and RAX as key regulators in chemosensitive osteosarcoma

2020 ◽  
Author(s):  
HuaBin Wang ◽  
Yuanxiang Liu ◽  
Haitao Zeng
Keyword(s):  
Cell Proliferation ◽  
Cell Survival ◽  
Differentially Expressed ◽  
Cell Counting ◽  
Regulation Mechanism ◽  
Rt Pcr ◽  
P Values ◽  
Vegf Signaling ◽  
Differentially Expressed Mirnas ◽  
And Function

Abstract Background This study is trying to investigate the regulation mechanism of chemosensitive osteosarcoma. mRNA and miRNA profiles were explored between chemosensitive and chemoresistant osteosarcoma patients based on GSE39058 dataset. IPA was used for pathway and function enrichment. Another dataset GSE21257 with clinical characteristics was used for survival analysis, and 68 new enrolled osteosarcoma patients with chemotherapy responses were used for RT-PCR validation. Finally, lentiviruses infected U-2 OS cells were subjected to cell counting and real-time cell analyzer.Results A total of 567 differentially expressed genes and 34 differentially expressed miRNAs were screened out. These genes mainly involved in the biology functions of cell survival and cell proliferation, and enriched in the pathways of VEGF signaling, Paxillin signaling, and Inhibition of matrix matalloproteases. In 53 validation osteosarcoma patients from GSE21257, high-expression of TIMP2 and BAX, two common genes among the enriched biology functions, have favorable prognosis with p-values 0.052 and 0.027 respectively. In the 68 new enrolled patients, both TIMP2 and BAX were RT-PCR validated to be high-expressed in chemosensitive group with p-values 0.04 and 0.003 respectively. In addition, cell count and cell index either in TIMP2 or BAX infected U-2 OS cells were smaller compared with control cells within four consecutive days.Conclusions In summary, the biology functions of cell survival and cell proliferation were identified to be mainly inhibited in chemosensitive osteosarcoma patients. Two up-regulated genes, TIMP2 and BAX, were validated to be important regulators of cell proliferation and cell apoptosis in chemosensitive group. Further experimental evidences are still needed to consolidate this results.

scholarly journals Inhibitory effect of sodium butyrate on colorectal cancer cells and construction of the related molecular network

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yang Xi ◽  
Zhuang Jing ◽  
Wu Wei ◽  
Zhang Chun ◽  
Qi Quan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Sodium Butyrate ◽  
Molecular Network ◽  
Differentially Expressed ◽  
Cell Counting ◽  
Molecular Networks ◽  
Ppi Network ◽  
Invasion And Metastasis ◽  
Cerna Network ◽  
Proliferation Ability

Abstract Background Sodium butyrate (NaB) is produced through the fermentation of dietary fiber that is not absorbed and digested by the small intestine. Purpose Here, we aimed to investigate the effects of NaB on the proliferation, invasion, and metastasis of CRC cells and their potential underlying molecular mechanism(s). Methods The cell counting kit-8 (CCK-8) assay and EdU assay were used to detect cell proliferation ability, flow cytometry was used to investigate the induction of apoptosis and cell cycle progression, and the scratch-wound healing and transwell assays were used to evaluate cell migration and invasion, respectively. The human CRC genome information for tissues and CRC cells treated with NaB obtained from the NCBI GEO database was reannotated and used for differential RNA analysis. Functional and pathway enrichment analyses were performed for differentially expressed lncRNAs and mRNAs. A protein-protein interaction (PPI) network for the hub genes was constructed using the Cytoscape software. Targeted miRNAs were predicted based on the lnCeDB database, and a ceRNA network was constructed using the Cytoscape software. The Kaplan-Meier method was used to analyze patient prognosis using the clinical information and exon-seq data for CRC obtained from the Broad Institute’s GDAC Firehose platform. Results NaB decreased the proliferation ability of CRC cells in a dose- and time-dependent manner. The number of apoptotic CRC cells increased with the increase in NaB concentrations, and NaB induced a G1 phase block in CRC cells. Moreover, NaB suppressed the migratory and invasive capabilities of CRC cells. There were 666 differentially expressed mRNAs and 30 differentially expressed lncRNAs involved in the CRC inhibition by NaB. The PPI network and ceRNA network were constructed based on the differentially expressed mRNAs and lncRNAs. Three differentially expressed mRNAs, including HMGA2, LOXL2, and ST7, were significantly correlated with the prognosis of CRC. Conclusion NaB induces the apoptosis and inhibition of CRC cell proliferation, invasion, and metastasis by modulating complex molecular networks. RNA prediction and molecular network construction need to be the focus of further research in this direction.

scholarly journals Identification of New miRNA-mRNA Networks in the Development of Non-syndromic Cleft Lip With or Without Cleft Palate

2021 ◽  
Vol 9 ◽  
Author(s):  
Chengyi Fu ◽  
Shu Lou ◽  
Guirong Zhu ◽  
Liwen Fan ◽  
Xin Yu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cleft Palate ◽  
Negative Correlation ◽  
Cell Apoptosis ◽  
Cleft Lip ◽  
Target Genes ◽  
Craniofacial Development ◽  
Differentially Expressed ◽  
Differentially Expressed Mirnas

Objective: To identify new microRNA (miRNA)-mRNA networks in non-syndromic cleft lip with or without cleft palate (NSCL/P).Materials and Methods: Overlapping differentially expressed miRNAs (DEMs) were selected from cleft palate patients (GSE47939) and murine embryonic orofacial tissues (GSE20880). Next, the target genes of DEMs were predicted by Targetscan, miRDB, and FUNRICH, and further filtered through differentially expressed genes (DEGs) from NSCL/P patients and controls (GSE42589), MGI, MalaCards, and DECIPHER databases. The results were then confirmed by in vitro experiments. NSCL/P lip tissues were obtained to explore the expression of miRNAs and their target genes.Results: Let-7c-5p and miR-193a-3p were identified as DEMs, and their overexpression inhibited cell proliferation and promoted cell apoptosis. PIGA and TGFB2 were confirmed as targets of let-7c-5p and miR-193a-3p, respectively, and were involved in craniofacial development in mice. Negative correlation between miRNA and mRNA expression was detected in the NSCL/P lip tissues. They were also associated with the occurrence of NSCL/P based on the MGI, MalaCards, and DECIPHER databases.Conclusions: Let-7c-5p-PIGA and miR-193a-3p-TGFB2 networks may be involved in the development of NSCL/P.

Analysis of MicroRNA Transcriptomes Insights into the miR-148a-3p Inducer of Rumen Development in Goats

2020 ◽  
Author(s):  
Tao Zhong ◽  
Cheng Wang ◽  
Jiangtao Hu ◽  
Xiaoyong Chen ◽  
Lili Niu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Target Genes ◽  
Genetic Regulation ◽  
Mapk Signaling ◽  
Regulation Mechanism ◽  
Ras Signaling ◽  
Genome Wide ◽  
A Genome ◽  
Differentially Expressed Mirnas ◽  
And Function

Abstract Background: Rumen is an important digestive organ of ruminant. From fetal to adult stage, the morphology, structure and function of rumen have changed significantly. But the intrinsic genetic regulation is still limited. We previously reported a genome-wide expression profile of miRNAs in prenatal goat rumens. In the present study, we rejoined analyzed the transcriptomes of rumen miRNAs during prenatal (E60 and E135) and postnatal (D30 and D150) stages.Results: A total of 66 differentially expressed miRNAs (DEMs) were identified in the rumen tissues from D30 and D150 goats. Of these, 17 DEMs were consistently highly expressed in the rumens at the preweaning stages (E60, E135 and D30), while down-regulated at D150. Noteworthy, annotation analysis revealed that the target genes regulated by the DEMs were mainly enriched in MAPK signaling pathway, Jak-STAT signaling pathway and Ras signaling pathway. Interestingly, the expression of miR-148a-3p was significantly high in the embryonic stage and down-regulated at D150. The potential binding sites between miR-148a-3p and QKI were predicted by the TargetScan and verified by the dual luciferase report assay. The co-localization of miR-148a-3p and QKI was observed not in intestinal tracts but in rumen tissues by in situ hybridization. Moreover, the expression of miR-148a-3p in the epithelium was significantly higher than that in the other layers, suggesting that miR-148a-3p involve in the development of rumen epithelial cells by targeting QKI. Subsequently, miR-148a-3p inhibitor was found to induce the proliferation of GES-1 cells.Conclusions: Taken together, these results identified the DEMs involved in the development of rumen and provided an insight into the regulation mechanism of goat rumens during development.

scholarly journals 60S acidic ribosomal protein P1 (RPLP1) is elevated in human endometriotic tissue and in a murine model of endometriosis and is essential for endometriotic epithelial cell survival in vitro

2020 ◽  
Vol 26 (1) ◽  
pp. 53-64
Author(s):  
Zahraa Alali ◽  
Amanda Graham ◽  
Kimberly Swan ◽  
Rebecca Flyckt ◽  
Tommaso Falcone ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Ribosomal Protein ◽  
Cell Survival ◽  
Murine Model ◽  
Eutopic Endometrium ◽  
Ectopic Tissue ◽  
And Function ◽  
Matched Samples ◽  
Proliferation And Invasion

Abstract Endometriosis is a female disease which is defined as the presence of ectopic endometrial tissue and is dependent on estrogen for its survival in these ectopic locations. Expression of the ribosomal protein large P1 (RPLP1) is associated with cell proliferation and invasion in several pathologies, but a role in the pathophysiology of endometriosis has not been explored. In this study, we aimed to evaluate the expression and function of RPLP1 with respect to endometriosis pathophysiology. RPLP1 protein was localised by immunohistochemistry (IHC) in eutopic and ectopic tissue from 28 subjects with confirmed endometriosis and from 20 women without signs or symptoms of the disease, while transcript levels were evaluated by qRT-PCR in 77 endometriotic lesions and 55 matched eutopic endometrial biopsies, and protein expression was evaluated using western blotting in 20 of these matched samples. To evaluate the mechanism for enhanced lesion expression of RPLP1, an experimental murine model of endometriosis was used and RPLP1 expression was localized using IHC. In vitro studies using an endometriosis cell line coupled with shRNA knockdown was used to demonstrate its role in cell survival. Expression of RPLP1 mRNA and protein were significantly higher in ectopic lesion tissue compared to paired eutopic endometrium and immunohistochemical localisation revealed predominant localisation to epithelial cells. This pattern of lesion RPLP1 was recapitulated in mice with experimentally induced endometriosis. Stable knockdown of RPLP1 protein resulted in a significant decrease in cell survival in vitro. These studies reveal that RPLP1 is associated with cell proliferation and/or survival and may play a role in the pathophysiology of endometriosis.

Differential expression of microRNAs in porcine placentas on Days 30 and 90 of gestation

2010 ◽  
Vol 22 (8) ◽  
pp. 1175 ◽  
Author(s):  
Lijie Su ◽  
Shuhong Zhao ◽  
Mengjin Zhu ◽  
Mei Yu
Keyword(s):  
Differential Expression ◽  
Differentially Expressed ◽  
Locked Nucleic Acid ◽  
Chain Reaction ◽  
Stem Loop ◽  
Non Invasive ◽  
Differentially Expressed Mirnas ◽  
Non Coding Rnas ◽  
Polymerase Chain ◽  
And Function

The porcine placenta is classified as a non-invasive epitheliochorial type. To meet the increasing demands for nutrients by the rapidly growing conceptus and/or fetus, the placental microscopic folds undergo significant morphological and biochemical changes during two periods critical for conceptus and/or fetus, namely Days 30–40 and after Day 90 of gestation. MicroRNAs (miRNAs) are a class of small non-coding RNAs that can modulate gene activity by inhibiting the translation or regulation of mRNA degradation. In the present study, we identified 17 differentially expressed miRNAs in porcine placenta on Days 30 and 90 of gestation using a locked nucleic acid (LNA) microRNA array. Stem–loop real-time reverse transcription–polymerase chain reaction confirmed the differential expression of eight selected miRNAs (miR-24, miR-125b, miR-92b, miR-106a, miR-17, let-7i, miR-27a and miR-20). Analysis of targets and the pathways in which these miRNAs are involved revealed that the differentially expressed miRNAs target many genes that are important in various processes, including cell growth, trophoblast differentiation, angiogenesis and formation and maintenance of adherens junctions. The results of the present study suggest potential roles for these differentially expressed miRNAs in porcine placental growth and function.

scholarly journals Melatonin Promotes the Proliferation of Chicken Sertoli Cells by Activating the ERK/Inhibin Alpha Subunit Signaling Pathway

Molecules ◽  
2020 ◽  
Vol 25 (5) ◽  
pp. 1230 ◽  
Author(s):  
Ke Xu ◽  
Jun Wang ◽  
Hongyu Liu ◽  
Jing Zhao ◽  
Wenfa Lu
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Sertoli Cells ◽  
Cell Counting ◽  
Erk Signaling ◽  
Alpha Subunit ◽  
Nuclear Antigen ◽  
Physiological Processes ◽  
Underlying Mechanisms ◽  
And Function

Melatonin influences physiological processes such as promoting proliferation and regulating cell development and function, and its effects on chicken Sertoli cells are unknown. Therefore, we investigated the effects of melatonin on cell proliferation and its underlying mechanisms in chicken Sertoli cells. Chicken Sertoli cells were exposed to varying melatonin concentrations (1, 10, 100, and 1000 nM), and the melatonin-induced effects on cell proliferation were measured by Cell Counting Kit 8 (CCK-8), 5-ethynyl-2’-deoxyuridine (EdU), real-time qPCR, and western blotting. We found that 1000 nM melatonin significantly (p < 0.05) promoted cell proliferation in chicken Sertoli cells. Furthermore, melatonin significantly (p < 0.05) increased the expression of inhibin alpha subunit (INHA), and the silencing of INHA reversed the melatonin-induced effects on Sertoli cell proliferation. We also found that melatonin activates the extracellular-regulated protein kinase (ERK) signaling pathway. To explore the role of the ERK signaling pathway in melatonin-induced cell proliferation, PD98059 (an inhibitor of EKR1/2) was used to pre-treat chicken Sertoli cells. The melatonin-induced proliferation of chicken Sertoli cells was reversed by PD98059, with decreased cell viability, weakened cell proliferation, and down-regulated expression of the proliferating cell nuclear antigen (PCNA), cyclin D1 (CCND1) and INHA. In summary, our results indicate that melatonin promotes the proliferation of chicken Sertoli cells by activating the ERK/inhibin alpha subunit signaling pathway.

scholarly journals Dysregulation of autophagy-associated microRNAs in condyloma acuminatum

2020 ◽  
Author(s):  
Shi Wu ◽  
Dan Lu ◽  
Xinkai Zheng ◽  
Jin Xu ◽  
Zhen Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Light Chain ◽  
Target Genes ◽  
Condyloma Acuminatum ◽  
Differentially Expressed ◽  
Control Group ◽  
Healthy Controls ◽  
Related Protein ◽  
Ki 67 ◽  
Differentially Expressed Mirnas

Abstract Objectives This study was designed to investigate the miRNAs that regulate the cell proliferation of condyloma acuminatum (CA) lesions and their targets.Methods The expression of Ki-67 in 26 CA patients compared with 10 healthy controls was assessed by immunohistochemistry. And the different miRNAs in 4 CA patients and 4 control cases were analyzed by bioinformatics. PCR was used to validate the expression of screened miRNA and its corresponding target genes.Results The expression of Ki-67 was abnormally increased in CA compared with healthy controls ( P <0.05). The comparison of the control group with the CA group revealed 81 differentially expressed miRNAs, of which 56 were downregulated and 25 were upregulated. Two of the differentially expressed miRNAs, miR-30a-5p and miR-514a-3p, are associated with cell proliferation and their target genes are autophagy-related protein (Atg) 5 and Atg12, and Atg3 and Atg12, respectively. PCR results showed that the expression levels of miR-30a-5p and miR-514a-3p were decreased in CA patients compared with healthy controls ( P <0.05), whereas the expression of Atg5, Atg12 and Atg3 was increased ( P <0.05). The expression of the autophagy proteins microtubule-associated protein 1 light chain 3 (LC3) and P62/SQSTM1 (P62) was abnormally increased in the local lesion tissue of the 26 patients with CA compared with the 10 healthy controls, as assessed by immunohistochemistry ( P <0.05).Conclusions Our results suggest that autophagy levels may be modulated by has-miRNA30a-5p and has-miRNA514a-3p in CA patients, leading to dysregulated cell proliferation.

Src Kinases Act Downstream Akt and Are Required for the Transforming Properties of Constitutively Activated Forms of STAT5A and STAT5B

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2378-2378
Author(s):  
Remy Nyga ◽  
Lea Savay ◽  
Ingrid Marcq ◽  
Aline Regnier ◽  
Gandhi Damaj ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cell Survival ◽  
Conflicts Of Interest ◽  
Cell Counting ◽  
Parp Cleavage ◽  
Blue Dye ◽  
Mouse Bone Marrow ◽  
Src Kinases ◽  
Dependent Manner

Abstract Abstract 2378 Background: Stat5A and Stat5B transcription factors play an important role in the control of hematopoietic cell proliferation and survival and are constitutively activated in number of hematological neoplasia. Moreover, expression of constitutively active Stat5 (caStat5) mutants in primary hematopoietic cells can lead to leukaemia. The transforming properties of CaStat5 have been previously shown to require Akt activation. However, the mechanisms by which CaStat5 mutants and Akt are activated remain enigmatic. In this study we aimed to determine the roles of src kinases in these processes, Methods: For this purpose, we used murine Ba/F3 cells transfected or not with CaSta5A (Stat5A1*6) or CaStat5B (Stat51*B6) or with the oncogenic fusion proteins Tel-JAK2 and Tel-Abl as controls. Primary hematopoietic progenitors obtained from mouse bone marrow were also used in this sutdy. Cells were treated or not with the pan-src inhibitors PP1, PP2, and SU 6656 (and with PP3 an inactive analogue of PP1 as a control), imatinib (Abl inhibitor) and AG490 (JAK inhibitor). In some experiments cells were treated with U0126 (MEK inhibitor) or with the highly transducible TaT-dominant negative (dn) Akt fusion protein. Cell proliferation was assessed by cell counting. Cell death was evaluated using the trypan blue dye exclusion test. Cell apoptosis was assessed by analysing annexin V staining using flow cytometry and PARP cleavage using western blot. Expression of kinases and their phosphotylated forms were examined by western blot. Results: CaStat5A and CaStat5B cells were shown to express constitutively phosphorylated Lyn, Hck, Src kinases as well as Akt, IKK and ERK1/2. Stat1, Stat3, and JAK family members (TYK2 and JAK1-3) were not phosphorylated in these cells. Use of pan-Src inhibitors inhibited proliferation of CaStat5 cells and induced apoptosis of a fraction of these cells, in a dose-dependent manner. By contrast, imatinib and AG490 had no effect on the growth and survival of CaStat5 cells. Moreover, pan-src inhibitors prevented Erk but not Akt, IKK or STAT5 phosphorylation. By contrast, inhibition of Akt by means of TaT-dnAkt abolished Lyn, Src and ERK1/2 phosphorylation. Importantly, inhibition of MAPK did not interfere with Akt phosphorylation and did not interfere with CaStat5 cell survival. Conclusion: Altogether our data indicate that Akt acts upstream in the CaStat5-associated signalling cascade, then activates src kinases and thereby promotes MAPK-dependent cell proliferation and MAPK-independent cell survival. These results shed light onto a hitherto undescribed role of Src kinases acting downstream Akt in the mechanisms of action of CaStat5. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Differentially Expressed Long Noncoding RNAs Involved in FUBP1 Promoting Hepatocellular Carcinoma Cells Proliferation

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Xianpeng Li ◽  
Huaixi Yu ◽  
Feng Xu ◽  
Yifeng Wu ◽  
Jifang Sheng
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Lines ◽  
Noncoding Rna ◽  
Target Genes ◽  
Expression Profiles ◽  
Differentially Expressed ◽  
Cell Counting ◽  
Rt Pcr ◽  
Upstream Element ◽  
Hcc Cells

Background. Far upstream element-binding protein 1 (FUBP1) is reported to be involved in cancer development by regulating the transcription of c-myc gene through binding to far upstream element. Highly expressed FUBP1 was negatively correlated with survival rate of patients with hepatocellular carcinoma (HCC) and could promote the proliferation of HCC cells. However, the downstream mechanism of FUBP1 has not yet been clearly explained. This study is aimed at identifying the expression profiles of long noncoding RNA (lncRNA) in HCC cells in response to FUBP1 overexpression and at investigating the possible lncRNAs that participated in cell proliferation process regulated by FUBP1. Methods. The overexpression of FUBP1 was mediated by lentiviral infection on 3 different types of HCC cell lines (MHCC97-H, MHCC97-L, and Huh-7). The expression of target genes was detected by quantitative reverse transcription-PCR (RT-PCR) and western blotting assays. Microarray and quantitative RT-PCR were applied to screen the differentially expressed lncRNAs in HCC cells after FUBP1 overexpression. The Cell Counting Kit-8 assay was used to confirm the growth vitality of HCC cells. Results. The growth vitality of HCC cells was significantly increased after lentivirus infection. A total of 12 lncRNAs had the same expression trend in the 3 HCC cell lines in response to FUBP1 overexpression, including 3 upregulated lncRNAs and 9 downregulated lncRNAs. Coexpression analysis of dysregulated lncRNAs-mRNAs network showed that lnc-LYZ-2 was the lncRNA most relevant to FUBP1. Inhibition of lnc-LYZ-2 could significantly relieve the proproliferation effect of FUBP1 on HCC cells, suggesting that lnc-LYZ-2 was partially involved in proproliferation regulation of FUBP1. Conclusions. Our results indicated that FUBP1 induced the abnormal expression of lncRNAs and the FUBP1-lncRNAs coexpression network in HCC cells, which could provide theoretical and experimental basis for FUBP1-lncRNAs network involved in HCC development.

scholarly journals MiR-125b-5p enclosed in hypoxic HK2 cell-derived extracellular vesicles alleviates renal ischemia-reperfusion injury by regulating NLRC5

2021 ◽  
Author(s):  
Kai Xu ◽  
Lifeng Zhang ◽  
Lei Zhang ◽  
Lei Zhang ◽  
Ze Zhang ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Bioinformatics Analysis ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Differentially Expressed ◽  
Luciferase Reporter ◽  
Rt Pcr ◽  
Differentially Expressed Mirnas ◽  
The Relationship ◽  
Hk2 Cells

IntroductionIn this study, we validated the changes in microRNA (miRNA) expression in hypoxic human kidney 2 (HK2) cell-derived extracellular vesicles (EVs). Additionally, we investigated the mechanism by which miRNA that are derived from EVs alleviated renal ischemia-reperfusion (I/R) injury.Material and methodsHK2 cells were treated in a hypoxic chamber (1% O2) for 12 h.EVs were obtained as supernatant from ultracentrifugation and characterized. After examining 16 differentially expressed EV-miRNAs between normoxic and hypoxic conditions by RT-PCR and bioinformatics analysis, miR-125b-5p was selected for further analysis. Normoxic and hypoxic HK2 cells-derived EVs as well as EVs that were isolated from miR-125b-5p negative control (miR-NC)-transfected or miR-125b-5p mimic (miR-MI)-transfected HK2 cells were injected in mice with renal I/R injury. The degree of renal injury was assessed by periodic acid-Schiff staining, renal tubule injury score, and plasma creatinine levels. Bioinformatics analysis was performed to determine the potential target genes of differentially expressed miRNAs. RT-PCR,western blotting, luciferase reporter assay, and immunohistochemistry were performed to investigate the relationship between miR-125b-5p and the NLR family CARD domain containing 5 (NLRC5).ResultsRT-PCR revealed that from 16 differentially expressed miRNAs, four EV-miRNAs were upregulated. Animal study showed that miR-125b-5p overexpression in EVs alleviated renal I/R injury. Bioinformatics analysis predicted that NLRC5 was targeted by miR-125b-5p. Moreover, the relationship between miR-125b-5p and NLRC5 was also validated.ConclusionsThere were several miRNAs that were upregulated (including miR-125b-5p) in hypoxic HK2 cells. Hypoxia induced EVs that alleviate renal IRI, can be attributed to miR-125b-5p for targeting NLRC5.

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