Sang In Lee1, Hyojun Park2, Sung Joo Kim3, Kyo Won Lee4, Du Yeon Shin5, Jin Kyung Son4, Ju Hee Hong6, Seung Han Kim7, Hye Jin Cho8, Jae Berm Park4, Tae Min Kim9. 1. Department of Animal Biotechnology, Kyungpook National University, Sangju, Gyeongsangbuk-do, Republic of Korea. 2. School of Medicine, Sungkyunkwan University, Gangnam-gu, Seoul, Republic of Korea. 3. School of Medicine, Sungkyunkwan University, Gangnam-gu, Seoul, Republic of Korea; Gennbio Co Ltd, Gangnam-gu, Seoul, Republic of Korea. 4. Department of Surgery, Samsung Medical Center, Seoul, Republic of Korea. 5. Transplantation Research Center, Stem Cell & Regenerative Medicine Institute, Samsung Medical Center, Seoul, Republic of Korea. 6. Department of Health Sciences & Technology, Samsung Advanced Institute for Health Sciences & Technology, Graduate School, Sungkyunkwan University, Seoul, Republic of Korea. 7. Gennbio Co Ltd, Gangnam-gu, Seoul, Republic of Korea. 8. Graduate School of International Agricultural Technology, Seoul National University, Gangwon-do, Republic of Korea. 9. Graduate School of International Agricultural Technology, Seoul National University, Gangwon-do, Republic of Korea. Electronic address: taemin21@snu.ac.kr.
Abstract
BACKGROUND: Ischemia/reperfusion injury (IRI) is inevitable in kidney transplantation (KT) and may lead to impaired tubular epithelial cell function and reduce graft function and survival. Renal IRI is a complex cellular and molecular event; therefore, investigating the genetic or molecular pathways associated with the early phase of KT would improve our understanding of IRI in KT. MicroRNAs (miRNAs) play a critical role in various pathologic events associated with IRI. METHODS: We compared the expression profile of miRNAs extracted from 2 blood plasma samples, 1 from periphery and the other form gonadal veins immediately after reperfusion, in a total 5 cases of KT. RESULTS: We observed that the total RNA yield was higher in postreperfusion plasma and that a subset of miRNAs was upregulated (miR-let-7a-3p, miR-143-3p, and miR-214-3p) or downregulated (let-7d-3p, let-7d-3p, miR-1246, miR-1260b, miR-1290, and miR-130b-3p) in postreperfusion plasma. Gene ontology analyses revealed that these subsets target different biological functions. Twenty-four predicted genes were commonly targeted by the upregulated miRNAs, and gene ontology enrichment and pathway analyses revealed that these were associated with various cellular activities such as signal transduction or with components such as exosomes and membranous organelles. CONCLUSION: We present 2 subsets of miRNAs that were differentially upregulated or downregulated in postreperfusion plasma. Our findings may enhance our understanding of miRNA-mediated early molecular events related to IRI in KT.
BACKGROUND: Ischemia/reperfusion injury (IRI) is inevitable in kidney transplantation (KT) and may lead to impaired tubular epithelial cell function and reduce graft function and survival. Renal IRI is a complex cellular and molecular event; therefore, investigating the genetic or molecular pathways associated with the early phase of KT would improve our understanding of IRI in KT. MicroRNAs (miRNAs) play a critical role in various pathologic events associated with IRI. METHODS: We compared the expression profile of miRNAs extracted from 2 blood plasma samples, 1 from periphery and the other form gonadal veins immediately after reperfusion, in a total 5 cases of KT. RESULTS: We observed that the total RNA yield was higher in postreperfusion plasma and that a subset of miRNAs was upregulated (miR-let-7a-3p, miR-143-3p, and miR-214-3p) or downregulated (let-7d-3p, let-7d-3p, miR-1246, miR-1260b, miR-1290, and miR-130b-3p) in postreperfusion plasma. Gene ontology analyses revealed that these subsets target different biological functions. Twenty-four predicted genes were commonly targeted by the upregulated miRNAs, and gene ontology enrichment and pathway analyses revealed that these were associated with various cellular activities such as signal transduction or with components such as exosomes and membranous organelles. CONCLUSION: We present 2 subsets of miRNAs that were differentially upregulated or downregulated in postreperfusion plasma. Our findings may enhance our understanding of miRNA-mediated early molecular events related to IRI in KT.