Urine microRNA as potential biomarkers of autosomal dominant polycystic kidney disease progression: description of miRNA profiles at baseline

Autosomal dominant polycystic kidney disease (ADPKD) is clinically heterogenic. Biomarkers are needed to predict prognosis and guide management. We aimed to profile microRNA (miRNA) in ADPKD to gain molecular insight and evaluate biomarker potential. Small-RNA libraries were generated from urine spe...

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Published in:PloS one 2014-01, Vol.9 (1), p.e86856-e86856
Main Authors: Ben-Dov, Iddo Z, Tan, Ying-Cai, Morozov, Pavel, Wilson, Patricia D, Rennert, Hanna, Blumenfeld, Jon D, Tuschl, Thomas
Format: Article
Language:English
Subjects:
Adult
Aged
Analysis
Biological markers
Biology
Biomarkers
Biomarkers - urine
Cancer
Cell culture
Chronic kidney failure
Cistrons
Cysts
Development and progression
Disease Progression
Epigenesis, Genetic
Epithelial cells
Etiology
Female
Fetus
Fetuses
Gene expression
Gene Library
High-Throughput Nucleotide Sequencing
Hospitals
Humans
Inflammation
Kidney diseases
Kidney transplantation
Kidney Tubules - metabolism
Kidney Tubules - pathology
Laboratories
Male
Medical research
Medicine
MicroRNA
MicroRNAs
MicroRNAs - genetics
MicroRNAs - urine
Middle Aged
miRNA
Molecular biology
Nephrology
Pathogenesis
Pathology
Patients
Polycystic kidney
Polycystic kidney disease
Polycystic Kidney, Autosomal Dominant - diagnosis
Polycystic Kidney, Autosomal Dominant - genetics
Polycystic Kidney, Autosomal Dominant - pathology
Polycystic Kidney, Autosomal Dominant - urine
Primary Cell Culture
Prognosis
Proteins
Regulation
Ribonucleic acid
RNA
RNA polymerase
Suppressors
Urine
Urothelium - metabolism
Urothelium - pathology
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cited_by cdi_FETCH-LOGICAL-c758t-6b64c6d9c13b78a7336c235a9ad1baf8a8179f0a8723fa8b5f421a3fff0a75813
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container_end_page e86856
container_issue 1
container_start_page e86856
container_title PloS one
container_volume 9
creator Ben-Dov, Iddo Z
Tan, Ying-Cai
Morozov, Pavel
Wilson, Patricia D
Rennert, Hanna
Blumenfeld, Jon D
Tuschl, Thomas
description Autosomal dominant polycystic kidney disease (ADPKD) is clinically heterogenic. Biomarkers are needed to predict prognosis and guide management. We aimed to profile microRNA (miRNA) in ADPKD to gain molecular insight and evaluate biomarker potential. Small-RNA libraries were generated from urine specimens of ADPKD patients (N = 20) and patients with chronic kidney disease of other etiologies (CKD, N = 20). In this report, we describe the miRNA profiles and baseline characteristics. For reference, we also examined the miRNA transcriptome in primary cultures of ADPKD cyst epithelia (N = 10), normal adult tubule (N = 8) and fetal tubule (N = 7) epithelia. In primary cultures of ADPKD kidney cells, miRNA cistrons mir-143(2) (9.2-fold), let-7i(1) (2.3-fold) and mir-3619(1) (12.1-fold) were significantly elevated compared to normal tubule epithelia, whereas mir-1(4) members (19.7-fold), mir-133b(2) (21.1-fold) and mir-205(1) (3.0-fold) were downregulated (P
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Biomarkers are needed to predict prognosis and guide management. We aimed to profile microRNA (miRNA) in ADPKD to gain molecular insight and evaluate biomarker potential. Small-RNA libraries were generated from urine specimens of ADPKD patients (N = 20) and patients with chronic kidney disease of other etiologies (CKD, N = 20). In this report, we describe the miRNA profiles and baseline characteristics. For reference, we also examined the miRNA transcriptome in primary cultures of ADPKD cyst epithelia (N = 10), normal adult tubule (N = 8) and fetal tubule (N = 7) epithelia. In primary cultures of ADPKD kidney cells, miRNA cistrons mir-143(2) (9.2-fold), let-7i(1) (2.3-fold) and mir-3619(1) (12.1-fold) were significantly elevated compared to normal tubule epithelia, whereas mir-1(4) members (19.7-fold), mir-133b(2) (21.1-fold) and mir-205(1) (3.0-fold) were downregulated (P&lt;0.01). Expression of the dysregulated miRNA in fetal tubule epithelia resembled ADPKD better than normal adult cells, except let-7i, which was lower in fetal cells. In patient biofluid specimens, mir-143(2) members were 2.9-fold higher in urine cells from ADPKD compared to other CKD patients, while expression levels of mir-133b(2) (4.9-fold) and mir-1(4) (4.4-fold) were lower in ADPKD. We also noted increased abundance mir-223(1) (5.6-fold), mir-199a(3) (1.4-fold) and mir-199b(1) (1.8-fold) (P&lt;0.01) in ADPKD urine cells. In ADPKD urine microvesicles, miR-1(2) (7.2-fold) and miR-133a(2) (11.8-fold) were less abundant compared to other CKD patients (P&lt;0.01). We found that in ADPKD urine specimens, miRNA previously implicated as kidney tumor suppressors (miR-1 and miR-133), as well as miRNA of presumed inflammatory and fibroblast cell origin (miR-223/miR-199), are dysregulated when compared to other CKD patients. Concordant with findings in the primary tubule epithelial cell model, this suggests roles for dysregulated miRNA in ADPKD pathogenesis and potential use as biomarkers. 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Biomarkers are needed to predict prognosis and guide management. We aimed to profile microRNA (miRNA) in ADPKD to gain molecular insight and evaluate biomarker potential. Small-RNA libraries were generated from urine specimens of ADPKD patients (N = 20) and patients with chronic kidney disease of other etiologies (CKD, N = 20). In this report, we describe the miRNA profiles and baseline characteristics. For reference, we also examined the miRNA transcriptome in primary cultures of ADPKD cyst epithelia (N = 10), normal adult tubule (N = 8) and fetal tubule (N = 7) epithelia. In primary cultures of ADPKD kidney cells, miRNA cistrons mir-143(2) (9.2-fold), let-7i(1) (2.3-fold) and mir-3619(1) (12.1-fold) were significantly elevated compared to normal tubule epithelia, whereas mir-1(4) members (19.7-fold), mir-133b(2) (21.1-fold) and mir-205(1) (3.0-fold) were downregulated (P&lt;0.01). Expression of the dysregulated miRNA in fetal tubule epithelia resembled ADPKD better than normal adult cells, except let-7i, which was lower in fetal cells. In patient biofluid specimens, mir-143(2) members were 2.9-fold higher in urine cells from ADPKD compared to other CKD patients, while expression levels of mir-133b(2) (4.9-fold) and mir-1(4) (4.4-fold) were lower in ADPKD. We also noted increased abundance mir-223(1) (5.6-fold), mir-199a(3) (1.4-fold) and mir-199b(1) (1.8-fold) (P&lt;0.01) in ADPKD urine cells. In ADPKD urine microvesicles, miR-1(2) (7.2-fold) and miR-133a(2) (11.8-fold) were less abundant compared to other CKD patients (P&lt;0.01). We found that in ADPKD urine specimens, miRNA previously implicated as kidney tumor suppressors (miR-1 and miR-133), as well as miRNA of presumed inflammatory and fibroblast cell origin (miR-223/miR-199), are dysregulated when compared to other CKD patients. Concordant with findings in the primary tubule epithelial cell model, this suggests roles for dysregulated miRNA in ADPKD pathogenesis and potential use as biomarkers. We intend to assess prognostic potential of miRNA in a followup analysis.</description><subject>Adult</subject><subject>Aged</subject><subject>Analysis</subject><subject>Biological markers</subject><subject>Biology</subject><subject>Biomarkers</subject><subject>Biomarkers - urine</subject><subject>Cancer</subject><subject>Cell culture</subject><subject>Chronic kidney failure</subject><subject>Cistrons</subject><subject>Cysts</subject><subject>Development and progression</subject><subject>Disease Progression</subject><subject>Epigenesis, Genetic</subject><subject>Epithelial cells</subject><subject>Etiology</subject><subject>Female</subject><subject>Fetus</subject><subject>Fetuses</subject><subject>Gene expression</subject><subject>Gene Library</subject><subject>High-Throughput Nucleotide Sequencing</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Kidney diseases</subject><subject>Kidney transplantation</subject><subject>Kidney Tubules - metabolism</subject><subject>Kidney Tubules - pathology</subject><subject>Laboratories</subject><subject>Male</subject><subject>Medical research</subject><subject>Medicine</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - urine</subject><subject>Middle Aged</subject><subject>miRNA</subject><subject>Molecular biology</subject><subject>Nephrology</subject><subject>Pathogenesis</subject><subject>Pathology</subject><subject>Patients</subject><subject>Polycystic kidney</subject><subject>Polycystic kidney disease</subject><subject>Polycystic Kidney, Autosomal Dominant - diagnosis</subject><subject>Polycystic Kidney, Autosomal Dominant - genetics</subject><subject>Polycystic Kidney, Autosomal Dominant - pathology</subject><subject>Polycystic Kidney, Autosomal Dominant - urine</subject><subject>Primary Cell Culture</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Regulation</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA polymerase</subject><subject>Suppressors</subject><subject>Urine</subject><subject>Urothelium - 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diagnosis</topic><topic>Polycystic Kidney, Autosomal Dominant - genetics</topic><topic>Polycystic Kidney, Autosomal Dominant - pathology</topic><topic>Polycystic Kidney, Autosomal Dominant - urine</topic><topic>Primary Cell Culture</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Regulation</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA polymerase</topic><topic>Suppressors</topic><topic>Urine</topic><topic>Urothelium - metabolism</topic><topic>Urothelium - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ben-Dov, Iddo Z</creatorcontrib><creatorcontrib>Tan, Ying-Cai</creatorcontrib><creatorcontrib>Morozov, Pavel</creatorcontrib><creatorcontrib>Wilson, Patricia D</creatorcontrib><creatorcontrib>Rennert, Hanna</creatorcontrib><creatorcontrib>Blumenfeld, Jon D</creatorcontrib><creatorcontrib>Tuschl, Thomas</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing &amp; Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological &amp; Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science &amp; Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>Advanced Technologies &amp; Aerospace Collection</collection><collection>Agricultural &amp; Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing &amp; Allied Health Database (Alumni Edition)</collection><collection>Meteorological &amp; Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ben-Dov, Iddo Z</au><au>Tan, Ying-Cai</au><au>Morozov, Pavel</au><au>Wilson, Patricia D</au><au>Rennert, Hanna</au><au>Blumenfeld, Jon D</au><au>Tuschl, Thomas</au><au>Long, David</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Urine microRNA as potential biomarkers of autosomal dominant polycystic kidney disease progression: description of miRNA profiles at baseline</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-01-29</date><risdate>2014</risdate><volume>9</volume><issue>1</issue><spage>e86856</spage><epage>e86856</epage><pages>e86856-e86856</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Autosomal dominant polycystic kidney disease (ADPKD) is clinically heterogenic. Biomarkers are needed to predict prognosis and guide management. We aimed to profile microRNA (miRNA) in ADPKD to gain molecular insight and evaluate biomarker potential. Small-RNA libraries were generated from urine specimens of ADPKD patients (N = 20) and patients with chronic kidney disease of other etiologies (CKD, N = 20). In this report, we describe the miRNA profiles and baseline characteristics. For reference, we also examined the miRNA transcriptome in primary cultures of ADPKD cyst epithelia (N = 10), normal adult tubule (N = 8) and fetal tubule (N = 7) epithelia. In primary cultures of ADPKD kidney cells, miRNA cistrons mir-143(2) (9.2-fold), let-7i(1) (2.3-fold) and mir-3619(1) (12.1-fold) were significantly elevated compared to normal tubule epithelia, whereas mir-1(4) members (19.7-fold), mir-133b(2) (21.1-fold) and mir-205(1) (3.0-fold) were downregulated (P&lt;0.01). Expression of the dysregulated miRNA in fetal tubule epithelia resembled ADPKD better than normal adult cells, except let-7i, which was lower in fetal cells. In patient biofluid specimens, mir-143(2) members were 2.9-fold higher in urine cells from ADPKD compared to other CKD patients, while expression levels of mir-133b(2) (4.9-fold) and mir-1(4) (4.4-fold) were lower in ADPKD. We also noted increased abundance mir-223(1) (5.6-fold), mir-199a(3) (1.4-fold) and mir-199b(1) (1.8-fold) (P&lt;0.01) in ADPKD urine cells. In ADPKD urine microvesicles, miR-1(2) (7.2-fold) and miR-133a(2) (11.8-fold) were less abundant compared to other CKD patients (P&lt;0.01). We found that in ADPKD urine specimens, miRNA previously implicated as kidney tumor suppressors (miR-1 and miR-133), as well as miRNA of presumed inflammatory and fibroblast cell origin (miR-223/miR-199), are dysregulated when compared to other CKD patients. Concordant with findings in the primary tubule epithelial cell model, this suggests roles for dysregulated miRNA in ADPKD pathogenesis and potential use as biomarkers. We intend to assess prognostic potential of miRNA in a followup analysis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24489795</pmid><doi>10.1371/journal.pone.0086856</doi><tpages>e86856</tpages><oa>free_for_read</oa></addata></record>
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subjects Adult
Aged
Analysis
Biological markers
Biology
Biomarkers
Biomarkers - urine
Cancer
Cell culture
Chronic kidney failure
Cistrons
Cysts
Development and progression
Disease Progression
Epigenesis, Genetic
Epithelial cells
Etiology
Female
Fetus
Fetuses
Gene expression
Gene Library
High-Throughput Nucleotide Sequencing
Hospitals
Humans
Inflammation
Kidney diseases
Kidney transplantation
Kidney Tubules - metabolism
Kidney Tubules - pathology
Laboratories
Male
Medical research
Medicine
MicroRNA
MicroRNAs
MicroRNAs - genetics
MicroRNAs - urine
Middle Aged
miRNA
Molecular biology
Nephrology
Pathogenesis
Pathology
Patients
Polycystic kidney
Polycystic kidney disease
Polycystic Kidney, Autosomal Dominant - diagnosis
Polycystic Kidney, Autosomal Dominant - genetics
Polycystic Kidney, Autosomal Dominant - pathology
Polycystic Kidney, Autosomal Dominant - urine
Primary Cell Culture
Prognosis
Proteins
Regulation
Ribonucleic acid
RNA
RNA polymerase
Suppressors
Urine
Urothelium - metabolism
Urothelium - pathology
title Urine microRNA as potential biomarkers of autosomal dominant polycystic kidney disease progression: description of miRNA profiles at baseline
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