Down-regulation of human long non-coding RNA LINC01187 is associated with nephropathies
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Down-regulation of human long non-coding RNA LINC01187 is associated with nephropathies. / Manolakou, Theodora; Kaltezioti, Valeria; Prakoura, Niki; Kavvadas, Panagiotis; Reichelt-Wurm, Simone; Gakiopoulou, Harikleia; Banas, Miriam; Banas, Bernhard; Lindenmeyer, Maja T; Cohen, Clemens D; Boor, Peter; Djudjaj, Sonja; Boumpas, Dimitrios T; Chatziantoniou, Christos; Charonis, Aristidis; Politis, Panagiotis K.
in: J CELL MOL MED, Jahrgang 27, Nr. 9, 05.2023, S. 1192-1205.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Down-regulation of human long non-coding RNA LINC01187 is associated with nephropathies
AU - Manolakou, Theodora
AU - Kaltezioti, Valeria
AU - Prakoura, Niki
AU - Kavvadas, Panagiotis
AU - Reichelt-Wurm, Simone
AU - Gakiopoulou, Harikleia
AU - Banas, Miriam
AU - Banas, Bernhard
AU - Lindenmeyer, Maja T
AU - Cohen, Clemens D
AU - Boor, Peter
AU - Djudjaj, Sonja
AU - Boumpas, Dimitrios T
AU - Chatziantoniou, Christos
AU - Charonis, Aristidis
AU - Politis, Panagiotis K
N1 - © 2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
PY - 2023/5
Y1 - 2023/5
N2 - Chronic kidney diseases affect a substantial percentage of the adult population worldwide. This observation emphasizes the need for novel insights into the molecular mechanisms that control the onset and progression of renal diseases. Recent advances in genomics have uncovered a previously unanticipated link between the non-coding genome and human kidney diseases. Here we screened and analysed long non-coding RNAs (lncRNAs) previously identified in mouse kidneys by genome-wide transcriptomic analysis, for conservation in humans and differential expression in renal tissue from healthy and diseased individuals. Our data suggest that LINC01187 is strongly down-regulated in human kidney tissues of patients with diabetic nephropathy and rapidly progressive glomerulonephritis, as well as in murine models of kidney diseases, including unilateral ureteral obstruction, nephrotoxic serum-induced glomerulonephritis and ischemia/reperfusion. Interestingly, LINC01187 overexpression in human kidney cells in vitro inhibits cell death indicating an anti-apoptotic function. Collectively, these data suggest a negative association of LINC01187 expression with renal diseases implying a potential protective role.
AB - Chronic kidney diseases affect a substantial percentage of the adult population worldwide. This observation emphasizes the need for novel insights into the molecular mechanisms that control the onset and progression of renal diseases. Recent advances in genomics have uncovered a previously unanticipated link between the non-coding genome and human kidney diseases. Here we screened and analysed long non-coding RNAs (lncRNAs) previously identified in mouse kidneys by genome-wide transcriptomic analysis, for conservation in humans and differential expression in renal tissue from healthy and diseased individuals. Our data suggest that LINC01187 is strongly down-regulated in human kidney tissues of patients with diabetic nephropathy and rapidly progressive glomerulonephritis, as well as in murine models of kidney diseases, including unilateral ureteral obstruction, nephrotoxic serum-induced glomerulonephritis and ischemia/reperfusion. Interestingly, LINC01187 overexpression in human kidney cells in vitro inhibits cell death indicating an anti-apoptotic function. Collectively, these data suggest a negative association of LINC01187 expression with renal diseases implying a potential protective role.
KW - Animals
KW - Humans
KW - Mice
KW - Diabetic Nephropathies/metabolism
KW - Down-Regulation/genetics
KW - Glomerulonephritis/metabolism
KW - Kidney/metabolism
KW - RNA, Long Noncoding/metabolism
U2 - 10.1111/jcmm.17014
DO - 10.1111/jcmm.17014
M3 - SCORING: Journal article
C2 - 37056054
VL - 27
SP - 1192
EP - 1205
JO - J CELL MOL MED
JF - J CELL MOL MED
SN - 1582-1838
IS - 9
ER -