4.4 Article

Divergent regulation of lncRNA expression by ischemia in adult and aging mice

期刊

GEROSCIENCE
卷 44, 期 1, 页码 429-445

出版社

SPRINGER
DOI: 10.1007/s11357-021-00460-9

关键词

lncRNA; Acute kidney injury; Ischemia-reperfusion injury

资金

  1. Hungarian Research Fund [OTKA SNN-114619, ANN-110810]
  2. New National Excellence Program of the Ministry of Human Capacities [UNKP-17-4-I-SE-79]
  3. University of Pecs [300021]
  4. Semmelweis University
  5. National Research, Development and Innovation Fund of Hungary [NVKP_16-1-2016-0042]
  6. Economic Development and Innovation Operative Program Grant [GINOP 2.3.2-15-2016-00048]
  7. [EFOP-3.6.3-VEKOP-16-2017-00009]

向作者/读者索取更多资源

Elderly patients are more susceptible to acute kidney injury (AKI), with long noncoding RNAs (lncRNAs) playing a key role in cellular processes. This study found that both aging and ischemia-reperfusion injury (IRI) can affect the expression of renal lncRNAs, suggesting a versatile and complex role of lncRNAs in aging and kidney injury. Furthermore, significant changes were observed in the expression levels of lncRNAs in the control kidneys of old mice.
Elderly patients have increased susceptibility to acute kidney injury (AKI). Long noncoding RNAs (lncRNA) are key regulators of cellular processes, and have been implicated in both aging and AKI. Our aim was to study the effects of aging and ischemia-reperfusion injury (IRI) on the renal expression of lncRNAs. Adult and old (10- and 26-30-month-old) C57BL/6 N mice were subjected to unilateral IRI followed by 7 days of reperfusion. Renal expression of 90 lncRNAs and mRNA expression of injury, regeneration, and fibrosis markers was measured by qPCR in the injured and contralateral control kidneys. Tubular injury, regeneration, and fibrosis were assessed by histology. Urinary lipocalin-2 excretion was increased in old mice prior to IRI, but plasma urea was similar. In the control kidneys of old mice tubular cell necrosis and apoptosis, mRNA expression of kidney injury molecule-1, fibronectin-1, p16, and p21 was elevated. IRI increased plasma urea concentration only in old mice, but injury, regeneration, and fibrosis scores and their mRNA markers were similar in both age groups. AK082072 and Y lncRNAs were upregulated, while H19 and RepA transcript were downregulated in the control kidneys of old mice. IRI upregulated Miat, Igf2as, SNHG5, SNHG6, RNCR3, Malat1, Air, Linc1633, and Neat1 v1, while downregulated Linc1242. LncRNAs H19, AK082072, RepA transcript, and Six3os were influenced by both aging and IRI. Our results indicate that both aging and IRI alter renal lncRNA expression suggesting that lncRNAs have a versatile and complex role in aging and kidney injury. An Ingenuity Pathway Analysis highlighted that the most downregulated H19 may be linked to aging/senescence through p53.

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