Assessment of the MicroRNA System in Salt-Sensitive Hypertension

Naraba, Hiroaki; Iwai, Naoharu

doi:10.1291/hypres.28.819

Cited by 34 publications

(25 citation statements)

References 32 publications

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“…Some genes other than Ccl2 in this chromosomal region might be responsible for hypertension. In this regard, it is worth noting that we recently investigated the expression profiles of microRNAs in the kidneys of DS and LEW, and found no significant differences between the two strains (27). Direct evidence that anti-MCP-1 therapy could ameliorate salt-sensitive hypertension in DS will be needed to support our hypothesis.…”

Section: Discussionmentioning

confidence: 69%

The Monocyte Chemotactic Protein-1 Gene May Contribute to Hypertension in Dahl Salt-Sensitive Rats

et al. 2007

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In a previous study, we performed a genome-wide quantitative trait loci (QTLs) analysis for blood pressure using F2 rats derived from Dahl salt-sensitive (DS) and Lewis (LEW) rats and identified two QTLs that influenced blood pressure levels. Although we determined that one of the causative genes in the chromosome (Ch) 1 region seemed to be Klk1, we did not perform detailed analyses on the Ch10 QTL region. The purpose of the present study was to identify candidate genes that influence blood pressure in the Ch10 QTL region.Using microarray analysis, we compiled a list of the genes that are differentially expressed between the two strains and that were localized to the Ch10 QTL region. Subsequent reverse transcription-polymerase chain reaction (RT-PCR) and Northern blot analysis identified that, while the expression levels of Ccl2 mRNA were not different between the kidneys of DS and LEW rats fed a normal diet, those in DS were 10-fold higher than those in LEW under a high-salt diet. Although the promoter reporter assay failed to identify causative nucleotide changes that led to the differential expression, monocyte chemotactic protein-1 (MCP-1) release from isolated monocytes were significantly higher in DS than in LEW. Intriguingly, this Ch10 QTL for blood pressure was also a possible QTL for urinary albumin excretion. Since Ccl2 is well known to be involved in various types of renal injury, it is likely that a higher expression of Ccl2 might aggravate macrophage infiltration, which in turn could aggravate tubulointerstitial injury, and thereby accelerate salt-sensitive hypertension. Thus, Ccl2 appears to be a interesting candidate gene for salt-sensitive hypertension in DS.(Hypertens Res 2007; 30: [185][186][187][188][189][190][191][192][193]

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Section: Discussionmentioning

confidence: 69%

The Monocyte Chemotactic Protein-1 Gene May Contribute to Hypertension in Dahl Salt-Sensitive Rats

et al. 2007

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“…Global miRNA profiling of human hypertensive nephrosclerosis biopsies also revealed a number of differentially expressed miRNAs, including miR-200a, miR-200b, miR-141, miR-429, and miR-192 (150). Similar profiling has been performed in Dahl salt-sensitive rats (103). miR-29b is upregulated in renal medullary tissues in Dahl salt-sensitive rats fed a high-salt diet, and miR-29b overexpression in cultured cells can suppress collagen expression (85).…”

Section: Other Renal Diseases and Conditionsmentioning

confidence: 65%

Mini-review: emerging roles of microRNAs in the pathophysiology of renal diseases

Bhatt

Kato

Natarajan

2016

American Journal of Physiology-Renal Physiology

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MicroRNAs (miRNA) are endogenously produced short noncoding regulatory RNAs that can repress gene expression by posttranscriptional mechanisms. They can therefore influence both normal and pathological conditions in diverse biological systems. Several miRNAs have been detected in kidneys, where they have been found to be crucial for renal development and normal physiological functions as well as significant contributors to the pathogenesis of renal disorders such as diabetic nephropathy, acute kidney injury, lupus nephritis, polycystic kidney disease, and others, due to their effects on key genes involved in these disease processes. miRNAs have also emerged as novel biomarkers in these renal disorders. Due to increasing evidence of their actions in various kidney segments, in this mini-review we discuss the functional significance of altered miRNA expression during the development of renal pathologies and highlight emerging miRNA-based therapeutics and diagnostic strategies for early detection and treatment of kidney diseases.

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“…S4A in the supplementary material). Second, candidates for kidney-enriched miRNAs were selected from previous publications on human, mouse, rat and zebrafish (Sun et al, 2004;Naraba and Iwai, 2005;Wienholds et al, 2005) and re-analyzed by RT-PCR, comparing four organs of adult mice and different stages of Xenopus development (see Fig. S4B in the supplementary material).…”

Section: Research Articlementioning

confidence: 99%

“…However, little information is available regarding the role of miRNAs in kidney development. Expression analyses have identified several miRNAs that are expressed in the kidney (Sun et al, 2004;Naraba and Iwai, 2005;Kato et al, 2007) and conditional alleles eliminating Dicer from mouse podocytes have demonstrated that miRNAs are required for the maintenance of functional glomeruli (Harvey et al, 2008;Ho et al, 2008;Shi et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

The miR-30 miRNA family regulates Xenopus pronephros development and targets the transcription factor Xlim1/Lhx1

2009

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*MicroRNAs (miRNAs) are small non-coding RNA molecules that regulate gene expression at the post-transcriptional level. They are involved in diverse biological processes, such as development, differentiation, cell proliferation and apoptosis. To study the role of miRNAs during pronephric kidney development of Xenopus, global miRNA biogenesis was eliminated by knockdown of two key components: Dicer and Dgcr8. These embryos developed a range of kidney defects, including edema formation, delayed renal epithelial differentiation and abnormal patterning. To identify a causative miRNA, mouse and frog kidneys were screened for putative candidates. Among these, the miR-30 family showed the most prominent kidney-restricted expression. Moreover, knockdown of miR-30a-5p phenocopied most of the pronephric defects observed upon global inhibition of miRNA biogenesis. Molecular analyses revealed that miR-30 regulates the LIM-class homeobox factor Xlim1/Lhx1, a major transcriptional regulator of kidney development. miR-30 targeted Xlim1/Lhx1 via two previously unrecognized binding sites in its 3ЈUTR and thereby restricted its activity. During kidney development, Xlim1/Lhx1 is required in the early stages, but is downregulated subsequently. However, in the absence of miR-30 activity, Xlim1/Lhx1 is maintained at high levels and, therefore, may contribute to the delayed terminal differentiation of the amphibian pronephros.

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Assessment of the MicroRNA System in Salt-Sensitive Hypertension

Cited by 34 publications

References 32 publications

The Monocyte Chemotactic Protein-1 Gene May Contribute to Hypertension in Dahl Salt-Sensitive Rats

The Monocyte Chemotactic Protein-1 Gene May Contribute to Hypertension in Dahl Salt-Sensitive Rats

Mini-review: emerging roles of microRNAs in the pathophysiology of renal diseases

The miR-30 miRNA family regulates Xenopus pronephros development and targets the transcription factor Xlim1/Lhx1

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