miR-181a and inflammation: miRNA homeostasis response to inflammatory stimuli in vivo

Xie, Weidong; Li, Zhongxin; Li, Mengnan; Xu, Ning; Zhang, Yaou

doi:10.1016/j.bbrc.2012.11.097

Cited by 75 publications

(62 citation statements)

References 17 publications

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“…interleukin-1β, interleukin-6 and TNFa (39,40). miR-181a is also a known mitochondrial miRNA ("mitomiR"), acting on the expression of genes at the intersection of mitochondrial function, cellular senescence and response to inflammation (41).…”

Section: Discussionmentioning

confidence: 99%

Signatures of miR-181a on the Renal Transcriptome and Blood Pressure

Marques

Romaine

Denniff

et al. 2015

Mol Med

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MicroRNA-181a binds to the 3' untranslated region of messenger RNA (mRNA) for renin, a rate-limiting enzyme of the renin-angiotensin system. Our objective was to determine whether this molecular interaction translates into a clinically meaningful effect on blood pressure and whether circulating miR-181a is a measurable proxy of blood pressure. In 200 human kidneys from the TRANScriptome of renaL humAn TissuE (TRANSLATE) study, renal miR-181a was the sole negative predictor of renin mRNA and a strong correlate of circulating miR-181a. Elevated miR-181a levels correlated positively with systolic and diastolic blood pressure in TRANSLATE, and this association was independent of circulating renin. The association between serum miR-181a and systolic blood pressure was replicated in 199 subjects from the Genetic Regulation of Arterial Pressure of Humans In the Community (GRAPHIC) study. Renal immunohistochemistry and in situ hybridization showed that colocalization of miR-181a and renin was most prominent in collecting ducts where renin is not released into the systemic circulation. Analysis of 69 human kidneys characterized by RNA sequencing revealed that miR-181a was associated with downregulation of four mitochondrial pathways and upregulation of 41 signaling cascades of adaptive immunity and inflammation. We conclude that renal miR-181a has pleiotropic effects on pathways relevant to blood pressure regulation and that circulating levels of miR-181a are both a measurable proxy of renal miR-181a expression and a novel biochemical correlate of blood pressure. Online address: http://www.molmed.org doi: 10.2119/molmed.2015.00096 Address correspondence to Maciej Tomaszewski, Institute of CardiovascularSciences, AV Hill Building, Dover Street, Manchester, M13 9PT, United Kingdom. Phone: +44-(0)116-275-0232; E-mail: maciej.tomaszewski@manchester.ac.uk. Submitted April 29, 2015; Accepted for publication August 17, 2015; Published Online (www.molmed.org ) August 24, 2015 m i R -1 8 1 a , T H E K I D N E Y A N D B L O O D P R E S S U R E7 4 0 | M a r q u E s E T a L . | M O L M E D 2 1 : 7 3 9 -7 4 8 , 2 0 1 5

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Section: Discussionmentioning

confidence: 99%

Signatures of miR-181a on the Renal Transcriptome and Blood Pressure

Marques

Romaine

Denniff

et al. 2015

Mol Med

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“…Hence, an increasing number of studies are beginning to focus on preventing and/or reducing allergic airway responses through targeting IL-13 and its signaling pathway. For example, Ramalingam et al [11] diverse immune responses and immunologic disorders [12][13][14]. Using a miRNA microarray assay, we previously showed that miRNA-143 (miR-143) was the most significantly downregulated miRNA in nasal mucosal tissues from AR patients compared with tissues from healthy control subjects, suggesting that miR-143 may be involved in the pathologic process of AR [15].…”

Section: Introductionmentioning

confidence: 99%

miR-143 inhibits interleukin-13-induced inflammatory cytokine and mucus production in nasal epithelial cells from allergic rhinitis patients by targeting IL13Rα1

Teng

Zhang

Liu

et al. 2015

Biochemical and Biophysical Research Communications

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“…MiR-181a is involved in the development and differentiation of lymphoid and myeloid cells [13], and plays a very important role in the host inflammatory response [14]. In the CNS, it influences the outcome of cerebral ischemia [15].…”

Section: Introductionmentioning

confidence: 99%

microRNA s (9, 138, 181A, 221, and 222) and mesial temporal lobe epilepsy in developing brains

Ashhab

Omran²,

Kong

et al. 2013

Translational Neuroscience

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Background: Recently, microRNAs (miRNAs) have attracted much attention as novel players in the pathogenesis of mesial temporal lobe epilepsy (MTLE) in mature and developing brains. This study aimed to investigate the expression dynamics of miR-9, miR-138, miR-181a, miR-221, and miR-222 in the hippocampus of an immature rat model during the three stages of MTLE development and in children with MTLE. Methodology: qPCR was used to measure expression levels during the three stages of MTLE development (2 h, 3, and 8 weeks after induction of lithium-pilocarpine status epilepticus, representing the acute, latent, and chronic stages, respectively. Expression levels were also measured in hippocampi obtained from children with MTLE and normal controls. Results: In the rat model, miR-9 was significantly upregulated during the acute and chronic stages relative to controls, but not during the latent stage. MiR-138, miR-221 and miR-222 were all downregulated during all three stages of MTLE development. MiR-181a was downregulated during the acute stage, upregulated during the chronic stage, and unaltered during the latent stage. In children, miR-9 and miR-181a were upregulated, while miR-138, miR-221, and miR-222 were downregulated. Conclusion: Modulation of these miRNAs may be a new strategy in designing antiepileptic and anticonvulsant therapies for the developing brain.

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miR-181a and inflammation: miRNA homeostasis response to inflammatory stimuli in vivo

Cited by 75 publications

References 17 publications

Signatures of miR-181a on the Renal Transcriptome and Blood Pressure

Signatures of miR-181a on the Renal Transcriptome and Blood Pressure

miR-143 inhibits interleukin-13-induced inflammatory cytokine and mucus production in nasal epithelial cells from allergic rhinitis patients by targeting IL13Rα1

microRNA s (9, 138, 181A, 221, and 222) and mesial temporal lobe epilepsy in developing brains

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