MicroRNA-146a and microRNA-146b expression and anti-inflammatory function in human airway smooth muscle

Comer, Brian S.; Camoretti-Mercado, Blanca; Kogut, Paul; Halayko, Andrew J.; Solway, Julian; Gerthoffer, William T.

doi:10.1152/ajplung.00174.2014

Cited by 112 publications

(103 citation statements)

References 55 publications

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“…Since miR-18b was upregulated, it is likely that PTEN is regulated by other miRNA-mediated mechanisms. Furthermore, expression of miR-146b increased 14-21 dpi, which may have contributed to regulating inflammatory responses as previously reported (8).…”

Section: Discussionsupporting

confidence: 78%

microRNAs Regulate Host Immune Response and Pathogenesis During Influenza Infection in Rhesus Macaques

et al. 2016

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microRNAs (miRNAs) are small noncoding RNAs that are key regulators of biological processes, including the immune response to viral infections. Differential expression levels of cellular miRNAs and their predicted targets have been described in the lungs of H1N1-infected BALB/c mice, the lungs of H5N1 influenza-infected cynomolgus macaques, and in peripheral blood mononuclear cells (PBMCs) of critically ill patients infected with 2009 pandemic H1N1. However, a longitudinal analysis of changes in the expression of miRNAs and their targets during influenza infection and how they relate to viral replication and host response has yet to be carried out. In the present study, we conducted a comprehensive analysis of innate and adaptive immune responses as well as the expression of several miRNAs and their validated targets in both peripheral blood and bronchoalveolar lavage (BAL) collected from rhesus macaques over the course of infection with the 2009 H1N1 virus A/Mexico/4108/2009 (MEX4108). We describe a distinct set of differentially expressed miRNAs in BAL and PBMCs, which regulate the expression of genes involved in inflammation, immune response, and regulation of cell cycle and apoptosis.

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Section: Discussionsupporting

confidence: 78%

microRNAs Regulate Host Immune Response and Pathogenesis During Influenza Infection in Rhesus Macaques

et al. 2016

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“…[25][26][27]30 These activities suggest that miR-146a-PEINPs may inhibit renal fibrosis in patients with kidney disease. miR-146a has also been reported to suppress expression of …”

Section: Discussionmentioning

confidence: 96%

“…[15][16][17][18]24 miR146a has been reported to inhibit inflammation by suppressing target mRNAs, such as those encoding tumor necrosis factor receptor-associated factor 6 (TRAF6), interleukin-1 receptor-associated kinase 1 (IRAK1), and Toll-like receptor 4 (TLR4), resulting in the inhibition of NF-κB in several organs. [25][26][27][28][29] Recently, miR-146a was reported to inhibit the TGF-β 1 -Smad signaling pathway by suppressing Smad4. 30 Increased miR-146a expression has been observed in kidney samples of diabetic nephropathy patients.…”

Section: Introductionmentioning

confidence: 99%

“…We also investigated changes in expression of TRAF6, IRAK1, and TLR4, which have been reported to be targets of miR-146a. [25][26][27][28][29] Of these, TRAF6 expression was higher in obstructed than in sham-operated kidneys, an increase significantly inhibited by miR-146a-PEI-NPs, but not by control-miR-PEI-NPs (Figure 11). The expression levels of IRAK1 and TLR4 were also higher in obstructed than in sham-operated kidneys, but these increases were not significantly inhibited by either miR-146a-PEI-NPs or control-miR-PEI-NPs.…”

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confidence: 99%

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Delivery of microRNA-146a with polyethylenimine nanoparticles inhibits renal fibrosis in vivo

Morishita¹,

Imai²,

Yoshizawa³

et al. 2015

IJN

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Renal fibrosis is the final common pathway leading to end-stage renal disease. Although microRNA (miR) was recently shown to be involved in the development of renal fibrosis, few studies have focused on the effects on renal fibrosis of exogenous miR delivered in an in vivo therapeutic setting. The study reported here investigated the effects of miR-146a delivery using polyethylenimine nanoparticles (PEI-NPs) on renal fibrosis in vivo. PEI-NPs bearing miR-146 or control-miR (nitrogen/phosphate ratio: 6) were injected into the tail vein of a mouse model of renal fibrosis induced by unilateral ureteral obstruction. PEI-NPs bearing miR-146 significantly enhanced miR-146a expression in the obstructed kidney compared with the control group, while inhibiting the renal fibrosis area, expression of alpha-smooth muscle actin, and infiltration of F4/80-positive macrophages into the obstructed kidney. In addition, PEI-NPs bearing miR-146a inhibited the transforming growth factor beta 1–Smad and tumor necrosis factor receptor-associated factor 6–nuclear factor kappa B signaling pathways. Control-miR-PEI-NPs did not show any of these effects. These results suggest that the delivery of miR-146a attenuated renal fibrosis by inhibiting pro-fibrotic and inflammatory signaling pathways and that the delivery of appropriate miRs may be a therapeutic option for preventing renal fibrosis in vivo.

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“…These cells have been well-characterized previously, e.g. [14] . All peer-reviewed) is the author/funder.…”

Section: Methodsmentioning

confidence: 99%

Traction force screening enabled by compliant PDMS elastomers

Yoshie

Koushki

Kaviani

et al. 2017

Preprint

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Abstract:Acto-myosin contractility is an essential element of many aspects of cellular biology, and manifests as traction forces that cells exert on their surroundings. The central role of these forces makes them a novel principal therapeutic target in diverse diseases. This requires accurate and higher capacity measurements of traction forces; however, existing methods are largely low throughput, limiting their utility in broader applications. To address this need, we employ Fourier-transform traction force microscopy in a parallelized 96-well format, which we refer to as contractile force screening (CFS). Critically, rather than the frequently employed hydrogel polyacrylamide (PAA), we fabricate these plates using polydimethylsiloxane (PDMS) rubber. Key to this approach is that the PDMS used is very compliant, with a lower-bound Young's modulus of approximately 0.7 kPa. We subdivide these monolithic substrates spatially into biochemically independent wells, creating a uniform multiwell platform for traction force screening. We demonstrate the utility and versatility of this platform by quantifying the compound and dose-dependent contractility responses of human airway smooth muscle cells and retinal pigment epithelial cells.

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MicroRNA-146a and microRNA-146b expression and anti-inflammatory function in human airway smooth muscle

Cited by 112 publications

References 55 publications

microRNAs Regulate Host Immune Response and Pathogenesis During Influenza Infection in Rhesus Macaques

microRNAs Regulate Host Immune Response and Pathogenesis During Influenza Infection in Rhesus Macaques

Delivery of microRNA-146a with polyethylenimine nanoparticles inhibits renal fibrosis in vivo

Traction force screening enabled by compliant PDMS elastomers

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