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The Role of MicroRNAs in the Regulation of K(+) Channels in Epithelial Tissue.

Pilmore E, Hamilton KL - Front Physiol (2015)

Bottom Line: MiRs are now in the "limelight" as these non-coding pieces of RNA (generally ~22 nucleotides long) result in altered translation and function of proteins.Interestingly, the role of miRs in modulating K(+) channels of epithelial tissues is only emerging now.This minireview focuses on recent novel findings into the role of miRs in the regulation of K(+) channels of epithelia.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Otago School of Medical Sciences, University of Otago Dunedin, New Zealand.

ABSTRACT
Our understanding of the modulation of proteins has shifted in direction with the discovery of microRNAs (miRs) over twenty years ago. MiRs are now in the "limelight" as these non-coding pieces of RNA (generally ~22 nucleotides long) result in altered translation and function of proteins. Indeed, miRs are now reported to be potential biomarkers of disease. Epithelial K(+) channels play many roles in electrolyte and fluid homeostasis of the human body and have been suggested to be therapeutic targets of disease. Interestingly, the role of miRs in modulating K(+) channels of epithelial tissues is only emerging now. This minireview focuses on recent novel findings into the role of miRs in the regulation of K(+) channels of epithelia.

No MeSH data available.


Related in: MedlinePlus

The actions of miRs on epithelial K+ channels. (A) The action of miR-194 and miR-802 on upregulation of KIR1.1. Upper Panel: MiR-194 inhibits Intersectin 1, which mitigates the inhibition of KIR1.1 by intersectin 1 and increases KIR1.1. Lower Panel: miR-802 inhibits caveolin 1 which relieves the inhibition of KIR1.1 by caveolin 1 and increases KIR1.1. (B) The action of miR-205 on KIR4.1 in a native human corneal epithelial cells (HCECs) it to suppress KIR4.1 causing the cells to depolarize, which activates voltage-gated Ca2+ channels in HCECs, thus, increasing the healing process. (C) The action of miR-204 on KIR7.1 in retinal pigment epithelium. The effect of miR-204 on the increased expression of KIR7.1 was caused by miR-204's suppressing action on TGF-βR2, through an unknown mechanism, followed by reduced signaling of protein kinase C which resulted in increased expression of KIR7.1. (D) MiR-7 regulates the expression of KIR2.1 in small-cell lung cancer cells (SCLCs). When miR-7 levels was elevated, the mRNA for KIR2.1 was reduced which reduced the expression of KIR2.1 at the membrane. There was a inverse correlation between MiR-7 expression levels and the expression of KIR2.1 and multi-drug resitance protein 1 which resulted in increased chemosenetivity to SCLCs.
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Figure 2: The actions of miRs on epithelial K+ channels. (A) The action of miR-194 and miR-802 on upregulation of KIR1.1. Upper Panel: MiR-194 inhibits Intersectin 1, which mitigates the inhibition of KIR1.1 by intersectin 1 and increases KIR1.1. Lower Panel: miR-802 inhibits caveolin 1 which relieves the inhibition of KIR1.1 by caveolin 1 and increases KIR1.1. (B) The action of miR-205 on KIR4.1 in a native human corneal epithelial cells (HCECs) it to suppress KIR4.1 causing the cells to depolarize, which activates voltage-gated Ca2+ channels in HCECs, thus, increasing the healing process. (C) The action of miR-204 on KIR7.1 in retinal pigment epithelium. The effect of miR-204 on the increased expression of KIR7.1 was caused by miR-204's suppressing action on TGF-βR2, through an unknown mechanism, followed by reduced signaling of protein kinase C which resulted in increased expression of KIR7.1. (D) MiR-7 regulates the expression of KIR2.1 in small-cell lung cancer cells (SCLCs). When miR-7 levels was elevated, the mRNA for KIR2.1 was reduced which reduced the expression of KIR2.1 at the membrane. There was a inverse correlation between MiR-7 expression levels and the expression of KIR2.1 and multi-drug resitance protein 1 which resulted in increased chemosenetivity to SCLCs.

Mentions: Wang and colleagues (Lin et al., 2011) provided the first evidence that mirR-802 regulated membrane expression and activity of KIR1.1 by modulating caveolin-1 (Figure 2A). Initially, the authors performed a miR microarray assay on mouse kidney of animals fed a high K+ diet to identify potential miRs that might modulate KIR1.1. One miR identified was miR-802. The authors used multiple approaches to determine the role of miR-802 in the regulation of KIR1.1. Using Northern blot and PCR experiments, they demonstrated that miR-802 was elevated in the kidney of mice fed a high K+ diet. Additionally, using qRT-PCR, they reported increased levels of pre-miR-802 in CCDs isolated from mice fed a high K+ diet. Therefore, Lin et al. (2011) established that miR-802 was present in the mouse CCDs and the miR was modulated by high K+ diet.


The Role of MicroRNAs in the Regulation of K(+) Channels in Epithelial Tissue.

Pilmore E, Hamilton KL - Front Physiol (2015)

The actions of miRs on epithelial K+ channels. (A) The action of miR-194 and miR-802 on upregulation of KIR1.1. Upper Panel: MiR-194 inhibits Intersectin 1, which mitigates the inhibition of KIR1.1 by intersectin 1 and increases KIR1.1. Lower Panel: miR-802 inhibits caveolin 1 which relieves the inhibition of KIR1.1 by caveolin 1 and increases KIR1.1. (B) The action of miR-205 on KIR4.1 in a native human corneal epithelial cells (HCECs) it to suppress KIR4.1 causing the cells to depolarize, which activates voltage-gated Ca2+ channels in HCECs, thus, increasing the healing process. (C) The action of miR-204 on KIR7.1 in retinal pigment epithelium. The effect of miR-204 on the increased expression of KIR7.1 was caused by miR-204's suppressing action on TGF-βR2, through an unknown mechanism, followed by reduced signaling of protein kinase C which resulted in increased expression of KIR7.1. (D) MiR-7 regulates the expression of KIR2.1 in small-cell lung cancer cells (SCLCs). When miR-7 levels was elevated, the mRNA for KIR2.1 was reduced which reduced the expression of KIR2.1 at the membrane. There was a inverse correlation between MiR-7 expression levels and the expression of KIR2.1 and multi-drug resitance protein 1 which resulted in increased chemosenetivity to SCLCs.
© Copyright Policy
Related In: Results  -  Collection

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Figure 2: The actions of miRs on epithelial K+ channels. (A) The action of miR-194 and miR-802 on upregulation of KIR1.1. Upper Panel: MiR-194 inhibits Intersectin 1, which mitigates the inhibition of KIR1.1 by intersectin 1 and increases KIR1.1. Lower Panel: miR-802 inhibits caveolin 1 which relieves the inhibition of KIR1.1 by caveolin 1 and increases KIR1.1. (B) The action of miR-205 on KIR4.1 in a native human corneal epithelial cells (HCECs) it to suppress KIR4.1 causing the cells to depolarize, which activates voltage-gated Ca2+ channels in HCECs, thus, increasing the healing process. (C) The action of miR-204 on KIR7.1 in retinal pigment epithelium. The effect of miR-204 on the increased expression of KIR7.1 was caused by miR-204's suppressing action on TGF-βR2, through an unknown mechanism, followed by reduced signaling of protein kinase C which resulted in increased expression of KIR7.1. (D) MiR-7 regulates the expression of KIR2.1 in small-cell lung cancer cells (SCLCs). When miR-7 levels was elevated, the mRNA for KIR2.1 was reduced which reduced the expression of KIR2.1 at the membrane. There was a inverse correlation between MiR-7 expression levels and the expression of KIR2.1 and multi-drug resitance protein 1 which resulted in increased chemosenetivity to SCLCs.
Mentions: Wang and colleagues (Lin et al., 2011) provided the first evidence that mirR-802 regulated membrane expression and activity of KIR1.1 by modulating caveolin-1 (Figure 2A). Initially, the authors performed a miR microarray assay on mouse kidney of animals fed a high K+ diet to identify potential miRs that might modulate KIR1.1. One miR identified was miR-802. The authors used multiple approaches to determine the role of miR-802 in the regulation of KIR1.1. Using Northern blot and PCR experiments, they demonstrated that miR-802 was elevated in the kidney of mice fed a high K+ diet. Additionally, using qRT-PCR, they reported increased levels of pre-miR-802 in CCDs isolated from mice fed a high K+ diet. Therefore, Lin et al. (2011) established that miR-802 was present in the mouse CCDs and the miR was modulated by high K+ diet.

Bottom Line: MiRs are now in the "limelight" as these non-coding pieces of RNA (generally ~22 nucleotides long) result in altered translation and function of proteins.Interestingly, the role of miRs in modulating K(+) channels of epithelial tissues is only emerging now.This minireview focuses on recent novel findings into the role of miRs in the regulation of K(+) channels of epithelia.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Otago School of Medical Sciences, University of Otago Dunedin, New Zealand.

ABSTRACT
Our understanding of the modulation of proteins has shifted in direction with the discovery of microRNAs (miRs) over twenty years ago. MiRs are now in the "limelight" as these non-coding pieces of RNA (generally ~22 nucleotides long) result in altered translation and function of proteins. Indeed, miRs are now reported to be potential biomarkers of disease. Epithelial K(+) channels play many roles in electrolyte and fluid homeostasis of the human body and have been suggested to be therapeutic targets of disease. Interestingly, the role of miRs in modulating K(+) channels of epithelial tissues is only emerging now. This minireview focuses on recent novel findings into the role of miRs in the regulation of K(+) channels of epithelia.

No MeSH data available.


Related in: MedlinePlus