↓ Skip to main content

MiR-126 Regulates Growth Factor Activities and Vulnerability to Toxic Insult in Neurons

Overview of attention for article published in Molecular Neurobiology, November 2014
Altmetric Badge

Mentioned by

twitter
1 tweeter

Citations

dimensions_citation
27 Dimensions

Readers on

mendeley
37 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
MiR-126 Regulates Growth Factor Activities and Vulnerability to Toxic Insult in Neurons
Published in
Molecular Neurobiology, November 2014
DOI 10.1007/s12035-014-8989-x
Pubmed ID
Authors

Woori Kim, Haneul Noh, Yenarae Lee, Jeha Jeon, Arthi Shanmugavadivu, Donna L. McPhie, Kwang-Soo Kim, Bruce M. Cohen, Hyemyung Seo, Kai C. Sonntag

Abstract

Dysfunction of growth factor (GF) activities contributes to the decline and death of neurons during aging and in neurodegenerative diseases. In addition, neurons become more resistant to GF signaling with age. Micro (mi)RNAs are posttranscriptional regulators of gene expression that may be crucial to age- and disease-related changes in GF functions. MiR-126 is involved in regulating insulin/IGF-1/phosphatidylinositol-3-kinase (PI3K)/AKT and extracellular signal-regulated kinase (ERK) signaling, and we recently demonstrated a functional role of miR-126 in dopamine neuronal cell survival in models of Parkinson's disease (PD)-associated toxicity. Here, we show that elevated levels of miR-126 increase neuronal vulnerability to ubiquitous toxicity mediated by staurosporine (STS) or Alzheimer's disease (AD)-associated amyloid beta 1-42 peptides (Aβ1-42). The neuroprotective factors IGF-1, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and soluble amyloid precursor protein α (sAPPα) could diminish but not abrogate the toxic effects of miR-126. In miR-126 overexpressing neurons derived from Tg6799 familial AD model mice, we observed an increase in Aβ1-42 toxicity, but surprisingly, both Aβ1-42 and miR-126 promoted neurite sprouting. Pathway analysis revealed that miR-126 overexpression downregulated elements in the GF/PI3K/AKT and ERK signaling cascades, including AKT, GSK-3β, ERK, their phosphorylation, and the miR-126 targets IRS-1 and PIK3R2. Finally, inhibition of miR-126 was neuroprotective against both STS and Aβ1-42 toxicity. Our data provide evidence for a novel mechanism of regulating GF/PI3K signaling in neurons by miR-126 and suggest that miR-126 may be an important mechanistic link between metabolic dysfunction and neurotoxicity in general, during aging, and in the pathogenesis of specific neurological disorders, including PD and AD.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 37 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 37 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 12 32%
Student > Bachelor 5 14%
Student > Master 5 14%
Researcher 4 11%
Student > Doctoral Student 3 8%
Other 3 8%
Unknown 5 14%
Readers by discipline Count As %
Medicine and Dentistry 11 30%
Biochemistry, Genetics and Molecular Biology 6 16%
Neuroscience 5 14%
Agricultural and Biological Sciences 4 11%
Pharmacology, Toxicology and Pharmaceutical Science 1 3%
Other 3 8%
Unknown 7 19%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 20 November 2014.
All research outputs
#11,577,177
of 13,029,326 outputs
Outputs from Molecular Neurobiology
#1,716
of 2,145 outputs
Outputs of similar age
#238,878
of 294,124 outputs
Outputs of similar age from Molecular Neurobiology
#27
of 36 outputs
Altmetric has tracked 13,029,326 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,145 research outputs from this source. They receive a mean Attention Score of 4.9. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 294,124 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 36 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.