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The mechanism of botulinum A on Raynaud syndrome

Overview of attention for article published in Drug Design, Development and Therapy, June 2018
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Title
The mechanism of botulinum A on Raynaud syndrome
Published in
Drug Design, Development and Therapy, June 2018
DOI 10.2147/dddt.s161113
Pubmed ID
Authors

Yanwen Zhou, Ying Liu, Yunhua Hao, Ya Feng, Lizhen Pan, Wuchao Liu, Bing Li, Libin Xiao, Lingjing Jin, Zhiyu Nie

Abstract

Botulinum neurotoxin type A (BoNT/A) is emerging as a treatment modality for Raynaud's phenomenon (RP). However, the mechanism of the role of BoNT/A in antagonizing the constriction of arteriola in RP remains unclear. We tested the constriction of arteriole diameter and the distribution of adrenergic receptors on the rat cremaster modle. Moreover, we measured the secretion of norepinephrine (NE), protein level changes and related receptors on cultured rat superior cervical ganglia neurons(SCGNs), a model of sympathetic neuron. Based on our results, the inhibition of arteriole vasoconstriction was increased with increasing doses of BoNT/A. BoNT/A, prazosin, and BQ123 treatment can result in significant inhibition of arteriole vasoconstriction with the same electrical stimulation. The inhibition effect of prazosin was equivalent to BoNT/A, while BQ123 has a synergistic effect with BoNT/A. After treating SCGNs using BoNT/A for 30 min, the decrease in fluorescence intensity of FM1-43 slowed down which was correlated with the doses of BoNT/A. Furthermore, release of NE in the supernatant was significantly decreased as measured by enzyme-linked immunosorbent assay, 24 h after a high dose of BoNT/A (25 µ/mL). Cleaved-SNAP-25 was detected by Western blotting 24 h following BoNT/A (50 µ/mL) treatment. Moreover, receptor SV2C, GM1, and FGFR3 were detected on sympathetic neurons, similarly to cholinergic neurons. Our study showed that BoNT/A could significantly inhibit electrical stimulation-induced arteriole vasoconstriction through the sympathetic pathway. The mechanism was similar to the cholinergic one, in which the vesicle release of sympathetic neurons could be inhibited by cleavage of SNAP-25. The end result was blocked vesicle fusion with the presynaptic membrane after BoNT/A treatment, inhibiting the release of the NE.

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Mendeley readers

Mendeley readers

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Geographical breakdown

Country Count As %
Unknown 33 100%

Demographic breakdown

Readers by professional status Count As %
Other 4 12%
Researcher 3 9%
Student > Postgraduate 3 9%
Student > Doctoral Student 2 6%
Student > Ph. D. Student 2 6%
Other 4 12%
Unknown 15 45%
Readers by discipline Count As %
Medicine and Dentistry 11 33%
Biochemistry, Genetics and Molecular Biology 2 6%
Neuroscience 2 6%
Unspecified 1 3%
Business, Management and Accounting 1 3%
Other 0 0%
Unknown 16 48%
Attention Score in Context

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 01 November 2018.
All research outputs
#20,663,600
of 25,385,509 outputs
Outputs from Drug Design, Development and Therapy
#1,436
of 2,268 outputs
Outputs of similar age
#267,264
of 342,877 outputs
Outputs of similar age from Drug Design, Development and Therapy
#47
of 63 outputs
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So far Altmetric has tracked 2,268 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.1. This one is in the 22nd percentile – i.e., 22% of its peers scored the same or lower than it.
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