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Inflammatory Regulation by Driving Microglial M2 Polarization: Neuroprotective Effects of Cannabinoid Receptor-2 Activation in Intracerebral Hemorrhage

Overview of attention for article published in Frontiers in immunology, February 2017
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Title
Inflammatory Regulation by Driving Microglial M2 Polarization: Neuroprotective Effects of Cannabinoid Receptor-2 Activation in Intracerebral Hemorrhage
Published in
Frontiers in immunology, February 2017
DOI 10.3389/fimmu.2017.00112
Pubmed ID
Authors

Li Lin, Tao Yihao, Feng Zhou, Niu Yin, Tan Qiang, Zheng Haowen, Chen Qianwei, Tang Jun, Zhang Yuan, Zhu Gang, Feng Hua, Yang Yunfeng, Chen Zhi

Abstract

The cannabinoid receptor-2 (CB2R) was initially thought to be the "peripheral cannabinoid receptor." Recent studies, however, have documented CB2R expression in the brain in both glial and neuronal cells, and increasing evidence suggests an important role for CB2R in the central nervous system inflammatory response. Intracerebral hemorrhage (ICH), which occurs when a diseased cerebral vessel ruptures, accounts for 10-15% of all strokes. Although surgical techniques have significantly advanced in the past two decades, ICH continues to have a high mortality rate. The aim of this study was to investigate the therapeutic effects of CB2R stimulation in acute phase after experimental ICH in rats and its related mechanisms. Data showed that stimulation of CB2R using a selective agonist, JWH133, ameliorated brain edema, brain damage, and neuron death and improved neurobehavioral outcomes in acute phase after ICH. The neuroprotective effects were prevented by SR144528, a selective CB2R inhibitor. Additionally, JWH133 suppressed neuroinflammation and upregulated the expression of microglial M2-associated marker in both gene and protein level. Furthermore, the expression of phosphorylated cAMP-dependent protein kinase (pPKA) and its downstream effector, cAMP-response element binding protein (CREB), were facilitated. Knockdown of CREB significantly inversed the increase of M2 polarization in microglia, indicating that the JWH133-mediated anti-inflammatory effects are closely associated with PKA/CREB signaling pathway. These findings demonstrated that CB2R stimulation significantly protected the brain damage and suppressed neuroinflammation by promoting the acquisition of microglial M2 phenotype in acute stage after ICH. Taken together, this study provided mechanism insight into neuroprotective effects by CB2R stimulation after ICH.

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Mendeley readers

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 > Bachelor 9 24%
Student > Doctoral Student 5 14%
Student > Master 5 14%
Student > Ph. D. Student 4 11%
Researcher 3 8%
Other 4 11%
Unknown 7 19%
Readers by discipline Count As %
Neuroscience 9 24%
Medicine and Dentistry 7 19%
Biochemistry, Genetics and Molecular Biology 5 14%
Pharmacology, Toxicology and Pharmaceutical Science 3 8%
Immunology and Microbiology 2 5%
Other 3 8%
Unknown 8 22%
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 23 February 2017.
All research outputs
#19,951,180
of 25,382,440 outputs
Outputs from Frontiers in immunology
#22,585
of 31,531 outputs
Outputs of similar age
#312,989
of 433,728 outputs
Outputs of similar age from Frontiers in immunology
#307
of 403 outputs
Altmetric has tracked 25,382,440 research outputs across all sources so far. This one is in the 18th percentile – i.e., 18% of other outputs scored the same or lower than it.
So far Altmetric has tracked 31,531 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.4. This one is in the 21st percentile – i.e., 21% 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 433,728 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 24th percentile – i.e., 24% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 403 others from the same source and published within six weeks on either side of this one. This one is in the 13th percentile – i.e., 13% of its contemporaries scored the same or lower than it.