↓ Skip to main content

HSP60 plays a regulatory role in IL-1β-induced microglial inflammation via TLR4-p38 MAPK axis

Overview of attention for article published in Journal of Neuroinflammation, February 2016
Altmetric Badge

Mentioned by

twitter
1 X user
facebook
1 Facebook page

Citations

dimensions_citation
99 Dimensions

Readers on

mendeley
81 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
HSP60 plays a regulatory role in IL-1β-induced microglial inflammation via TLR4-p38 MAPK axis
Published in
Journal of Neuroinflammation, February 2016
DOI 10.1186/s12974-016-0486-x
Pubmed ID
Authors

Shalini Swaroop, Nabonita Sengupta, Amol Ratnakar Suryawanshi, Yogita K Adlakha, Anirban Basu

Abstract

IL-1β, also known as "the master regulator of inflammation", is a potent pro-inflammatory cytokine secreted by activated microglia in response to pathogenic invasions or neurodegeneration. It initiates a vicious cycle of inflammation and orchestrates various molecular mechanisms involved in neuroinflammation. The role of IL-1β has been extensively studied in neurodegenerative disorders; however, molecular mechanisms underlying inflammation induced by IL-1β are still poorly understood. The objective of our study is the comprehensive identification of molecular circuitry involved in IL-1β-induced inflammation in microglia through protein profiling. To achieve our aim, we performed the proteomic analysis of N9 microglial cells with and without IL-1β treatment at different time points. Expression of HSP60 in response to IL-1β administration was checked by quantitative real-time PCR, immunoblotting, and immunofluorescence. Interaction of HSP60 with TLR4 was determined by co-immunoprecipitation. Inhibition of TLR4 was done using TLR4 inhibitor to reveal its effect on IL-1β-induced inflammation. Further, effect of HSP60 knockdown and overexpression were assessed on the inflammation in microglia. Specific MAPK inhibitors were used to reveal the downstream MAPK exclusively involved in HSP60-induced inflammation in microglia. Total 21 proteins were found to be differentially expressed in response to IL-1β treatment in N9 microglial cells. In silico analysis of these proteins revealed unfolded protein response as one of the most significant molecular functions, and HSP60 turned out to be a key hub molecule. IL-1β induced the expression as well as secretion of HSP60 in extracellular milieu during inflammation of N9 cells. Secreted HSP60 binds to TLR4 and inhibition of TLR4 suppressed IL-1β-induced inflammation to a significant extent. Our knockdown and overexpression studies demonstrated that HSP60 increases the phosphorylation of ERK, JNK, and p38 MAPKs in N9 cells during inflammation. Specific inhibition of p38 by inhibitors suppressed HSP60-induced inflammation, thus pointed towards the major role of p38 MAPK rather than ERK1/2 and JNK in HSP60-induced inflammation. Furthermore, silencing of upstream modulator of p38, i.e., MEK3/6 also reduced HSP60-induced inflammation. IL-1β induces expression of HSP60 in N9 microglial cells that further augments inflammation via TLR4-p38 MAPK axis.

X Demographics

X Demographics

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

Mendeley readers

The data shown below were compiled from readership statistics for 81 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 1%
France 1 1%
Unknown 79 98%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 17 21%
Student > Master 16 20%
Student > Doctoral Student 6 7%
Student > Bachelor 5 6%
Other 4 5%
Other 8 10%
Unknown 25 31%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 16 20%
Neuroscience 11 14%
Agricultural and Biological Sciences 9 11%
Medicine and Dentistry 9 11%
Pharmacology, Toxicology and Pharmaceutical Science 3 4%
Other 5 6%
Unknown 28 35%
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 08 February 2016.
All research outputs
#18,437,241
of 22,842,950 outputs
Outputs from Journal of Neuroinflammation
#2,074
of 2,640 outputs
Outputs of similar age
#287,419
of 397,125 outputs
Outputs of similar age from Journal of Neuroinflammation
#63
of 82 outputs
Altmetric has tracked 22,842,950 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,640 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.6. This one is in the 12th percentile – i.e., 12% 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 397,125 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 15th percentile – i.e., 15% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 82 others from the same source and published within six weeks on either side of this one. This one is in the 14th percentile – i.e., 14% of its contemporaries scored the same or lower than it.