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Mesenchymal stem cells exert anti-proliferative effect on lipopolysaccharide-stimulated BV2 microglia by reducing tumour necrosis factor-α levels

Overview of attention for article published in Journal of Neuroinflammation, September 2014
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Title
Mesenchymal stem cells exert anti-proliferative effect on lipopolysaccharide-stimulated BV2 microglia by reducing tumour necrosis factor-α levels
Published in
Journal of Neuroinflammation, September 2014
DOI 10.1186/s12974-014-0149-8
Pubmed ID
Authors

Shinsmon Jose, Shi Wei Tan, Yin Yin Ooi, Rajesh Ramasamy, Sharmili Vidyadaran

Abstract

BackgroundProgression of neurodegenerative diseases occurs when microglia, upon persistent activation, perpetuate a cycle of damage in the central nervous system. Use of mesenchymal stem cells (MSC) has been suggested as an approach to manage microglia activation based on their immunomodulatory functions. In the present study, we describe the mechanism through which bone marrow-derived MSC modulate the proliferative responses of lipopolysaccharide-stimulated BV2 microglia.MethodsBV2 microglia were cultured with MSC and stimulated with 1 ¿g/ml lipopolysaccharide. Using an inducible nitric oxide synthase inhibitor, tritiated thymidine (3H-TdR) incorporation assay was performed to determine the role of nitric oxide in the anti-proliferative effect of MSC. We also studied apoptosis and the cell cycle of both cell types using flow cytometry and explored their cytokine profile using protein and cytometric arrays. Moreover, the role of IL-6 and TNF-¿ in immunomodulation was deduced using specific blocking antibodies and recombinant proteins.ResultsMSC reduces microglia proliferation upon lipopolysaccharide stimulation by 21 to 28% and modulates the levels of nitric oxide, IL-6 and TNF-¿. The role of nitric oxide in conferring the anti-proliferative effect of MSC was ruled out. Furthermore, we found that MSC exert their anti-proliferative effect by restoring the percentage of BV2 cells at S and G2/M phase to levels similar to unstimulated cells. MSC undergo a G0/G1 arrest while exerting this effect. We have also identified that MSC-mediated modulation of microglia is independent of IL-6, whilst reduction of TNF-¿ in co-culture is critical for inhibition of microglia proliferation.ConclusionsOur study demonstrates that MSC inhibit microglia proliferation independent of nitric oxide and IL-6, although reduction of TNF-¿ is critical for this effect. The inhibition of proliferation is through cell cycle modulation. These findings shed light on the mechanisms of microglial immunomodulation by MSC.

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 45 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Malaysia 1 2%
Unknown 44 98%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 14 31%
Student > Bachelor 9 20%
Researcher 8 18%
Student > Master 4 9%
Student > Doctoral Student 3 7%
Other 4 9%
Unknown 3 7%
Readers by discipline Count As %
Agricultural and Biological Sciences 12 27%
Medicine and Dentistry 8 18%
Neuroscience 5 11%
Biochemistry, Genetics and Molecular Biology 5 11%
Immunology and Microbiology 3 7%
Other 7 16%
Unknown 5 11%

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 05 September 2014.
All research outputs
#3,052,505
of 4,507,652 outputs
Outputs from Journal of Neuroinflammation
#440
of 659 outputs
Outputs of similar age
#74,032
of 116,198 outputs
Outputs of similar age from Journal of Neuroinflammation
#24
of 31 outputs
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