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Title: | Asprosin Exerts Pro-Inflammatory Effects in THP-1 Macrophages Mediated via the Toll-like Receptor 4 (TLR4) Pathway |
Authors: | Shabir, K Gharanei, S Orton, S Patel, V Chauhan, P Karteris, E Randeva, HS Brown, JE Kyrou, I |
Keywords: | asprosin;adipokines;inflammation;THP-1 macrophages;Toll-like receptor 4;TLR4 |
Issue Date: | 23-Dec-2022 |
Publisher: | MDPI |
Citation: | Shabir, K. et al. (2023) 'Asprosin Exerts Pro-Inflammatory Effects in THP-1 Macrophages Mediated via the Toll-like Receptor 4 (TLR4) Pathway', International Journal of Molecular Sciences, 24 (1), 227, pp. 1 - 16. doi: 10.3390/ijms24010227. |
Abstract: | Copyright © 2022 by the authors. Adipose tissue is a dynamic endocrine organ, secreting a plethora of adipokines which play a key role in regulating metabolic homeostasis and other physiological processes. An altered adipokine secretion profile from adipose tissue depots has been associated with obesity and related cardio-metabolic diseases. Asprosin is a recently described adipokine that is released in response to fasting and can elicit orexigenic and glucogenic effects. Circulating asprosin levels are elevated in a number of cardio-metabolic diseases, including obesity and type 2 diabetes. In vitro studies have reported pro-inflammatory effects of asprosin in a variety of tissues. The present study aimed to further elucidate the role of asprosin in inflammation by exploring its potential effect(s) in THP-1 macrophages. THP-1 monocytes were differentiated to macrophages by 48 h treatment with dihydroxyvitamin D3. Macrophages were treated with 100 nM recombinant human asprosin, 100 ng/mL lipopolysaccharide (LPS), and 10 μM caffeic acid phenethyl ester (CAPE; an inhibitor of NFκB activation) or 1 µM TAK-242 (a Toll-like receptor 4, TLR4, inhibitor). The expression and secretion of pertinent pro-inflammatory mediators were measured by qPCR, Western blot, ELISA and Bioplex. Asprosin stimulation significantly upregulated the expression and secretion of the pro-inflammatory cytokines: tumour necrosis factor α (TNFα), interleukin-1β (IL-1β), IL-8 and IL-12 in vitro. This pro-inflammatory response in THP-1 macrophages was partly attenuated by the treatments with CAPE and was significantly inhibited by TAK-242 treatment. Asprosin-induced inflammation is significantly counteracted by TLR4 inhibition in THP-1 macrophages, suggesting that asprosin exerts its pro-inflammatory effects, at least in part, via the TLR4 signalling pathway. |
Description: | Data Availability Statement: Data are contained within the paper and its Supplementary Material: the following supporting information can be downloaded at: https://www.mdpi.com/article/10.3390/ijms24010227/s1. |
URI: | https://bura.brunel.ac.uk/handle/2438/26325 |
DOI: | https://doi.org/10.3390/ijms24010227 |
ISSN: | 1661-6596 |
Other Identifiers: | ORCID iDs: Kiran Shabir https://orcid.org/0000-0003-1633-1552; Seley Gharanei https://orcid.org/0000-0002-5935-8950; Emmanouil Karteris https://orcid.org/0000-0003-3231-7267; Ioannis Kyrou https://orcid.org/0000-0002-6997-3439. 227 |
Appears in Collections: | Brunel Medical School Research Papers |
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