The activation state of macrophages alters their ability to suppress preadipocyte apoptosis

Molgat, André S.D.; Gagnon, AnneMarie; Foster, Charlie; Sorisky, Alexander

doi:10.1530/joe-12-0114

Cited by 14 publications

(11 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…5B). This value is very stable across the batches of THP-1-MacCM that we have produced, and the same applies to TNFa levels (Molgat et al 2012). IL1b strongly stimulated IKKb phosphorylation from undetectable basal levels and also resulted in complete IkB degradation in human preadipocytes.…”

Section: Resultssupporting

confidence: 54%

See 1 more Smart Citation

The role of interleukin 1β in the anti-adipogenic action of macrophages on human preadipocytes

Gagnon

Foster

Landry

et al. 2013

Journal of Endocrinology

Self Cite

View full text Add to dashboard Cite

When adipose tissue accumulates in obesity, the ability of preadipocytes to differentiate permits a hyperplastic expansion of functional adipocytes that preserves insulin sensitivity. Adipose infiltration by macrophages is associated with an adipogenic deficit and the appearance of inflamed, insulin-resistant hypertrophied adipocytes. Interleukin 1b (IL1b) has been reported to account for the anti-adipogenic action of macrophages in a mouse model. Using the THP-1 human macrophage cell line and human primary preadipocytes, our objective was to determine whether IL1b was necessary for the ability of conditioned medium from THP-1 macrophages (THP-1-MacCM) to: i) stimulate human preadipocyte inhibitor of kB kinase b (IKKb) and ii) inhibit human adipocyte differentiation. IL1b is present in THP-1-MacCM, and THP-1-MacCM or IL1b (500 pg/ml; its concentration in THP-1-MacCM) acutely stimulated IKKb phosphorylation and inhibitor of kB (IkB) degradation in preadipocytes. IL1b was sufficient to inhibit adipogenesis on its own, and this was blocked by SC-514, an IKKb inhibitor, as has been reported for THP-1-MacCM. IkB degradation by IL1b-immunodepleted THP-1-MacCM was attenuated, whereas IKKb phosphorylation and the inhibition of adipocyte differentiation were unchanged. Therefore, in contrast to what has been suggested for mouse cell models, IL1b is not required for the ability of MacCM to inhibit adipogenesis in human cell models.

show abstract

Section: Resultssupporting

confidence: 54%

“…Furthermore, the amount of TNFa was not actually quantified in their conditioned medium. At 20 pg/ml, the concentration measured in THP-1-MacCM (Molgat et al 2012), TNFa had no effect on human adipocyte differentiation. As a positive control, TNFa at 25 000 pg/ml was anti-adipogenic.…”

Section: Discussionmentioning

confidence: 81%

The role of interleukin 1β in the anti-adipogenic action of macrophages on human preadipocytes

Gagnon

Foster

Landry

et al. 2013

Journal of Endocrinology

Self Cite

View full text Add to dashboard Cite

show abstract

“…This mild inflammatory condition is characterized by changes in the macrophage population in adipose tissue [ 2 , 3 ]. An increase in proinflammatory type-1 macrophages (M1), which promotes insulin resistance, is evident in the adipose tissue of obese people, who also demonstrate reduced numbers of type-2 macrophages (M2), which are insulin sensitizing [ 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

Human ADMC-Derived Adipocyte Thermogenic Capacity Is Regulated by IL-4 Receptor

Lizcano

Vargas

Gómez

et al. 2017

Stem Cells International

View full text Add to dashboard Cite

Type two innate immune system is anti-inflammatory and may play an important role as the means whereby “browning” is induced in subcutaneous adipocytes. It was shown that IL-4 may influence the fate of adipose cell precursors by promoting differentiation towards more thermogenic adipocytes in mice. Here, we investigated the influence of IL-4 and IL-4 receptor, a type two immune cytokine pathway, on the metabolic activity and thermogenic potential of human adipocytes differentiated from adipose-derived mesenchymal stem cells (ADMSCs) obtained from subcutaneous samples of healthy women undergoing abdominoplasty. Western blot analysis, qPCR, and biochemical analyses were performed 10 days after ADMSC differentiation into mature adipocytes was induced. IL-4 receptor was expressed in both precursor and differentiated adipocytes, and IL-4 treatment increased phosphorylation Y641 of signal transducer and activator of transcription 6 (STAT6) in both cell types. IL-4 treatment also increased expression of thermogenic proteins PGC-1α, UCP-1, and CITED1. In addition, IL-4 increased the secretion of adiponectin, leptin, and FGF21 and promoted lipolysis in differentiated adipocytes. In conclusion, IL-4 may directly modulate differentiation of human adipocytes towards a beige phenotype acting through IL-4 receptors on both adipose precursors and differentiated human adipocytes, metabolic effect that must be considered in some antiallergic drugs.

show abstract

“…Obesity is defined as a long-term positive caloric imbalance leading to adipose tissue expansion, which may occur via increases in adipocyte size (hypertrophy), number (hyperplasia) or both [1,2]. Obese individuals presented a chronic low-grade inflammation that involves excessive adipocyte hypertrophy, immune cell infiltration, extracellular matrix overproduction, increased production of pro-inflammatory adipokines and redox imbalance [3,4,5].…”

Section: Introductionmentioning

confidence: 99%

“…Hypertrofic adipose tissue growth is associated with adipose tissue inflammation [2]. Therefore, an increase in pro-inflammatory adipokines secreted by infiltrated macrophages and hypertrophied adipocytes, as well as an elevated production of reactive oxygen species (ROS), can decrease the differentiation capacity of preadipocytes and inhibit adipogenesis [4,5,9,10].…”

Section: Introductionmentioning

confidence: 99%

Neuroendocrine Inflammatory Responses in Overweight/Obese Infants

et al. 2016

View full text Add to dashboard Cite

Childhood obesity is related to a cascade of neuroendocrine inflammatory changes. However, there remains a gap in the current literature regarding the possible occurrence of these changes in overweight/obese infants. The objective of this study was to evaluate adipokines, cortisol, brain-derived neurotrophic factor (BDNF) and redox status in overweight/obese infants versus normal-weight peers. A cross-sectional study was conducted with 50 infants (25 in the overweight/obese group and 25 in the normal-weight group) between 6 and 24 months. Plasma levels of leptin, adiponectin, resistin, soluble tumor necrosis factor (TNF) receptors, chemokines, BDNF, serum cortisol and redox status were measured. Unpaired Student's t-test was used to analyze the results and a probability of p<0.05 was acceptable for rejection of the null hypothesis. The Pearson correlation was used to verify the association between the biomarkers analyzed in each group. Plasma levels of leptin (p = 0.0001), adiponectin (p = 0.0007) and BDNF (p = 0.003), and serum cortisol (p = 0.048) were significantly higher in overweight/obese infants than normal-weight infants. In contrast, the concentration of thiobarbituric acid reactive substances (TBARS) (p = 0.004), and catalase (p = 0.045) and superoxide dismutase activity (p = 0.02) were lower in overweight/obese infants than normal-weight peers. All the results together indicate neuroendocrine inflammatory response changes in overweight/obese infants between 6 and 24 months. Although there is already an environment that predisposes for a subsequent pro-inflammatory response, neuroendocrine secretion changes that permit the control of the inflammatory process in this age interval can be observed.

show abstract

The activation state of macrophages alters their ability to suppress preadipocyte apoptosis

Cited by 14 publications

References 37 publications

The role of interleukin 1β in the anti-adipogenic action of macrophages on human preadipocytes

The role of interleukin 1β in the anti-adipogenic action of macrophages on human preadipocytes

Human ADMC-Derived Adipocyte Thermogenic Capacity Is Regulated by IL-4 Receptor

Neuroendocrine Inflammatory Responses in Overweight/Obese Infants

Contact Info

Product

Resources

About