The contribution of IL-6 to beta 3 adrenergic receptor mediated adipose tissue remodeling

Buzelle, Samyra Lopes; MacPherson, Rebecca E. K.; Peppler, Willem T.; Castellani, L; Wright, David C.

doi:10.14814/phy2.12312

Cited by 19 publications

(19 citation statements)

References 44 publications

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“…Western blotting procedures were completed as previously described. 26 Briefly, proteins were transferred onto a nitrocellulose membrane, incubated with indicated primary antibodies overnight, the corresponding secondary antibody for 1 hour, and imaged using enhanced chemiluminescence on a FluorChem HD imaging system (a Innotect, Santa Clara, CA). Antibodies used were purchased from AbCam (Toronto, ON, Canada; b-actin Cat # 8227; Citrate synthase (CS) Cat # ab129095; AntiUbiquinol-Cytochrome C Reductase (CORE1) Cat # 110252; Cytochrome C Oxidase Subunit IV (COXIV) Cat # ab16056; GAPDH Cat # 8245; uncoupling protein 1 (UCP-1) Cat # 10983), Millipore (Etobicoke, ON, Canada; Peroxisome proliferator-activated receptor gamma coactivator 1-a (PGC-1a) Cat # AB3242, Mitosciences (Toronto, ON, Canada; Cytochrome C (CytC) Cat # MSA06; Pyruvate dehydrogenase subunit E1a (PDH-E1a) Cat # MSP03); and Cell Signaling (Danvers, MA; MyD88 Cat # 4283; pSTAT3 Cat # 9138; STAT3 Cat # 8768).…”

Section: Western Blottingmentioning

confidence: 99%

Habitual physical activity protects against lipopolysaccharide-induced inflammation in mouse adipose tissue

et al. 2016

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Sepsis is a systemic inflammatory response to infection, with no preventative strategies. In this study, we identify a role for habitual physical activity in the prevention of adipose tissue inflammation induced by a model of sepsis, lipopolysaccharide (LPS). Male C57BL/6J mice (8 weeks old) were housed with access to voluntary wheel running (VWR) or sedentary (SED) for 10 weeks. Mice were then injected with LPS (2 mg/kg) or saline (SAL), and tissues were removed 6 hours postinjection. VWR attenuated body, epididymal adipose tissue (eWAT), and subcutaneous inguinal adipose tissue (iWAT) mass gain, improved glucose tolerance, increased markers of mitochondrial biogenesis in iWAT and eWAT, and increased UCP-1 protein content in iWAT. In iWAT, VWR attenuated the LPS induced increase in mRNA expression of TNF-a, MCP-1, and follistatin, along with phosphorylation of STAT3. In addition, VWR had a main effect for reducing iWAT mRNA expression of IL-1b, IL-6, and SOCS3. In eWAT, VWR had a main effect for reducing mRNA expression of IL-1b, MCP-1, IL-6, and follistatin. Further, VWR increased SOCS3 mRNA expression and phosphorylation of STAT3 in SAL mice, thus the relative change in response to LPS for these markers was attenuated. The protective effect of prior physical activity occurred in conjunction with increases in the protein content of a component of the LPS binding complex, MyD88. Overall, the results from this study demonstrate that habitual physical activity can attenuate the LPS induced inflammatory response in adipose tissue and this occurs to a greater extent in iWAT compare with eWAT.

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Section: Western Blottingmentioning

confidence: 99%

Habitual physical activity protects against lipopolysaccharide-induced inflammation in mouse adipose tissue

et al. 2016

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“…Whole liver tissue was homogenized in a 30ϫ cocktail of cell lysis buffer, supplemented with phenylmethylsulfonyl fluoride, and protease inhibitor cocktail (Sigma-Aldrich). Western blotting procedures were completed similar to that which we have previously described (3). Nitrocellulose membranes were incubated with indicated primary antibodies overnight and then with corresponding secondary antibody for 1 h. These membranes were then imaged using enhanced chemiluminescence signals on a FluorChem HD imaging system (Alpha Innotect, Santa Clara, CA Real-time quantitative PCR.…”

Section: Ethicsmentioning

confidence: 99%

Voluntary wheel running attenuates lipopolysaccharide-induced liver inflammation in mice

Peppler

Anderson

Sutton

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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Peppler WT, Anderson ZG, Sutton CD, Rector RS, Wright DC. Voluntary wheel running attenuates lipopolysaccharide-induced liver inflammation in mice. Am J Physiol Regul Integr Comp Physiol 310: R934 -R942, 2016. First published February 17, 2016 doi:10.1152/ajpregu.00497.2015.-Sepsis induces an acute inflammatory response in the liver, which can lead to organ failure and death. Given the anti-inflammatory effects of exercise, we hypothesized that habitual physical activity could protect against acute sepsis-induced liver inflammation via mechanisms, including heat shock protein (HSP) 70/72. Male C57BL/6J mice (n ϭ 80, ϳ8 wk of age) engaged in physical activity via voluntary wheel running (VWR) or cage control (SED) for 10 wk. To induce sepsis, we injected (2 mg/kg ip) LPS or sterile saline (SAL), and liver was harvested 6 or 12 h later. VWR attenuated increases in body and epididymal adipose tissue mass, improved glucose tolerance, and increased liver protein content of PEPCK (P Ͻ 0.05). VWR attenuated increases in LPS-induced IL-6 signaling and mRNA expression of other inflammatory markers (TNF-␣, chemokine C-C motif ligand 2, inducible nitric oxide synthase, IL-10, IL-1␤) in the liver; however, this was not reflected at the whole body level, as systemic markers of inflammation were similar between SED and VWR. Insulin tolerance was greater in VWR compared with SED at 6 but not 12 h after LPS. The protective effect of VWR occurred in parallel with increases in the liver protein content of HSP70/72, a molecular chaperone that can protect against inflammatory challenges. This study provides novel evidence that physical activity protects against the inflammatory cascade induced by LPS in the liver and that these effects may be mediated via HSP70/72. lipopolysaccharide; inflammation; liver; physical activity; exercise SEPSIS IS A CONTINUUM OF CLINICAL events defined by the presence of infection and systemic inflammation (18). The worldwide incidence of sepsis was recently estimated at 437 cases per 100,000 person years between 2003 and 2015, with an associated fatality rate of 17% (11). This puts a significant burden on the health care system, and in the United States alone, the direct hospital costs associated with sepsis are over $24 billion (17).The infiltration of a host with both gram-negative and gram-positive bacterial species is often considered to be the cause of acute sepsis (34). LPS from Escherichia coli, a component of gram-negative bacteria, is often used to produce these effects in rodent models. Upon exposure to LPS, an inflammatory cascade is activated both systemically and at a tissue-specific level (1). Initial signaling involves a Toll-like receptor 4 (TLR4)-myeloid differentiation primary response gene 88 (MyD88) interaction that then propagates the inflammatory response (24). Increases in circulating inflammatory factors, such as TNF-␣, IL-6, and IL-1␤, occur rapidly and are regulated by the dose and duration of exposure (21,29,40). Clearance of inflammatory markers begins as early as 8 h post...

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“…Transient IL-6 family activation mediates Jak/Stat3-Tgfb3 signaling in progenitors and adipose tissue IL-6 cytokine family members are potent inducers of the Jak/Stat3 pathway, and IL-6 is induced by -adrenergic stimulation (40,(42)(43)(44).…”

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Jak-TGFβ cross-talk links transient adipose tissue inflammation to beige adipogenesis

et al. 2018

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The transient activation of inflammatory networks is required for adipose tissue remodeling including the "browning" of white fat in response to stimuli such as 3-adrenergic receptor activation. In this process, white adipose tissue acquires thermogenic characteristics through the recruitment of so-called beige adipocytes. We investigated the downstream signaling pathways impinging on adipocyte progenitors that promote de novo formation of adipocytes. We showed that the Jak family of kinases controlled TGF signaling in the adipose tissue microenvironment through Stat3 and thereby adipogenic commitment, a function that was required for beige adipocyte differentiation of murine and human progenitors. Jak/Stat3 inhibited TGF signaling to the transcription factors Srf and Smad3 by repressing local Tgfb3 and Tgfb1 expression before the core transcriptional adipogenic cascade was activated. This pathway cross-talk was triggered in stromal cells by ATGL-dependent adipocyte lipolysis and a transient wave of IL-6 family cytokines at the onset of adipose tissue remodeling induced by 3-adrenergic receptor stimulation. Our results provide insight into the activation of adipocyte progenitors and are relevant for the therapeutic targeting of adipose tissue inflammatory pathways.

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The contribution of IL-6 to beta 3 adrenergic receptor mediated adipose tissue remodeling

Cited by 19 publications

References 44 publications

Habitual physical activity protects against lipopolysaccharide-induced inflammation in mouse adipose tissue

Habitual physical activity protects against lipopolysaccharide-induced inflammation in mouse adipose tissue

Voluntary wheel running attenuates lipopolysaccharide-induced liver inflammation in mice

Jak-TGFβ cross-talk links transient adipose tissue inflammation to beige adipogenesis

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