Regulation of hepatocyte growth factor expression by NF-κB and PPARγ in adipose tissue

Yin, Jun; Lee, Jong Han; Zhang, Jin; Gao, Zhan‐Guo; Polotsky, Vsevolod Y.; Ye, Jianping

doi:10.1152/ajpendo.00687.2013

Cited by 16 publications

(15 citation statements)

References 47 publications

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“…Activated Mfs produce HGF (Yin et al, 2014), which accelerates wound healing and MSC migration. We postulated that a plausible mechanism by which maresin-Ls restored the reparative functions of db/db Mfs might, in part, be augmenting pro-healing growth factor production.…”

Section: Resultsmentioning

confidence: 99%

Maresin-like Lipid Mediators Are Produced by Leukocytes and Platelets and Rescue Reparative Function of Diabetes-Impaired Macrophages

Hong

Lü

Tian

et al. 2014

Chemistry & Biology

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SUMMARY Non-healing diabetic wounds are associated with impaired macrophage (Mf) function. Leukocytes and platelets (PLT) play crucial roles in wound healing by poorly understood mechanisms. Here, we report identification and characterization of novel maresin-like(L) mediators 14,22-dihydroxy-docosa-4Z,7Z,10Z,12E,16Z,19Z-hexaenoic acids, 14S,22-diHDHA (maresin-L1) and 14R,22-diHDHA (maresin-L2) that are produced by leukocytes and PLT and involved in wound healing. We show that 12-lipoxygenase-initiated 14S-hydroxylation or cytochrome P450 catalyzed 14R-hydroxylation, and P450-initiated ω(22)-hydroxylation are required for maresin-Ls biosynthesis. Maresin-L treatment restores reparative functions to diabetic Mfs, suggesting that maresin-Ls act as autocrine/paracrine factors responsible for, at least in part, the reparative functions of leukocytes and PLT in wounds. Additionally, maresin-L ameliorates Mfs inflammatory activation and have the potential to suppress the chronic inflammation in diabetic wounds caused by activation of Mfs. These findings provide initial insights into maresin-L biosynthesis and mechanism of action, and potentially offer a therapeutic option for better treatment of diabetic wounds.

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Section: Resultsmentioning

confidence: 99%

Maresin-like Lipid Mediators Are Produced by Leukocytes and Platelets and Rescue Reparative Function of Diabetes-Impaired Macrophages

Hong

Lü

Tian

et al. 2014

Chemistry & Biology

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“…Firstly, we analysed the classic pathway in chronic inflammatory processes involving NF-κB. 41,42 The literature provides detailed evidence that the NF-κB pathway in adipose tissue is modulated in obesity, 26,43,44 and the same signal route is suggested to be augmented in the adipose tissue of cachectic patients and animals. 14,34 Our results confirm that increased pro-inflammatory cytokine content in the adipose tissue was accompanied by higher expression of transcription factors key proteins, such as NF-κB p65.…”

Section: Discussionmentioning

confidence: 99%

White adipose tissue cells and the progression of cachexia: inflammatory pathways

Neves¹,

Neto

Yamashita

et al. 2015

Journal of Cachexia, Sarcopenia and Muscle

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BackgroundCachexia is a systemic syndrome leading to body wasting, systemic inflammation, and to metabolic chaos. It is a progressive condition, and little is known about its dynamics. Detection of the early signs of the disease may lead to the attenuation of the associated symptoms. The white adipose tissue is an organ with endocrine functions, capable of synthesising and secreting a plethora of proteins, including cytokines, chemokines, and adipokines. It is well established that different adipose tissue depots demonstrate heterogeneous responses to physiological and pathological stimuli. The present study aimed at providing insight into adipocyte involvement in inflammation along the progression of cachexia.MethodsEight‐weeks‐old male rats were subcutaneously inoculated with a Walker 256 carcinosarcoma cell suspension (2 × 107 cells in 1.0 mL; tumour‐bearing, T) or Phosphate‐buffered saline (control, C). The retroperitoneal, epididymal, and mesenteric adipose pads were excised on Days 0, 7, and 14 post‐tumour cell injection, and the adipocytes were isolated.ResultsMesenteric and epididymal adipocytes showed up‐regulation of IL‐1β protein expression and activation of the inflammasome pathway, contributing for whole tissue inflammation. The stromal vascular fraction of the retroperitoneal adipose tissue, on the other hand, seems to be the major contributor for the inflammation in this specific pad.ConclusionAdipocytes seem to play a relevant role in the establishment of white adipose tissue inflammation, through the activation of the NF‐κB and inflammasome pathways. In epididymal adipocytes, induction of the inflammasome may be detected already on Day 7 post‐tumour cell inoculation.

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“…As a major type of inflammatory cells, macrophages produce angiogenic factors, such as PDGF (34), HGF (35,36), and TGF-β (27,36). Macrophages are required for adipose tissue growth in lean mice (37,38) and obese mice (34).…”

Section: Obesitymentioning

confidence: 99%

Regulation of energy balance by inflammation: Common theme in physiology and pathology

Wang

2014

Rev Endocr Metab Disord

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119

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Inflammation regulates energy metabolism in both physiological and pathological conditions. Pro-inflammatory cytokines involves in energy regulation in several conditions, such as obesity, aging (calorie restriction), sports (exercise), and cancer (cachexia). Here, we introduce a view of integrative physiology to understand pro-inflammatory cytokines in the control of energy expenditure. In obesity, chronic inflammation is derived from energy surplus that induces adipose tissue expansion and adipose tissue hypoxia. In addition to the detrimental effect on insulin sensitivity, pro-inflammatory cytokines also stimulate energy expenditure and facilitate adipose tissue remodeling. In caloric restriction (CR), inflammatory status is decreased by low energy intake that less energy supply to immune cells, which favors energy saving in the body under caloric restriction. During physical exercise, inflammatory status is elevated due to muscle production of pro-inflammatory cytokines, which promote fatty acid mobilization from adipose tissue to meet the muscle energy demand. In cancer cachexia, chronic inflammation is elevated by the immune response in the fight against cancer. The energy expenditure from chronic inflammation contributes to weight loss. Immune tolerant cancer cells gains more nutrients during the inflammation. In these conditions, inflammation coordinates energy distribution and energy demand between tissues. If the body lacks response to the pro-inflammatory cytokines (Inflammation Resistance), the energy metabolism will be impaired leading to an increased risk for obesity. In contrast, super-induction of the inflammation activity leads to weight loss and malnutrition in cancer cachexia. In summary, inflammation is a critical component in the maintenance of energy balance in the body. Literature is reviewed in above fields to support this view.

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Regulation of hepatocyte growth factor expression by NF-κB and PPARγ in adipose tissue

Cited by 16 publications

References 47 publications

Maresin-like Lipid Mediators Are Produced by Leukocytes and Platelets and Rescue Reparative Function of Diabetes-Impaired Macrophages

Maresin-like Lipid Mediators Are Produced by Leukocytes and Platelets and Rescue Reparative Function of Diabetes-Impaired Macrophages

White adipose tissue cells and the progression of cachexia: inflammatory pathways

Regulation of energy balance by inflammation: Common theme in physiology and pathology

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