Microarray analysis identifies matrix metalloproteinases (MMPs) as key genes whose expression is up-regulated in human adipocytes by macrophage-conditioned medium

O’Hara, Adrian; Lim, Fei Ling; Mazzatti, Dawn J.; Trayhurn, Paul

doi:10.1007/s00424-009-0693-8

Cited by 97 publications

(111 citation statements)

References 52 publications

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“…In agreement with our results, an interesting study performed on the adipose tissue of mice reported the presence of several members of MMPs and TIMPs, except MMP-8 [26]. A microarray study showed that while various MMP family members were strongly upregulated in adipocytes in a culture-conditioned medium, MMP-8 upregulation was not observed [27]. These data support our findings and suggest that adipose tissue probably does not synthesize MMP-8 in amounts sufficient to interfere with MMP-8 systemic levels.…”

Section: Discussionsupporting

confidence: 92%

Evaluation of plasmatic MMP-8, MMP-9, TIMP-1 and MPO levels in obese and lean women

Andrade

Petruceli

Belo

et al. 2012

Clinical Biochemistry

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Section: Discussionsupporting

confidence: 92%

Evaluation of plasmatic MMP-8, MMP-9, TIMP-1 and MPO levels in obese and lean women

Andrade

Petruceli

Belo

et al. 2012

Clinical Biochemistry

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“…During AT expansion, the ECM actively remodels to accommodate the growth. We and others have demonstrated that several ECM components are upregulated during fat mass expansion in states of obesity (102,103). AT fibrosis, with its associated reduced plasticity, is therefore a key hallmark of the metabolically dysfunctional AT.…”

Section: Angiogenesis a Rate-limiting Step For At Expansion And Remomentioning

confidence: 89%

Adipose tissue remodeling and obesity

Sun¹,

Kusminski²,

Scherer³

2011

J. Clin. Invest.

1,552

1,381

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To fulfill its role as the major energy-storing tissue, adipose has several unique properties that cannot be seen in any other organ, including an almost unlimited capacity to expand in a non-transformed state. As such, the tissue requires potent mechanisms to remodel, acutely and chronically. Adipocytes can rapidly reach the diffusional limit of oxygen during growth; hypoxia is therefore an early determinant that limits healthy expansion. Proper expansion requires a highly coordinated response among many different cell types, including endothelial precursor cells, immune cells, and preadipocytes. There are therefore remarkable similarities between adipose expansion and growth of solid tumors, a phenomenon that presents both an opportunity and a challenge, since pharmacological interventions supporting healthy adipose tissue adaptation can also facilitate tumor growth. IntroductionAdipose tissue (AT) can respond rapidly and dynamically to alterations in nutrient deprivation and excess through adipocyte hypertrophy and hyperplasia, thereby fulfilling its major role in wholebody energy homeostasis. AT remodeling is an ongoing process that is pathologically accelerated in the obese state, and thus, features such as reduced angiogenic remodeling, ECM overproduction, a heightened state of immune cell infiltration and subsequent proinflammatory responses prevail in many obese fat-pads (1). However, not all AT expansion is necessarily associated with pathological changes. The concept of the "metabolically healthy obese" state (2) suggests that some individuals can preserve systemic insulin sensitivity on the basis of "healthy" AT expansion, bypassing all of the aforementioned pathological consequences associated with obesity (3), thereby also avoiding the obesity-associated lipotoxic side effects. Many physiologically relevant processes important for human AT remodeling can be studied in rodent models, with the added advantage that processes related to AT expansion and reduction can occur at an extremely rapid rate. A 24-hour fast in a mouse is associated with a dramatic loss of AT mass and an acute remodeling process that involves rapid infiltration of macrophages; moreover, merely 24 to 48 hours of exposure to a high-fat diet (HFD) can cause a prompt increase in adipocyte size (4). AT is therefore an ideal model system to study rapid alterations in tissue expansion and reduction, as it adapts to a differential nutrient supply. Here, we will focus on key aspects of the intricate dynamics of AT remodeling and subsequent inflammatory consequences that arise from obesity.

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“…MMP9 and PM20D1 are metalloproteinases. MMPs (including MMP9) are known to be upregulated in human adipocytes, 58 and have been associated with obesity in rodent models. 59,60 PRKG1, a guanosine 3 0 ,5 0 -monophosphate (cGMP)-dependent protein kinase is important in regulating foraging behavior, food acquisition and energy balance.…”

Section: Epigenetic Factors In Obesitymentioning

confidence: 99%

Epigenetic regulation in obesity

2011

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The availability to the DNA strand and the activity of the transcription machinery is crucial for the cell to use the information in the DNA. The epigenetic mechanisms DNA methylation, modification of histone tails, other chromatin-modifying processes and interference by small RNAs regulate the cell-type-specific DNA expression. Epigenetic marks can be more or less plastic perpetuating responses to various molecular signals and environmental stimuli, but in addition apparently stochastic epigenetic marks have been found. There is substantial evidence from animal and man demonstrating that both transient and more long-term epigenetic mechanisms have a role in the regulation of the molecular events governing adipogenesis and glucose homeostasis. Intrauterine exposure such as poor maternal nutrition has consistently been demonstrated to contribute to a particular epigenotype and thereby developmental metabolic priming of the exposed offspring in animal and man. Epigenetic modifications can be passed not only from one cell generation to the next, but metabolic disease-related epigenotypes have been proposed to also be transmitted germ-line. Future more comprehensive knowledge on epigenetic regulation will complement genome sequence data for the understanding of the complex etiology of obesity and related disorder.

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Microarray analysis identifies matrix metalloproteinases (MMPs) as key genes whose expression is up-regulated in human adipocytes by macrophage-conditioned medium

Cited by 97 publications

References 52 publications

Evaluation of plasmatic MMP-8, MMP-9, TIMP-1 and MPO levels in obese and lean women

Evaluation of plasmatic MMP-8, MMP-9, TIMP-1 and MPO levels in obese and lean women

Adipose tissue remodeling and obesity

Epigenetic regulation in obesity

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