Matrix Metalloproteinases Are Differentially Expressed in Adipose Tissue during Obesity and Modulate Adipocyte Differentiation

Chavey, Carine; Mari, Bernard; Monthouel, Marie-Noëlle; Bonnafous, Stéphanie; Anglard, Patrick; Obberghen, Emmanuel Van; Tartare‐Deckert, Sophie

doi:10.1074/jbc.m209196200

Cited by 400 publications

(396 citation statements)

References 41 publications

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“…In the same study, Alexander et al noted that MMP3 Ϫ/Ϫ mice backcrossed onto another background (FVB/N) became obese with age (17). In contrast to our study, both Maquoi et al (5), in an earlier study, and Chavey et al (4) found that MMP3 expression levels were upregulated in adipose tissue isolated from obese mice. The reasons for these disparities with our results are unclear.…”

Section: Discussioncontrasting

confidence: 74%

“…However, we have previously shown that the expression level of endothelial cell-specific molecule 2, a corollary of endothelial contamination, was consistent among these subjects (14). MMPs may play an important role in adipose tissue remodeling (4,5). In two previous studies, Chavey et al (4) and Maquoi et al (5) examined the expression levels of various MMPs and TIMPs (tissue inhibitors of MMP) in adipose tissue from mouse models of obesity.…”

Section: Discussionmentioning

confidence: 87%

“…One of the genes most notably upregulated in preadipocytes/stromal vascular cells isolated from obese subjects was MMP9, and this upregulation was confirmed by real-time PCR (3). Matrix metalloproteinase 9 (MMP9) is a member of a large family of MMPs, which have been proposed to be involved in adipose tissue remodeling (4,5). Therefore, other MMP family members, in addition to MMP9, may potentially contribute to the etiology of obesity (4,5).…”

mentioning

confidence: 92%

“…Matrix metalloproteinase 9 (MMP9) is a member of a large family of MMPs, which have been proposed to be involved in adipose tissue remodeling (4,5). Therefore, other MMP family members, in addition to MMP9, may potentially contribute to the etiology of obesity (4,5).…”

mentioning

confidence: 99%

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Differential Expression of Matrix Metalloproteinase 3 (MMP3) in Preadipocytes/Stromal Vascular Cells From Nonobese Nondiabetic Versus Obese Nondiabetic Pima Indians

et al. 2006

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Prior microarray studies comparing global gene expression patterns in preadipocytes/stromal vascular cells isolated from nonobese nondiabetic versus obese nondiabetic Pima Indians showed that matrix metalloproteinase 9 (MMP9) is upregulated in obese subjects. The current study targeted analysis of nine additional MMP genes that cluster to a region on chromosome 11q22 that is linked to BMI and percent body fat. Differential-display PCR showed that MMP3 is downregulated in preadipocytes/stromal vascular cells from obese subjects, and real-time PCR showed that MMP3 expression levels are negatively correlated with percent body fat. To determine whether variants within MMP3 are responsible for its altered expression, MMP3 was sequenced, and seven representative variants were genotyped in 1,037 Pima subjects for association analyses. Two variants were associated with both BMI and type 2 diabetes, and two additional variants were associated with type 2 diabetes alone; however, none of these variants were associated with MMP3 expression levels. We propose that the MMP3 pathway is altered in human obesity, but this alteration may be the result of a combination of genetic variation within the MMP3 locus itself, as well as variation in additional factors, either primary or secondary to obesity, that regulate expression of the MMP3 gene. Diabetes 55: 3160 -3165, 2006

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Section: Discussioncontrasting

confidence: 74%

Section: Discussionmentioning

confidence: 87%

mentioning

confidence: 92%

mentioning

confidence: 99%

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Differential Expression of Matrix Metalloproteinase 3 (MMP3) in Preadipocytes/Stromal Vascular Cells From Nonobese Nondiabetic Versus Obese Nondiabetic Pima Indians

et al. 2006

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“…23 mRNA levels for MMP-2, MMP-3, MMP-12, MMP-14, MMP-19 and TIMP-1 are strongly induced in obese adipose tissues in a genetic or a diet-induced model of obesity. 24 The treatment of cultured preadipocytes with either synthetic MMP inhibitors or neutralizing antibodies decreases differentiation. 22 These previous studies using cultured adipocytes suggest that MMP activity is required for adipocyte conversion.…”

Section: Discussionmentioning

confidence: 99%

Macrophages regulate tumor necrosis factor-α expression in adipocytes through the secretion of matrix metalloproteinase-3

et al. 2008

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Objective: Adipocytes accumulated in the visceral area change their function to induce tumor necrosis factor-a (TNF-a) secretion with concomitant matrix metalloproteinase (MMP)-3 induction in mice. This study was performed to clarify the role of macrophages (Mf)-secreted MMP on the functional changes in adipocytes using a culture system. Design: Cultures of 3T3-L1 adipocytes with THP-1 Mf or the Mf-conditioned medium were used to investigate the role of Mf-MMP on the TNF-a gene in 3T3-L1 adipocytes by the addition of MMP inhibitors. For animal experiments, male C57BL/6J mice were rendered insulin resistant by feeding a high-fat diet, and the expression of an Mf marker F4/80, and MMP-3 genes in mesenteric and subcutaneous fat tissue specimens were examined. Results: Mf-conditioned media (Mf-CM) increased the levels of TNF-a mRNA expression in 3T3-L1 adipocytes, and these adipocyte responses were abolished by treatment with GM6001, a broad-spectrum MMP inhibitor, or NNGH (N-isobutyl-N-(4-methoxyphenylsulfonyl)-glycylhydroxamic acid), an MMP-3 inhibitor. The activated form of MMP-3 enhanced glycerol release as well as TNF-a protein secretion from 3T3-L1 adipocytes. The incubation of adipocytes with MMP-3 inhibited insulin-induced glucose uptake in adipocytes. Furthermore, a high-fat intake increased the expression of MMP-3, decreased the insulin-induced glucose uptake of adipocytes and induced expression of F4/80 in mesenteric fat tissue of C57BL/6 mice. Conclusion: Mf may cause a pathological link with surrounding adipocytes through the secretion of MMP-3 followed by TNF-a expression in adipocytes in visceral fat tissue.

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Adipose Tissue in Health and Disease

Leff¹,

Granneman²

2010

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Obesity, being an epidemy these days, is the trigger of metabolic disturbances such as cardiovascular disease, type 2 diabetes, and insulin resistance. Defined as an increase in fat storage, adipose tissue has been put under the spotlight as the culprit of these conditions, as it is composed not only by adipocytes but of any immune system cell and a singular extracellular matrix. Its behavior under acute and chronic hypercaloric states is quite different; persistent hypertrophy in the latter creates hypoxia, resulting in the release of reactive oxygen species and proinflammatory cytokines that impact on the immune response type of the resident leucocytes, mainly macrophages. Hypertrophy over hyperplasia, adipose tissue macrophages-M1 phenotype polarization, and the adipokines/myokines profile are thought to be regulated by foreign microRNAs, delivered from surrounding or distant cells by exosomes through the bloodstream. In this chapter, we focus on adipose tissue immunometabolism and how obesity causes the chronic inflammatory state, and, subsequently, this stablishes a pathologic adiposity, characterized by dyslipidemia and insulin resistance (IR).

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Matrix Metalloproteinases Are Differentially Expressed in Adipose Tissue during Obesity and Modulate Adipocyte Differentiation

Cited by 400 publications

References 41 publications

Differential Expression of Matrix Metalloproteinase 3 (MMP3) in Preadipocytes/Stromal Vascular Cells From Nonobese Nondiabetic Versus Obese Nondiabetic Pima Indians

Differential Expression of Matrix Metalloproteinase 3 (MMP3) in Preadipocytes/Stromal Vascular Cells From Nonobese Nondiabetic Versus Obese Nondiabetic Pima Indians

Macrophages regulate tumor necrosis factor-α expression in adipocytes through the secretion of matrix metalloproteinase-3

Adipose Tissue in Health and Disease

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