Autotaxin Is Released from Adipocytes, Catalyzes Lysophosphatidic Acid Synthesis, and Activates Preadipocyte Proliferation

Ferry, Gilles; Tellier, Edwige; Try, Anne; Grès, Sandra; Naime, Isabelle; Simon, Marie; Rodriguez, Marianne; Boucher, Jérémie; Tack, Ivan; Gesta, Stéphane; Chomarat, Pascale; Dieu, Marc; Raes, Martine; Galizzi, J P; Valet, Philippe; Boutin, Jean A.; Saulnier-Blache, Jean Sébastien

doi:10.1074/jbc.m301158200

Cited by 212 publications

(213 citation statements)

References 42 publications

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“…We demonstrated that the expression of autotaxin was substantially up-regulated during adipocyte differentiation in culture, as well as in adipocytes from obese, diabetic db/ db mice when compared to non-obese mice [2]. These observations suggested a possible involvement of autotaxin in the normal or pathological development of adipose tissue and/or pathologies associated with obesity.…”

Section: Introductionmentioning

confidence: 64%

“…We obtained 3T3F442A adipocytes as previously described [2]. Briefly, confluent 3T3F442A preadipocytes were cultured in a differentiating medium consisting of DMEM supplemented with 10% fetal calf serum plus 50 nmol/l insulin.…”

Section: Cell Linesmentioning

confidence: 99%

“…3T3F442A adipocytes were used after 7 days of culture. African green monkey (COS-7) cells were grown in DMEM supplemented with 10% FCS and transfected with pcDNA3 (Invitrogen) or with pcDNA-m autotaxin-FLAG [2], using DEAE dextran as previously reported [2].…”

Section: Cell Linesmentioning

confidence: 99%

“…Our group has described the existence of a new adipokine: autotaxin [2], which is a soluble protein of 120 M r belonging to the ectonucleotide-pyrophosphate pyrophosphatase phosphodiesterase (ENPP) family [3]. Autotaxin catalyses a lysophospholipase D-activity [2,4,5] leading to the hydrolysis of lysophosphatidylcholine (LPC) into lysophosphatidic acid (LPA), a bioactive phospholipid known to control several cellular events via activation of specific G-protein-coupled receptors [6].…”

Section: Introductionmentioning

confidence: 99%

“…Autotaxin catalyses a lysophospholipase D-activity [2,4,5] leading to the hydrolysis of lysophosphatidylcholine (LPC) into lysophosphatidic acid (LPA), a bioactive phospholipid known to control several cellular events via activation of specific G-protein-coupled receptors [6].…”

Section: Introductionmentioning

confidence: 99%

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Potential involvement of adipocyte insulin resistance in obesity-associated up-regulation of adipocyte lysophospholipase D/autotaxin expression

et al. 2005

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Aims/hypothesis: Autotaxin is a lysophospholipase D that is secreted by adipocytes and whose expression is substantially up-regulated in obese, diabetic db/db mice. The aim of the present study was to depict the physiopathological and cellular mechanisms involved in regulation of adipocyte autotaxin expression. Methods: Autotaxin mRNAs were quantified in adipose tissue from db/db mice (obese and highly diabetic type 2), gold-thioglucose-treated (GTG) mice (highly obese and moderately diabetic type 2), high-fat diet-fed (HFD) mice (obese and moderately diabetic type 2), streptozotocin-treated mice (thin and diabetic type 1), and massively obese humans with glucose intolerance. Results: When compared to non-obese controls, autotaxin expression in db/db mice was significantly increased, but not in GTG, HFD, or streptozotocin-treated mice. During db/db mice development, up-regulation of autotaxin occurred only 3 weeks after the emergence of hyperinsulinaemia, and simultaneously with the emergence of hyperglycaaemia. Adipocytes from db/db mice exhibited a stronger impairment of insulin-stimulated glucose uptake than non-obese and HFD-induced obese mice. Autotaxin expression was up-regulated by treatment with TNFα (insulin resistance-promoting cytokine), and down-regulated by rosiglitazone treatment (insulin-sensitising compound) in 3T3F442A adipocytes. Finally, adipose tissue autotaxin expression was significantly up-regulated in patients exhibiting both insulin resistance and impaired glucose tolerance. Conclusions/interpretation: The present work demonstrates the existence of a db/db-specific upregulation of adipocyte autotaxin expression, which could be related to the severe type 2 diabetes phenotype and adipocyte insulin resistance, rather than excess adiposity in itself. It also showed that type 2 diabetes in humans is also associated with up-regulation of adipocyte autotaxin expression.

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Section: Introductionmentioning

confidence: 64%

Section: Cell Linesmentioning

confidence: 99%

Section: Cell Linesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Potential involvement of adipocyte insulin resistance in obesity-associated up-regulation of adipocyte lysophospholipase D/autotaxin expression

et al. 2005

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Autotaxin is a novel target of microRNA‐101‐3p

Lyu

Zhang

2019

FEBS Open Bio

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Autotaxin (ATX), a vital enzyme that generates lysophosphatidic acid (LPA), affects many biological processes, including tumorigenesis, via the ATX–LPA axis. In this study, we demonstrate that microRNA‐101‐3p (miR‐101‐3p), a well‐known tumor suppressor, downregulates ATX expression at the posttranscriptional level. We found that miR‐101‐3p inhibits ATX regulation by directly targeting a conserved sequence in the ATX mRNA 3′UTR. Moreover, we observed an inverse correlation between ATX and miR‐101‐3p levels in various types of cancer cells. ATX is highly expressed in several human cancers. Here, we verified that ATX expression is significantly inhibited by miR‐101‐3p in U87 and HCT116 cells. ATX downregulation contributed to the suppression of migration, invasion, and proliferation mediated by miR‐101‐3p; furthermore, the tumor‐suppressing activity of miR‐101‐3p was partially reduced by the addition of LPA in U87 cells. Our data suggest that ATX is a novel target of miR‐101‐3p.

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