Tribbles expression in cumulus cells is related to oocyte maturation and fatty acid metabolism

Brisard, Daphné; Chesnel, Franck; Elis, Sébastien; Desmarchais, Alice; Sánchez-Lazo, Laura; Chasles, Manon; Maillard, Virginie; Uzbekova, Svetlana

doi:10.1186/1757-2215-7-44

Cited by 28 publications

(17 citation statements)

References 61 publications

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“…We hypothesize that in the COC, FAO may undergo an initial increase in activity as a response to etomoxir, increasing transcription of essential FAO genes, and briefly metabolizing lipids before inhibition. This hypothesis is supported by recent reports in mouse COC where expression of genes involved in FAO were altered after FAO inhibition (Brisard et al 2014). Abundance of genes involved in FAO is also increased in COC after treatment with rosiglitazone, an agent known to inhibit FAO (Dunning et al 2014).…”

Section: Discussionsupporting

confidence: 78%

Fatty acid metabolism during maturation affects glucose uptake and is essential to oocyte competence

Paczkowski¹,

Schoolcraft²,

Krisher³

2014

Reproduction

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Fatty acid b-oxidation (FAO) is essential for oocyte maturation in mice. The objective of this study was to determine the effect of etomoxir (a FAO inhibitor; 100 mM), carnitine (1 mM), and palmitic acid (1 or 100 mM) during maturation on metabolism and gene expression of the oocyte and cumulus cells, and subsequent embryo development in the mouse. Carnitine significantly increased embryo development, while there was a decrease in development following maturation with 100 mM palmitic acid or etomoxir (P!0.05) treatment. Glucose consumption per cumulus-oocyte complex (COC) was decreased after treatment with carnitine and increased following etomoxir treatment (P!0.05). Intracellular oocyte lipid content was decreased after carnitine or etomoxir exposure (P!0.05). Abundance of Slc2a1 (Glut1) was increased after etomoxir treatment in the oocyte and cumulus cells (P!0.05), suggesting stimulation of glucose transport and potentially the glycolytic pathway for energy production when FAO is inhibited. Abundance of carnitine palmitoyltransferase 2 (Cpt2) tended to increase in oocytes (PZ0.1) after treatment with 100 mM palmitic acid and in cumulus cells after exposure to 1 mM palmitic acid (PZ0.07). Combined with carnitine, 1 mM palmitic acid increased the abundance of Acsl3 (P!0.05) and Cpt2 tended to increase (PZ0.07) in cumulus cells, suggesting FAO was increased during maturation in response to stimulators and fatty acids. In conclusion, fatty acid and glucose metabolism are related to the mouse COC, as inhibition of FAO increases glucose consumption. Stimulation of FAO decreases glucose consumption and lipid stores, positively affecting subsequent embryo development, while an overabundance of fatty acid or reduced FAO negatively affects oocyte quality.

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Section: Discussionsupporting

confidence: 78%

Fatty acid metabolism during maturation affects glucose uptake and is essential to oocyte competence

Paczkowski¹,

Schoolcraft²,

Krisher³

2014

Reproduction

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“…Currently, three mammalian homologs of the tribbles gene are known. One of these, TRIB3, plays an important role in multiple signaling pathways, coordinating crucial cellular processes such as apoptosis, glucose and lipid metabolism, adipocyte differentiation, and cell stress (15,(24)(25)(26)(27). TRIB3 is overexpressed in many cancers, but whether TRIB3 is upregulated in GC has not been reported previously.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of TRIB3 promotes angiogenesis in human gastric cancer

et al. 2016

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Tribbles homolog 3 (TRIB3) plays important roles in many types of malignancies. However, whether TRIB3 is involved in the development or progression of gastric cancer (GC) remains unclear. In this study, we analyzed TRIB3 expression in GC tissues from 191 GC patients categorized with stage I to Ⅳ disease, to examine the role of TRIB3 in GC, and examined the relationship between TRIB3 and tumor angiogenesis. We found that TRIB3 expression was significantly higher in GC tissues than that in adjacent non-tumor tissues. TRIB3 expression was associated with VEGF-A and tumor microvessel density, as well as overall TNM stage, T stage, N stage, and distant metastasis in GC tissues. Furthermore, TRIB3 silencing downregulated VEGF-A expression in GC cells, which subsequently suppressed endothelial cell recruitment and vessel formation. In conclusion, overexpression of TRIB3 is associated with tumor angiogenesis and a poor prognosis in patients with GC. Our findings indicate that TRIB3 is a promising target for anti-angiogenic therapy in GC.

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“…Dunning et al () plus data herein showed that a major portion of FAO in the mouse cumulus‐oocyte complex derives from the cumulus cells. Expression of Cpt1b mRNA in the cumulus cells increases during meiotic maturation and Trib1 and Trib3 (Ser‐Thr kinases involved in FAO regulation) mRNA abundance increased in mouse cumulus cells during in vitro maturation, whereas Acaca transcript levels decreased under these conditions (Brisard et al, ). High FAO activity in cumulus cells suggests that these somatic cells are an important source of fatty acid‐derived energy during oocyte maturation.…”

Section: Discussionmentioning

confidence: 99%

Acetyl CoA carboxylase inactivation and meiotic maturation in mouse oocytes

Valsangkar

Downs

2015

Mol. Reprod. Dev.

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In mouse oocytes, meiotic induction by pharmacological activation of PRKA (adenosine monophosphate-activated protein kinase; formerly known as AMPK) or by hormones depends on stimulation of fatty acid oxidation (FAO). PRKA stimulates FAO by phosphorylating and inactivating acetyl CoA carboxylase (ACAC; formerly ACC), leading to decreased malonyl CoA levels and augmenting fatty-acid transport into mitochondria. We investigated a role for ACAC inactivation in meiotic resumption by testing the effect of two ACAC inhibitors, CP-640186 and Soraphen A, on mouse oocytes maintained in meiotic arrest in vitro. These inhibitors significantly stimulated the resumption of meiosis in arrested cumulus cell-enclosed oocytes, denuded oocytes, and follicle-enclosed oocytes. This stimulation was accompanied by an increase in FAO. Etomoxir, a malonyl CoA analogue, prevented meiotic resumption as well as the increase in FAO induced by ACAC inhibition. Citrate, an ACAC activator, and CBM-301106, an inhibitor of malonyl CoA decarboxylase, which converts malonyl CoA to acetyl CoA, suppressed both meiotic induction and FAO induced by follicle-stimulating hormone, presumably by maintaining elevated malonyl CoA levels. Mouse oocyte-cumulus cell complexes contain both isoforms of ACAC (ACACA and ACACB); when wild-type and Acacb(-/-) oocytes characteristics were compared, we found that these single-knockout oocytes showed a significantly higher FAO level and a reduced ability to maintain meiotic arrest, resulting in higher rates of germinal vesicle breakdown. Collectively, these data support the model that ACAC inactivation contributes to the maturation-promoting activity of PRKA through stimulation of FAO.

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Tribbles expression in cumulus cells is related to oocyte maturation and fatty acid metabolism

Cited by 28 publications

References 61 publications

Fatty acid metabolism during maturation affects glucose uptake and is essential to oocyte competence

Fatty acid metabolism during maturation affects glucose uptake and is essential to oocyte competence

Overexpression of TRIB3 promotes angiogenesis in human gastric cancer

Acetyl CoA carboxylase inactivation and meiotic maturation in mouse oocytes

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