Regulation and function of the cyclic nucleotide phosphodiesterase (PDE3) gene family

Shakur, Yasmin; Holst, Lena Stenson; Landström, Tova Rahn; Movsesian, Matthew A.; Degerman, Eva; Manganiello, Vincent C.

doi:10.1016/s0079-6603(00)66031-2

Cited by 194 publications

(198 citation statements)

References 183 publications

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“…Another component that contributes to complex and differential cAMP signaling, in addition to the presence of different cAMP effectors, is the phosphodiesterases which are differentially expressed in different cells [7,8]. Our results indicate that PDE3B and PDE4 control cAMP pools which negatively influence PKB phosphorylation induced primarily by insulin but to certain extent also by CL16243.…”

Section: Discussionmentioning

confidence: 74%

“…Adipocytes express mainly PDE3B and PDE4s. PDE3B, one of two members of the PDE3 family, has been shown to participate in a complex interplay between insulin and cAMP signalling networks, important for the regulation of insulin-induced glucose uptake and lipogenesis as well as insulin-induced inhibition of lipolysis in adipocytes [2,8]. On the other hand, little is known about the role for different PDE4 isoforms in adipocytes.…”

Section: Introductionmentioning

confidence: 99%

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Novel mechanisms of the regulation of Protein kinase B in adipocytes; implications for Protein kinase A, Epac, Phosphodiesterases 3 and 4

Zmuda-Trzebiatowska

Manganiello

Degerman

2007

Cellular Signalling

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Crosstalk between insulin and cAMP signalling pathways has a great impact on adipocyte metabolism. Whilst Protein kinase B (PKB) is a pivotal mediator of insulin action, in some cells regulation of PKB by cAMP has also been demonstrated. Here we provide evidence that, in a phosphatidyl inositol 3-kinase dependent manner, β3-adrenergic stimulation (using CL316243) in adipocytes induces PKB phosphorylation in the absence of insulin and also potentiates insulin-induced phosphorylation of PKB. Interestingly, insulin-and CL316243-induced PKB phosphorylation was found to be inhibited by pools of cAMP controlled by PDE3B and PDE4 (mainly in the context of insulin), whereas a cAMP pool controlling protein kinase A appeared to mediate stimulation of PKB phosphorylation (mainly in the context of CL316243).

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Section: Discussionmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Novel mechanisms of the regulation of Protein kinase B in adipocytes; implications for Protein kinase A, Epac, Phosphodiesterases 3 and 4

Zmuda-Trzebiatowska

Manganiello

Degerman

2007

Cellular Signalling

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“…Adipocytes express membrane-bound PDE3B and membrane bound as well as cytosolic PDE4s [3]. Insulin and cAMP-mediated activation of PDE3B has been shown to play an important role in the regulation of lipolysis, lipogenesis and glucose uptake in adipocytes [4][5][6]. Mechanisms for short-term regulation of PDE3B by insulin have been extensively studied and involve phosphatidylinositol 3-kinase (PI3K)-dependent phosphorylation and activation of the enzyme catalyzed by protein kinase B [7].…”

Section: Introductionmentioning

confidence: 99%

“…Mechanisms for short-term regulation of PDE3B by insulin have been extensively studied and involve phosphatidylinositol 3-kinase (PI3K)-dependent phosphorylation and activation of the enzyme catalyzed by protein kinase B [7]. Mechanisms for short-term regulation of PDE3B by cAMP may involve protein kinase A, Epacs (Exchange proteins directly activated by cAMP) and PKB [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Long-term regulation of cyclic nucleotide phosphodiesterase type 3B and 4 in 3T3-L1 adipocytes

Oknianska¹,

Zmuda-Trzebiatowska²,

Manganiello³

et al. 2007

Biochemical and Biophysical Research Communications

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Phosphodiesterase 3B (PDE3B), known to play an important role in acute insulin and cAMP-mediated regulation of lipid metabolism, and PDE4 are the main PDE types expressed in adipocytes. Here we show that members of all PDE4 isoforms are expressed in 3T3-L1 and primary mouse adipocytes. Long-term treatment of 3T3-L1 adipocytes with insulin induced up-regulation of PDE3B and PDE4D in a phosphatidylinositol 3-kinase-dependent manner whereas long-term treatment with β-adrenergic agonists induced down-regulation of PDE3B and up-regulation of PDE4D. Thus, PDE3B and PDE4D can be added to the list of genes regulated by insulin and cAMP-increasing hormones. Altered expression of PDE3B and PDE4D in response to long-term treatment with insulin and catecholamines may contribute to altered regulation of metabolism in diabetes.

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“…La PDE3 est codée par deux gènes, PDE3A et PDE3B : la PDE3A est l'isoforme de PDE3 dominante au niveau cardiaque [18] ; la PDE3B est exprimée dans le coeur de souris [17]. Dans de nombreuses espèces animales dont l'homme, les inhibiteurs de PDE3 exercent des effets inotrope et lusitrope positifs puissants, et sont aussi capables de potentialiser les effets d'une stimulation -AR sur le CEC cardiaque [16].…”

Section: Régulation Du Couplage Excitation-contraction (Cec) Cardiaquunclassified

Rôle des phosphodiestérases des nucléotides cycliques de types 3 et 4 dans le couplage excitation-contraction et les arythmies cardiaques

et al. 2013

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> Les phosphodiestérases des nucléotides cycliques (PDE) constituent une superfamille d'enzymes spécialisées dans la dégradation de l'AMPc et du GMPc. Les PDE de types 3 et 4 sont les deux familles majeures impliquées dans la régulation des taux d'AMPc cardiaques et dans le contrôle de l'inotropisme. Les protéines de ces deux familles sont codées par plusieurs gènes. Des études récentes du phénotype cardiaque de souris invalidées pour ces différents gènes ont permis de mieux comprendre leur rôle dans la régulation des acteurs du couplage excitationcontraction (CEC) cardiaque. En particulier, ces travaux soulignent le caractère local de la régu-lation des acteurs du CEC par les PDE, ainsi que leur rôle dans le maintien de l'homéostasie calcique intracellulaire et la prévention des troubles du rythme. < tégration du Ca 2+ dans ce compartiment, tandis que le reste du Ca 2+ est extrudé, principalement par l'échangeur Na + -Ca 2+ (NCX) et, dans une moindre mesure, par les pompes calciques de la membrane plasmique (PMCA) [2] (Figure 1). Ce processus, appelé couplage excitation-contraction (CEC), est sous le contrôle de la voie de l'adénosine 3',5'-monophosphate cyclique (AMPc) qui constitue un relais essentiel de la régulation nerveuse du coeur. La libération de noradrénaline des terminaisons sympathiques ou la décharge d'adrénaline par les glandes surrénales activent les récepteurs -adrénergiques (-AR), entraînant une activation, via les protéines G stimulatrices (G s ), des adénylate cyclases (AC) responsables de la synthèse d'AMPc. Classiquement, l'effet inotrope positif de l'AMPc est attribué à l'activation de la protéine kinase dépendante de l'AMPc (PKA) qui phosphoryle les LTCC et les RyR2, conduisant à une augmentation de la [Ca 2+ ] i et donc de la contraction. La PKA phosphoryle aussi le phospholamban (PLB), ce qui lève l'inhibition tonique exercée par cette protéine sur la SERCA2 et accélère le repompage du Ca 2+ dans le RS. Enfin, la PKA phosphoryle la troponine I (TnI) au niveau des myofilaments, ce qui diminue leur affinité pour le Ca 2+ . La phosphorylation du PLB et de la TnI concourent à une accélération

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Regulation and function of the cyclic nucleotide phosphodiesterase (PDE3) gene family

Cited by 194 publications

References 183 publications

Novel mechanisms of the regulation of Protein kinase B in adipocytes; implications for Protein kinase A, Epac, Phosphodiesterases 3 and 4

Novel mechanisms of the regulation of Protein kinase B in adipocytes; implications for Protein kinase A, Epac, Phosphodiesterases 3 and 4

Long-term regulation of cyclic nucleotide phosphodiesterase type 3B and 4 in 3T3-L1 adipocytes

Rôle des phosphodiestérases des nucléotides cycliques de types 3 et 4 dans le couplage excitation-contraction et les arythmies cardiaques

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