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Resistin and adenylyl cyclase-associated protein 1 (CAP1) regulate the expression of genes related to insulin resistance in BNL CL.2 mouse liver cells.

ABSTRACT: Resistin is an adipokine produced in white adipose tissue that is thought to modulate insulin sensitivity in peripheral tissues (such as liver, skeletal muscle or adipose tissue). Human and murine resistin molecules share only about 60% sequence homology. [1] Contrary to humans, in which resistin is secreted mostly by macrophages, Park and Ahima 2013 resistin in rodents is produced primarily by the mature adipocytes of the white adipose tissue. Although resistin can bind to toll-like receptor 4 (TLF4) activating proinflammatory responses in human and rodents, [3], [4], [5], [6], [7], [8] the inflammatory actions of resistin in human monocytes were found to be mediated by resistin binding to adenylyl cyclase-associated protein 1 (CAP1). [9] In this study, we aimed to investigate the in vitro effects of resistin on the expression of various genes related to insulin resistance in mouse liver cells. Using BNL CL.2 cells, we investigated the effect of resistin in untransfected or CAP1 siRNA-transfected cells on the expression of 84 key genes involved in insulin resistance.

SUBMITTER: Avtanski D

PROVIDER: S-EPMC6595414 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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Resistin and adenylyl cyclase-associated protein 1 (CAP1) regulate the expression of genes related to insulin resistance in BNL CL.2 mouse liver cells.

Avtanski Dimiter D Chen Karin K Poretsky Leonid L

Data in brief 20190608

Resistin is an adipokine produced in white adipose tissue that is thought to modulate insulin sensitivity in peripheral tissues (such as liver, skeletal muscle or adipose tissue). Human and murine resistin molecules share only about 60% sequence homology. [1] Contrary to humans, in which resistin is secreted mostly by macrophages, Park and Ahima 2013 resistin in rodents is produced primarily by the mature adipocytes of the white adipose tissue. Although resistin can bind to toll-like receptor 4 ...[more]

PMID: 31294061

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Project description:Background and purposeDespite the view that only ?2- as opposed to ?1-adrenoceptors (?ARs) couple to G(i), some data indicate that the ?1AR-evoked inotropic response is also influenced by the inhibition of Gi. Therefore, we wanted to determine if Gi exerts tonic receptor-independent inhibition upon basal adenylyl cyclase (AC) activity in cardiomyocytes.Experimental approachWe used the Gs-selective (R,R)- and the Gs- and G(i)-activating (R,S)-fenoterol to selectively activate ?2ARs (?1AR blockade present) in combination with Gi inactivation with pertussis toxin (PTX). We also determined the effect of PTX upon basal and forskolin-mediated responses. Contractility was measured ex vivo in left ventricular strips and cAMP accumulation was measured in isolated ventricular cardiomyocytes from adult Wistar rats.Key resultsPTX amplified both the (R,R)- and (R,S)-fenoterol-evoked maximal inotropic response and concentration-dependent increases in cAMP accumulation. The EC50 values of fenoterol matched published binding affinities. The PTX enhancement of the Gs-selective (R,R)-fenoterol-mediated responses suggests that Gi regulates AC activity independent of receptor coupling to Gi protein. Consistent with this hypothesis, forskolin-evoked cAMP accumulation was increased and inotropic responses to forskolin were potentiated by PTX treatment. In non-PTX-treated tissue, phosphodiesterase (PDE) 3 and 4 inhibition or removal of either constitutive muscarinic receptor activation of Gi with atropine or removal of constitutive adenosine receptor activation with CGS 15943 had no effect upon contractility. However, in PTX-treated tissue, PDE3 and 4 inhibition alone increased basal levels of cAMP and accordingly evoked a large inotropic response.Conclusions and implicationsTogether, these data indicate that Gi exerts intrinsic receptor-independent inhibitory activity upon AC. We propose that PTX treatment shifts the balance of intrinsic G(i) and Gs activity upon AC towards Gs, enhancing the effect of all cAMP-mediated inotropic agents.

Dataset Information

Resistin and adenylyl cyclase-associated protein 1 (CAP1) regulate the expression of genes related to insulin resistance in BNL CL.2 mouse liver cells.

Publications

Resistin and adenylyl cyclase-associated protein 1 (CAP1) regulate the expression of genes related to insulin resistance in BNL CL.2 mouse liver cells.

Similar Datasets

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