Heme oxygenase-2/adiponectin protein–protein interaction in metabolic syndrome

► HO-2 knockout mice present a metabolic syndrome-like phenotype. ► Inhibition of both HO-1 and HO-2 decreased adiponectin formation. ► Existence of protein–protein interaction between adiponectin and HO-2. ► HO-2 acts as a molecular chaperone. ► Increasing information on protein–protein complexes w...

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Vydané v:	Biochemical and biophysical research communications Ročník 432; číslo 4; s. 606 - 611
Hlavní autori:	Vanella, Luca, Li Volti, Giovanni, Guccione, Salvatore, Rappazzo, Giancarlo, Salvo, Eliana, Pappalardo, Morena, Forte, Stefano, Schwartzman, Michal L., Abraham, Nader G.
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States Elsevier Inc 22.03.2013
Predmet:	adipocytes adipogenesis Adiponectin Adiponectin - genetics Adiponectin - metabolism adipose tissue Animals anti-inflammatory activity culture media heme Heme oxygenase heme oxygenase (biliverdin-producing) Heme Oxygenase (Decyclizing) - genetics Heme Oxygenase (Decyclizing) - metabolism Heme Oxygenase-1 - genetics Heme Oxygenase-1 - metabolism insulin resistance lipid content Membrane Proteins - genetics Membrane Proteins - metabolism Metabolic syndrome Metabolic Syndrome - metabolism Mice Mice, Inbred C57BL Mice, Mutant Strains molecular chaperones obesity Protein interactions protein-protein interactions RNA, Small Interfering - genetics secretion small interfering RNA stem cells subcutaneous fat Two-Hybrid System Techniques MSCs HO ROS Heme oxygenase CoPP Metabolic syndrome Protein interactions Adiponectin
ISSN:	0006-291X, 1090-2104, 1090-2104
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Shrnutí:	► HO-2 knockout mice present a metabolic syndrome-like phenotype. ► Inhibition of both HO-1 and HO-2 decreased adiponectin formation. ► Existence of protein–protein interaction between adiponectin and HO-2. ► HO-2 acts as a molecular chaperone. ► Increasing information on protein–protein complexes will lead to the designing of new drugs. Insulin resistance with adipose tissue dysfunction and dysregulation in the production and secretion of adipokines is one of the hallmarks of metabolic syndrome. We have previously reported that increased levels of the heme oxygenase (HO) system, HO-1/HO-2 results in increased levels of adiponectin. Despite documentation of the existence of the anti-inflammatory axis HO-adiponectin, a possible protein–protein interaction between HO and adiponectin has not been examined. Here, we investigated the existence of protein interactions between HO-2 and adiponectin in the maintenance of adipocyte function during metabolic syndrome by integrating phenotypic and in silico studies. Compared to WT animals, HO-2 null mice displayed an increase in both visceral and subcutaneous fat content and reduced circulating adiponectin levels. The decrease in adiponectin was reversed by upregulation of HO-1. HO-2 depletion was associated with increased adipogenesis in cultured mesenchymal stem cells (MSCs) and decreased adiponectin levels in the culture media. In addition, HO-1 siRNA decreased adiponectin release. HO-2 was found to bind to the monomeric form of adiponectin, according to poses and calculated energies. HO-2-adiponectin interactions were validated by the two-hybrid system assay. In conclusion, protein–protein interactions between HO-2 and adiponectin highlight the role of HO-2 as a molecular chaperone for adiponectin assembly, while HO-1 increases adiponectin levels. Thus, crosstalk between HO-2 and HO-1 could be manipulated in a therapeutic approach to ameliorate the deleterious effects of obesity and the metabolic syndrome.
Bibliografia:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0006-291X 1090-2104 1090-2104
DOI:	10.1016/j.bbrc.2013.02.037