Adiponectin Protein Exists in Aortic Endothelial Cells

Noriyuki Komura,Norikazu Maeda,Iichiro Shimomura,Yoshihiro Tochino,Takuya Mori,Ayumu Hirata,Shinji Kihara,Tohru Funahashi,Hideaki Nakatsuji,Reury Fp Bacurau

doi:10.1371/journal.pone.0071271

Abstract

AimsInflammation is closely associated with the development of atherosclerosis and metabolic syndrome. Adiponectin, an adipose-derived secretory protein, possesses an anti-atherosclerotic property. The present study was undertaken to elucidate the presence and significance of adiponectin in vasculature.Methods and ResultsImmunofluorescence staining was performed in aorta of wild-type (WT) mice and demonstrated that adiponectin was co-stained with CD31. Thoracic aorta was cut through and then aortic intima was carefully shaved from aorta. Western blotting showed the existence of adiponectin protein in aortic intima, while there was no adiponectin mRNA expression. Adiponectin knockout (Adipo-KO) and WT mice were administered with a low-dose and short-term lipopolysaccharide (LPS) (1 mg/kg of LPS for 4 hours). The endothelium vascular adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were highly increased in Adipo-KO mice compared to WT mice after LPS administration.ConclusionsAdiponectin protein exists in aortic endothelium under steady state and may protect vasculature from the initiation of atherosclerosis.

Highlights

Obesity is the most common nutritional disorder in the industrial countries and is the common basis of atherosclerotic cardiovascular diseases [1]
Adiponectin protein exists in aortic endothelium under steady state and may protect vasculature from the initiation of atherosclerosis
Adiponectin was detected in aortic intima of wild-type (WT) mice and was costained with CD31 (Figure 1A upper panels), while adiponectin staining was absent in aortic intima of Adipo-KO mice as negative control (Figure 1A lower panels)

Summary

Introduction

Obesity is the most common nutritional disorder in the industrial countries and is the common basis of atherosclerotic cardiovascular diseases [1]. Adiponectin plays a central role in the development of metabolic syndrome and atherosclerosis [4]. We and others have suggested that low level of plasma adiponectin is closely associated with cardiovascular diseases and metabolic syndrome [5–8]. Chronic low-grade inflammation is closely associated with the development of metabolic syndrome and atherosclerosis [9]. Several studies reported that the exposure to LPS induces systemic inflammation, leading to the development of obesity-related disorders such as diabetes and atherosclerosis [10–15]. LPS accelerates the initial step of atherosclerosis through the increase of endothelial adhesion molecules. Adiponectin attractively suppressed the attachment of monocytes to endothelial cells, suggesting that adiponectin inhibits the initial step of atherosclerosis [6,18]. Little is known about the in vivo effect of adiponectin on LPS-induced increase of endothelial adhesion molecules in vasculature

Methods

Results

Conclusion