caa a22 4500 606235566 CHVBK 20210128101243.0 cr unu---uuuuu 210128e20150901xx s 000 0 eng 10.1007/s11010-015-2467-2 doi (NATIONALLICENCE)springer-10.1007/s11010-015-2467-2 Rosiglitazone suppresses HIV-1 Tat-induced vascular inflammation via Akt signaling [Elektronische Daten] [Wen Huang, Xuean Mo, Xianghong Wu, Wenjing Luo, Yanlan Chen] Peroxisome proliferator-activated receptor gamma (PPARƔ) contributes to human immunodeficiency virus (HIV)-1-induced dysfunction of brain endothelial cells. The aim of the present study was to evaluate the protection mechanism of PPARƔ against Tat-induced responses of adhesion molecules. We measured the protein expressions of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 in human brain microvascular endothelial cells (hCMEC/D3) and C57BL/6J mouse brain microvessels with Western blotting and immunofluorescent labeling. The mRNA levels of ICAM-1 and VCAM-1 were determined by real-time reverse-transcriptase polymerase chain reaction. HIV-1 Tat induced overexpression of ICAM-1 but not VCAM-1 in both hCMEC/D3 and brain microvessels, this response was attenuated by treatment with the PPARƔ agonist rosiglitazone. Tat-mediated upregulation of ICAM-1 and VCAM-1 levels were abolished by the addition of PPARƔ antagonist GW9662 and the Akt inhibitor KP3721, indicating that Akt signaling is involved in the PPARƔ-mediated protection of Tat-induced adhesion molecule upregulation. These results show that Akt signaling plays a key role in PPARƔ's vascular inflammatory effects that contribute to blood-brain barrier damage. Springer Science+Business Media New York, 2015 Peroxisome proliferator-activated receptor gamma nationallicence Human immunodeficiency virus-1 Tat protein nationallicence Adhesion molecules nationallicence Brain endothelial cells nationallicence Akt signaling pathway nationallicence Huang Wen Department of Neurology, First Affiliated Hospital, Guangxi Medical University, 530021, Nanning, People's Republic of China aut Mo Xuean School of Nursing, First Affiliated Hospital, Guangxi Medical University, 530021, Nanning, People's Republic of China aut Wu Xianghong Department of Vasculocardiology, First Affiliated Hospital, Guangxi Medical University, #6 Shuangyong Road, 530021, Nanning, Guangxi, People's Republic of China aut Luo Wenjing Department of Neurology, First Affiliated Hospital, Guangxi Medical University, 530021, Nanning, People's Republic of China aut Chen Yanlan Department of Neurology, First Affiliated Hospital, Guangxi Medical University, 530021, Nanning, People's Republic of China aut Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 407/1-2(2015-09-01), 173-179 0300-8177 407:1-2<173 2015 407 11010 https://doi.org/10.1007/s11010-015-2467-2 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s11010-015-2467-2 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Huang Wen Department of Neurology, First Affiliated Hospital, Guangxi Medical University, 530021, Nanning, People's Republic of China aut NATIONALLICENCE 700 1- Mo Xuean School of Nursing, First Affiliated Hospital, Guangxi Medical University, 530021, Nanning, People's Republic of China aut NATIONALLICENCE 700 1- Wu Xianghong Department of Vasculocardiology, First Affiliated Hospital, Guangxi Medical University, #6 Shuangyong Road, 530021, Nanning, Guangxi, People's Republic of China aut NATIONALLICENCE 700 1- Luo Wenjing Department of Neurology, First Affiliated Hospital, Guangxi Medical University, 530021, Nanning, People's Republic of China aut NATIONALLICENCE 700 1- Chen Yanlan Department of Neurology, First Affiliated Hospital, Guangxi Medical University, 530021, Nanning, People's Republic of China aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 407/1-2(2015-09-01), 173-179 0300-8177 407:1-2<173 2015 407 11010