The expression of human brain vascular smooth muscle cell AT receptor after the UL83 gene of HCMV inhibition by small interfering RNAs.
OBJECTIVE
To explore the role of angiotensin receptors (AT1 and AT2) and human cytomegalovirus (HCMV) infection in atherosclerosis, and to observe effect of HCMV UL83 gene on angiotensin receptor AT receptors.


METHODS
Cell model of RNA interference (RNAi) HCMV UL83 gene was set up by transfection RNAi into HCMV infected human cerebral artery vascular smooth muscle cells cultured in vitro by application of transfection technique and adoption of RT-PCR, etc. Effect of HCMV on gene expression of AT1 and AT2 receptors in human cerebral artery vascular smooth muscle cells cultured in vitro under the action of Ganciclovir (GCV), AT1 and AT2 receptor antagonists by immunofluorescence technique, RT-PCR and protein electrophoresis.


RESULTS
The duplication and protein expression of HCMV UL83 gene mRNA was successfully interfered using RNAi technique. After silencing HCMV UL83 gene, gene expression of AT1 receptor was down-regulated while that of AT2 was up-regulated. AT1 and AT2 receptor antagonists and GCV, under certain condition, could inhibit the activation on AT1 and AT2 receptor in human cerebral artery vascular smooth muscle cells induced by HCMV infection.


CONCLUSIONS
Cell model of HCMV infected UL83 silence gene was successfully set up in human cerebral artery vascular smooth muscle cells cultured in vitro. HCMV UL83 might play a role by activating AT1 receptor and inhibiting expression of AT2 receptor.
Wang
Jiawei
J
Department of Neurology, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Tuo
Houzhen
H
Wang
Ruijin
R
Li
Weirong
W
Feng
Zijing
Z
Chen
Jun
J
Wang
Dexin
D
D050197:Atherosclerosis / Q000378:metabolism / Q000821:virology; D015153:Blotting, Western; D002478:Cells, Cultured; D002536:Cerebral Arteries / Q000166:cytology; D003587:Cytomegalovirus / Q000235:genetics* / Q000502:physiology; D042783:Endothelial Cells / Q000378:metabolism / Q000821:virology; D015870:Gene Expression; D054884:Host-Pathogen Interactions; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism* / Q000821:virology; D010750:Phosphoproteins / Q000235:genetics*; D034622:RNA Interference; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics / Q000378:metabolism; D044139:Receptor, Angiotensin, Type 2 / Q000235:genetics / Q000378:metabolism; D011945:Receptors, Angiotensin / Q000235:genetics* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014162:Transfection / Q000379:methods; D014763:Viral Matrix Proteins / Q000235:genetics*
D010750:Phosphoproteins; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin; D014763:Viral Matrix Proteins; C065418:cytomegalovirus matrix protein 65kDa