PMID- 21030878
OWN - NLM
STAT- MEDLINE
DCOM- 20110329
LR  - 20220408
IS  - 1708-8267 (Electronic)
IS  - 1081-5589 (Linking)
VI  - 58
IP  - 8
DP  - 2010 Dec
TI  - MicroRNA-155 silencing enhances inflammatory response and lipid uptake in 
      oxidized low-density lipoprotein-stimulated human THP-1 macrophages.
PG  - 961-7
LID - 10.231/JIM.0b013e3181ff46d7 [doi]
AB  - It has been proposed that the inflammatory response of monocytes/macrophages 
      induced by oxidized low-density lipoprotein (oxLDL) is a key event in the 
      pathogenesis of atherosclerosis. MicroRNA-155 (miR-155) is an important regulator 
      of the immune system and has been shown to be involved in acute inflammatory 
      response. However, the function of miR-155 in oxLDL-stimulated inflammation and 
      atherosclerosis remains unclear. Here, we show that the exposure of human THP-1 
      macrophages to oxLDL led to a marked up-regulation of miR-155 in a dose-dependent 
      manner. Silencing of endogenous miR-155 in THP-1 cells using locked nucleic 
      acid-modified antisense oligonucleotides significantly enhanced oxLDL-induced 
      lipid uptake, up-regulated the expression of scavenger receptors (lectinlike 
      oxidized LDL receptor-1, cluster of differentiation 36 [CD36], and CD68), and 
      promoted the release of several cytokines including interleukin (IL)-6, -8, and 
      tumor necrosis factor alpha (TNF-alpha). Luciferase reporter assay showed that targeting 
      miR-155 promoted nuclear factor-kappa B (NF-kappaB) nuclear translocation and 
      potentiated the NF-kappaB-driven transcription activity. Moreover, miR-155 knockdown 
      resulted in a marked increase in the protein amount of myeloid differentiation 
      primary response gene 88 (MyD88), an important adapter protein used by Toll-like 
      receptors to activate the NF-kappaB pathway. Our data demonstrate that miR-155 serves 
      as a negative feedback regulator in oxLDL-stimulated THP-1 inflammatory responses 
      and lipid uptake and thus might have potential therapeutic implications in 
      atherosclerosis.
FAU - Huang, Ri-sheng
AU  - Huang RS
AD  - Department of Thoracic Surgery, Wenzhou Second People's Hospital, Wenzhou, China.
FAU - Hu, Guan-qiong
AU  - Hu GQ
FAU - Lin, Bin
AU  - Lin B
FAU - Lin, Zhi-yi
AU  - Lin ZY
FAU - Sun, Cheng-chao
AU  - Sun CC
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Investig Med
JT  - Journal of investigative medicine : the official publication of the American 
      Federation for Clinical Research
JID - 9501229
RN  - 0 (Cytokines)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (MIRN155 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (oxidized low density lipoprotein)
SB  - IM
MH  - Blotting, Western
MH  - Cell Line, Tumor
MH  - Chromatography, High Pressure Liquid
MH  - Cytokines/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Gene Expression Regulation/drug effects
MH  - Gene Knockdown Techniques
MH  - Gene Silencing/*drug effects
MH  - Humans
MH  - Inflammation/*chemically induced/genetics/metabolism
MH  - Lipid Metabolism/*drug effects
MH  - Lipoproteins, LDL/*pharmacology
MH  - Macrophages/*drug effects/metabolism
MH  - MicroRNAs/*genetics
MH  - Transfection
EDAT- 2010/10/30 06:00
MHDA- 2011/03/30 06:00
CRDT- 2010/10/30 06:00
PHST- 2010/10/30 06:00 [entrez]
PHST- 2010/10/30 06:00 [pubmed]
PHST- 2011/03/30 06:00 [medline]
AID - 10.231/JIM.0b013e3181ff46d7 [doi]
PST - ppublish
SO  - J Investig Med. 2010 Dec;58(8):961-7. doi: 10.231/JIM.0b013e3181ff46d7.