PMID- 29750294
OWN - NLM
STAT- MEDLINE
DCOM- 20181009
LR  - 20181009
IS  - 1791-244X (Electronic)
IS  - 1107-3756 (Linking)
VI  - 42
IP  - 2
DP  - 2018 Aug
TI  - LncRNA uc.48+ is involved in the diabetic immune and inflammatory responses 
      mediated by P2X7 receptor in RAW264.7 macrophages.
PG  - 1152-1160
LID - 10.3892/ijmm.2018.3661 [doi]
AB  - High glucose combined with high FFAs can contribute to the unfavorable 
      development of type 2 diabetes mellitus (T2DM) and monocytes/macrophages are 
      important in the occurrence and development of T2DM, which is regarded as a type 
      of low‑grade inflammation. Although our previous study demonstrated that 
      increased expression of P2X7 receptor (P2X7R) in peripheral blood monocytes may 
      alter the innate immune system and that long non‑coding (lnc)RNA uc.48+ was 
      involved in diabetic neuropathic pain, the involvement of uc.48+ mediated by the 
      P2X7R in monocyte/macrophages during T2DM has not been reported. In the present 
      study, the effectsof uc.48+ small interference RNA (siRNA) on factors, including 
      the mRNA and protein expression of P2X7R, apoptosis and proliferation, levels of 
      reactive oxygen species (ROS), cytokine levels, and expression of phosphorylated 
      (p‑) extracellular signal‑regulated kinase (ERK)1/2, were examined in RAW264.7 
      macrophages following exposure to high glucose and high plasma free fatty acids 
      (FFAs). After RAW264.7 cells were transfected with uc.48+ siRNA under high 
      glucose conditions and FFAs treatment, the mRNA expression levels of uc.48+ and 
      P2X7 receptor were detected by reverse transcription‑polymerase chain reaction. 
      The protein mass of P2X7 receptor and ERK signaling pathway were assessed by 
      western blotting. ROS and calcium concentrations, and culture supernatant 
      cytokine content [tumor necrosis factor‑alpha, interleukin (IL)‑10, IL‑1beta] were 
      detected by fluorescent probes and ELISA respectively. Cell viability and 
      apoptosis were determined by MTS test and flow cytometry, respectively. It was 
      found that treatment of RAW264.7 cells with high glucose and FFAs, which 
      exhibited increased expression of uc.48+, evoked P2X7R‑mediated immune and 
      inflammatory responses through several means, including cytokine secretion, ROS 
      formation, and activation of the ERK signaling pathway. The uc.48+ siRNA 
      regulated these factors and thus influenced the course and outcome of the immune 
      and inflammatory responses mediated by P2X7R.
FAU - Wu, Hong
AU  - Wu H
AD  - Department of Clinical Laboratory, First Affiliated Hospital, Medical School of 
      Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
FAU - Wen, Fang
AU  - Wen F
AD  - Department of Clinical Laboratory, First Affiliated Hospital, Medical School of 
      Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
FAU - Jiang, Mei
AU  - Jiang M
AD  - Department of Clinical Laboratory, First Affiliated Hospital, Medical School of 
      Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
FAU - Liu, Qiang
AU  - Liu Q
AD  - Institute of Blood Transfusion, Jiangxi Province Blood Center, Nanchang, Jiangxi 
      330077, P.R. China.
FAU - Nie, Yijun
AU  - Nie Y
AD  - Department of Clinical Laboratory, First Affiliated Hospital, Medical School of 
      Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20180509
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (Cytokines)
RN  - 0 (Fatty Acids, Nonesterified)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Receptors, Purinergic P2X7)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Adult
MH  - Animals
MH  - Cytokines/immunology
MH  - Diabetes Mellitus, Type 2/genetics/immunology
MH  - Fatty Acids, Nonesterified/immunology
MH  - Gene Expression Regulation
MH  - Glucose/*immunology
MH  - Humans
MH  - Hyperglycemia/genetics/*immunology
MH  - Inflammation/genetics/*immunology
MH  - Macrophages/*immunology/metabolism
MH  - Mice
MH  - Middle Aged
MH  - RAW 264.7 Cells
MH  - RNA Interference
MH  - RNA, Long Noncoding/genetics/*immunology
MH  - RNA, Small Interfering/genetics
MH  - Receptors, Purinergic P2X7/genetics/*immunology
EDAT- 2018/05/12 06:00
MHDA- 2018/10/10 06:00
CRDT- 2018/05/12 06:00
PHST- 2017/11/16 00:00 [received]
PHST- 2018/04/27 00:00 [accepted]
PHST- 2018/05/12 06:00 [pubmed]
PHST- 2018/10/10 06:00 [medline]
PHST- 2018/05/12 06:00 [entrez]
AID - 10.3892/ijmm.2018.3661 [doi]
PST - ppublish
SO  - Int J Mol Med. 2018 Aug;42(2):1152-1160. doi: 10.3892/ijmm.2018.3661. Epub 2018 
      May 9.