PMID- 29587203
OWN - NLM
STAT- MEDLINE
DCOM- 20181022
LR  - 20211204
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 58
DP  - 2018 May
TI  - Inhibitor of Bruton's tyrosine kinases, PCI-32765, decreases pro-inflammatory 
      mediators' production in high glucose-induced macrophages.
PG  - 145-153
LID - S1567-5769(18)30122-X [pii]
LID - 10.1016/j.intimp.2018.03.019 [doi]
AB  - Accumulating evidence has shown that macrophages play a vital role in development 
      and pathogenesis of diabetic nephropathy (DN) by secreting inflammatory 
      cytokines. Although Bruton's tyrosine kinases (Btk) is a biologically important 
      molecule implicated in immune regulation, the role of Btk in high glucose 
      (HG)-stimulated inflammatory response in macrophages and the mechanism involved 
      need further investigation. In our study, we used bone marrow-derived macrophages 
      (BMMs) to investigate the involvement of Btk on HG-induced inflammatory cytokines 
      expression and to explore the underlying mechanisms. We found that high glucose 
      induced phosphorylation of Btk, MAPKs and NF-kappaB, and the expression of downstream 
      inflammation cytokines monocyte chemo-attractant protein-1 (MCP-1), tumor 
      necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). Btk inhibitor 
      (PCI-32765) not only down-regulated ERK1/2 phosphorylation and NF-kappaB activation, 
      but also decreased the secretion of MCP-1, TNF-alpha and IL-1beta in HG-treated BMMs. 
      These results indicate that Btk plays an important role in HG-induced 
      inflammatory cytokines expression and that PCI-32765 may be used as an 
      immunoregulatory agent against hyperglycemia-induced inflammatory response in DN.
CI  - Copyright (c) 2018. Published by Elsevier B.V.
FAU - Fan, Zhe
AU  - Fan Z
AD  - Department of Nephrology, The First Affiliated Hospital, Anhui Medical 
      University, Hefei, Anhui, PR China.
FAU - Wang, Yan
AU  - Wang Y
AD  - Department of Nephrology, The First Affiliated Hospital, Anhui Medical 
      University, Hefei, Anhui, PR China.
FAU - Xu, Xingxin
AU  - Xu X
AD  - Department of Nephrology, The First Affiliated Hospital, Anhui Medical 
      University, Hefei, Anhui, PR China. Electronic address: xuxingxin.2008@163.com.
FAU - Wu, Yonggui
AU  - Wu Y
AD  - Department of Nephrology, The First Affiliated Hospital, Anhui Medical 
      University, Hefei, Anhui, PR China. Electronic address: wuyonggui@medmail.com.cn.
LA  - eng
PT  - Journal Article
DEP - 20180326
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (NF-kappa B)
RN  - 0 (Piperidines)
RN  - 0 (Pyrazoles)
RN  - 0 (Pyrimidines)
RN  - 1X70OSD4VX (ibrutinib)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.10.2 (Agammaglobulinaemia Tyrosine Kinase)
RN  - EC 2.7.10.2 (BTK protein, human)
RN  - EC 2.7.10.2 (Btk protein, mouse)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - IY9XDZ35W2 (Glucose)
RN  - JAC85A2161 (Adenine)
SB  - IM
MH  - Adenine/analogs & derivatives
MH  - Agammaglobulinaemia Tyrosine Kinase
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Bone Marrow Cells/physiology
MH  - Cells, Cultured
MH  - Cytokines/metabolism
MH  - Diabetic Nephropathies/drug therapy/*immunology
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Glucose/metabolism
MH  - Humans
MH  - Immunomodulation
MH  - Inflammation Mediators/metabolism
MH  - Macrophages/*drug effects/physiology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - NF-kappa B/metabolism
MH  - Phosphorylation
MH  - Piperidines
MH  - Protein-Tyrosine Kinases/*antagonists & inhibitors
MH  - Pyrazoles/*pharmacology
MH  - Pyrimidines/*pharmacology
MH  - Signal Transduction
OTO - NOTNLM
OT  - Bruton's tyrosine kinases
OT  - Diabetic nephropathy
OT  - Inflammation
OT  - NF-kappaB
EDAT- 2018/03/28 06:00
MHDA- 2018/10/23 06:00
CRDT- 2018/03/28 06:00
PHST- 2018/01/21 00:00 [received]
PHST- 2018/03/16 00:00 [revised]
PHST- 2018/03/19 00:00 [accepted]
PHST- 2018/03/28 06:00 [pubmed]
PHST- 2018/10/23 06:00 [medline]
PHST- 2018/03/28 06:00 [entrez]
AID - S1567-5769(18)30122-X [pii]
AID - 10.1016/j.intimp.2018.03.019 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2018 May;58:145-153. doi: 10.1016/j.intimp.2018.03.019. Epub 
      2018 Mar 26.