PMID- 34637964
OWN - NLM
STAT- MEDLINE
DCOM- 20220103
LR  - 20220103
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 581
DP  - 2021 Dec 3
TI  - CD38 activation by monosodium urate crystals contributes to inflammatory 
      responses in human and murine macrophages.
PG  - 6-11
LID - S0006-291X(21)01403-0 [pii]
LID - 10.1016/j.bbrc.2021.10.010 [doi]
AB  - Cluster of differentiation (CD) 38, a major enzyme for nicotinamide adenine 
      dinucleotide (NAD(+)) degradation, plays a key role in inflammation. Meanwhile, 
      intracellular NAD(+) decline is also associated with inflammatory responses. 
      However, whether CD38 activation is involved in gouty inflammation has not been 
      elucidated. The present study aimed to clarify the role of CD38 in monosodium 
      urate crystals (MSU)-triggered inflammatory responses. The results showed that 
      MSU crystals increased the protein expression of CD38 in time- and 
      concentration-dependent manner in THP-1 macrophages and mouse bone marrow-derived 
      macrophages (BMDMs). Moreover, intracellular NAD(+) levels were reduced by MSU 
      crystals along with the increased IL-1beta release. However, CD38 inhibition by 78c 
      elevated intracellular NAD(+) levels and suppressed IL-1beta release in MSU 
      crystals-treated THP-1 macrophages and BMDMs. Interestingly, CD38 inhibition 
      without significant elevation of intracellular NAD(+) also decreased IL-1beta 
      release driven by MSU crystals in THP-1 macrophages. In conclusion, the present 
      study revealed that MSU crystals could activate CD38 with the ensuing 
      intracellular NAD(+) decline to promote inflammatory responses in THP-1 
      macrophages and BMDMs, while CD38 inhibition could suppress MSU 
      crystals-triggered inflammatory responses, indicating that CD38 is a potential 
      therapeutic target for gout.
CI  - Copyright (c) 2021 Elsevier Inc. All rights reserved.
FAU - Wen, Shijie
AU  - Wen S
AD  - Department of Membrane Transport and Biopharmaceutics, Faculty of Pharmaceutical 
      Sciences, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa 
      University, Kakuma-machi, Kanazawa, Ishikawa, 920-1192, Japan.
FAU - Arakawa, Hiroshi
AU  - Arakawa H
AD  - Department of Membrane Transport and Biopharmaceutics, Faculty of Pharmaceutical 
      Sciences, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa 
      University, Kakuma-machi, Kanazawa, Ishikawa, 920-1192, Japan.
FAU - Tamai, Ikumi
AU  - Tamai I
AD  - Department of Membrane Transport and Biopharmaceutics, Faculty of Pharmaceutical 
      Sciences, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa 
      University, Kakuma-machi, Kanazawa, Ishikawa, 920-1192, Japan. Electronic 
      address: tamai@p.kanazawa-u.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20211007
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (IL1B protein, human)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Membrane Glycoproteins)
RN  - 0U46U6E8UK (NAD)
RN  - 268B43MJ25 (Uric Acid)
RN  - EC 3.2.2.5 (CD38 protein, human)
RN  - EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
SB  - IM
MH  - ADP-ribosyl Cyclase 1/agonists/*genetics/metabolism
MH  - Animals
MH  - Crystallization
MH  - Female
MH  - Gene Expression Regulation
MH  - Gout/etiology/genetics/metabolism/pathology
MH  - Humans
MH  - Hyperuricemia/etiology/genetics/metabolism/pathology
MH  - Inflammation
MH  - Interleukin-1beta/*genetics/metabolism
MH  - Macrophages/*drug effects/metabolism/pathology
MH  - Male
MH  - Membrane Glycoproteins/agonists/*genetics/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Models, Biological
MH  - NAD/metabolism
MH  - Primary Cell Culture
MH  - Signal Transduction
MH  - THP-1 Cells
MH  - Uric Acid/*pharmacology
OTO - NOTNLM
OT  - CD38
OT  - Gout
OT  - Hyperuricemia
OT  - Inflammation
OT  - Monosodium urate crystals
OT  - Nicotinamide adenine dinucleotide
EDAT- 2021/10/13 06:00
MHDA- 2022/01/04 06:00
CRDT- 2021/10/12 20:17
PHST- 2021/08/11 00:00 [received]
PHST- 2021/10/01 00:00 [accepted]
PHST- 2021/10/13 06:00 [pubmed]
PHST- 2022/01/04 06:00 [medline]
PHST- 2021/10/12 20:17 [entrez]
AID - S0006-291X(21)01403-0 [pii]
AID - 10.1016/j.bbrc.2021.10.010 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2021 Dec 3;581:6-11. doi: 10.1016/j.bbrc.2021.10.010. 
      Epub 2021 Oct 7.