PMID- 36697439
OWN - NLM
STAT- MEDLINE
DCOM- 20230130
LR  - 20230316
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 13
IP  - 1
DP  - 2023 Jan 25
TI  - Administration of anti-inflammatory M2 macrophages suppresses progression of 
      angiotensin II-induced aortic aneurysm in mice.
PG  - 1380
LID - 10.1038/s41598-023-27412-x [doi]
LID - 1380
AB  - Aortic aneurysm (AA) is a vascular disorder characterized pathologically by 
      inflammatory cell invasion and extracellular matrix (ECM) degradation. It is 
      known that regulation of the balance between pro-inflammatory M1 macrophages 
      (M1Ms) and anti-inflammatory M2 macrophages (M2Ms) plays a pivotal role in AA 
      stabilization. We investigated the effects of M2M administration in an 
      apolipoprotein E-deficient (apoE(-/-)) mouse model in which AA was induced by 
      angiotensin II (ATII) infusion. Mice received intraperitoneal administration of 1 
      million M2Ms 4 weeks after ATII infusion. Compared with a control group that was 
      administered saline, the M2M group exhibited reduced AA expansion; decreased 
      expression levels of interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha (TNF-alpha), 
      and monocyte chemoattractant protein-1 (MCP-1); and a lower M1M/M2M ratio. 
      Moreover, the M2M group exhibited upregulation of anti-inflammatory factors, 
      including IL-4 and IL-10. PKH26-labeled M2Ms accounted for 6.5% of cells in the 
      aneurysmal site and co-expressed CD206. Taken together, intraperitoneal 
      administration of M2Ms inhibited AA expansion by reducing the inflammatory 
      reaction via regulating the M1M/M2M ratio. This study shows that M2M 
      administration might be useful for the treatment of AA.
CI  - (c) 2023. The Author(s).
FAU - Ashida, Shinichi
AU  - Ashida S
AD  - Department of Cardiac Surgery, Nagoya University Graduate School of Medicine, 65 
      Tsurumai-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
FAU - Yamawaki-Ogata, Aika
AU  - Yamawaki-Ogata A
AD  - Department of Cardiac Surgery, Nagoya University Graduate School of Medicine, 65 
      Tsurumai-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
FAU - Tokoro, Masayoshi
AU  - Tokoro M
AD  - Department of Cardiac Surgery, Nagoya University Graduate School of Medicine, 65 
      Tsurumai-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
FAU - Mutsuga, Masato
AU  - Mutsuga M
AD  - Department of Cardiac Surgery, Nagoya University Graduate School of Medicine, 65 
      Tsurumai-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
FAU - Usui, Akihiko
AU  - Usui A
AD  - Department of Cardiac Surgery, Nagoya University Graduate School of Medicine, 65 
      Tsurumai-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
FAU - Narita, Yuji
AU  - Narita Y
AD  - Department of Cardiac Surgery, Nagoya University Graduate School of Medicine, 65 
      Tsurumai-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan. 
      ynarita@med.nagoya-u.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20230125
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 11128-99-7 (Angiotensin II)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Mice
MH  - Angiotensin II/metabolism
MH  - Anti-Inflammatory Agents/metabolism
MH  - *Aortic Aneurysm/chemically induced/drug therapy/metabolism
MH  - Disease Models, Animal
MH  - *Macrophages/metabolism
MH  - Mice, Inbred C57BL
MH  - Tumor Necrosis Factor-alpha/metabolism
PMC - PMC9877022
COIS- The authors declare no competing interests.
EDAT- 2023/01/26 06:00
MHDA- 2023/01/28 06:00
PMCR- 2023/01/25
CRDT- 2023/01/25 23:16
PHST- 2022/09/01 00:00 [received]
PHST- 2023/01/02 00:00 [accepted]
PHST- 2023/01/25 23:16 [entrez]
PHST- 2023/01/26 06:00 [pubmed]
PHST- 2023/01/28 06:00 [medline]
PHST- 2023/01/25 00:00 [pmc-release]
AID - 10.1038/s41598-023-27412-x [pii]
AID - 27412 [pii]
AID - 10.1038/s41598-023-27412-x [doi]
PST - epublish
SO  - Sci Rep. 2023 Jan 25;13(1):1380. doi: 10.1038/s41598-023-27412-x.