PMID- 36536281
OWN - NLM
STAT- MEDLINE
DCOM- 20221221
LR  - 20221230
IS  - 1528-3658 (Electronic)
IS  - 1076-1551 (Print)
IS  - 1076-1551 (Linking)
VI  - 28
IP  - 1
DP  - 2022 Dec 19
TI  - Single-cell transcriptomic analysis reveals differential cell subpopulations and 
      distinct phenotype transition in normal and dissected ascending aorta.
PG  - 158
LID - 10.1186/s10020-022-00584-4 [doi]
LID - 158
AB  - BACKGROUND: Acute thoracic aortic dissection (ATAD) is a fatal condition 
      characterized by tear of intima, formation of false lumen and rupture of aorta. 
      However, the subpopulations of normal and dissected aorta remain less studied. 
      METHODS: Single-cell RNA sequencing was performed including 5 patients with ATAD 
      and 4 healthy controls. Immunohistochemistry and immunofluorescence were used to 
      verify the findings. RESULTS: We got 8 cell types from human ascending aorta and 
      identified 50 subpopulations including vascular smooth muscle cells (VSMCs), 
      endothelial cells, fibroblasts, neutrophils, monocytes and macrophages. Six 
      transmembrane epithelial antigen of prostate 4 metalloreductase (STEAP4) was 
      identified as a new marker of synthetic VSMCs. CytoTRACE identified 
      subpopulations with higher differentiation potential in specified cell types 
      including synthetic VSMCs, enolase 1(+) fibroblasts and myeloid-derived 
      neutrophils. Synthetic VSMCs-derived C-X-C motif chemokine ligand 12 (CXCL12) 
      might interact with neutrophils and fibroblasts via C-X-C motif chemokine 
      receptor 4 (CXCR4) and atypical chemokine receptor 3 (ACKR3), respectively, which 
      might recruit neutrophils and induce transdifferentitation of fibroblasts into 
      synthetic VSMCs. CONCLUSION: We characterized signatures of different cell types 
      in normal and dissected human ascending aorta and identified a new marker for 
      isolation of synthetic VSMCs. Moreover, we proposed a potential mechanism that 
      synthetic VSMCs might interact with neutrophils and fibroblasts via 
      CXCL12-CXCR4/ACKR3 axis whereby deteriorating the progression of ATAD, which 
      might provide new insights to better understand the development and progression 
      of ATAD.
CI  - (c) 2022. The Author(s).
FAU - He, Yu-Bin
AU  - He YB
AD  - Department of Cardiovascular Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong 
      University, No.241, West Huaihai Road, Shanghai, 200030, China.
FAU - Jin, Hai-Zhen
AU  - Jin HZ
AD  - Department of Central Laboratory, Shanghai Chest Hospital, Shanghai Jiao Tong 
      University, Shanghai, China.
FAU - Zhao, Jin-Long
AU  - Zhao JL
AD  - Department of Cardiovascular Surgery, Shanghai Jiao Tong University Affiliated 
      Sixth People's Hospital, Shanghai, China.
FAU - Wang, Chong
AU  - Wang C
AD  - Department of Cardiovascular Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong 
      University, No.241, West Huaihai Road, Shanghai, 200030, China.
FAU - Ma, Wen-Rui
AU  - Ma WR
AD  - Department of Cardiac Surgery, Zhongshan Hospital, Fudan University, Shanghai, 
      China.
FAU - Xing, Jie
AU  - Xing J
AD  - Department of Biobank, Shanghai Chest Hospital, Shanghai Jiao Tong University, 
      Shanghai, China.
FAU - Zhang, Xiao-Bin
AU  - Zhang XB
AD  - Department of Cardiovascular Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong 
      University, No.241, West Huaihai Road, Shanghai, 200030, China.
FAU - Zhang, Yang-Yang
AU  - Zhang YY
AD  - Department of Cardiovascular Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong 
      University, No.241, West Huaihai Road, Shanghai, 200030, China.
FAU - Dai, Huang-Dong
AU  - Dai HD
AD  - Department of Cardiovascular Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong 
      University, No.241, West Huaihai Road, Shanghai, 200030, China.
FAU - Zhao, Nai-Shi
AU  - Zhao NS
AD  - Department of Cardiovascular Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong 
      University, No.241, West Huaihai Road, Shanghai, 200030, China.
FAU - Zhang, Jian-Feng
AU  - Zhang JF
AD  - Department of Cardiovascular Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong 
      University, No.241, West Huaihai Road, Shanghai, 200030, China. 
      jeff_cardiosur@163.com.
FAU - Zhang, Guan-Xin
AU  - Zhang GX
AD  - Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical 
      University, No.168, Changhai Road, Shanghai, China. gxzhang_ctsur@163.com.
FAU - Zhang, Jing
AU  - Zhang J
AUID- ORCID: 0000-0003-2265-565X
AD  - Department of Cardiovascular Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong 
      University, No.241, West Huaihai Road, Shanghai, 200030, China. 
      zhangjing_cvs@126.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20221219
PL  - England
TA  - Mol Med
JT  - Molecular medicine (Cambridge, Mass.)
JID - 9501023
SB  - IM
MH  - Male
MH  - Humans
MH  - *Aorta, Thoracic
MH  - Endothelial Cells
MH  - Transcriptome
MH  - Aorta
MH  - Phenotype
MH  - *Aortic Dissection
PMC - PMC9764678
OTO - NOTNLM
OT  - Acute thoracic aortic dissection
OT  - CXCL12
OT  - Cell differentiation trajectory
OT  - Cell-cell interaction
OT  - Phenotypic switch
OT  - Single-cell RNA sequencing
COIS- The authors declare that they have no conflict of interest.
EDAT- 2022/12/20 06:00
MHDA- 2022/12/22 06:00
PMCR- 2022/12/19
CRDT- 2022/12/19 23:43
PHST- 2022/05/17 00:00 [received]
PHST- 2022/12/01 00:00 [accepted]
PHST- 2022/12/19 23:43 [entrez]
PHST- 2022/12/20 06:00 [pubmed]
PHST- 2022/12/22 06:00 [medline]
PHST- 2022/12/19 00:00 [pmc-release]
AID - 10.1186/s10020-022-00584-4 [pii]
AID - 584 [pii]
AID - 10.1186/s10020-022-00584-4 [doi]
PST - epublish
SO  - Mol Med. 2022 Dec 19;28(1):158. doi: 10.1186/s10020-022-00584-4.