PMID- 14522421
OWN - NLM
STAT- MEDLINE
DCOM- 20031215
LR  - 20190513
IS  - 0008-6363 (Print)
IS  - 0008-6363 (Linking)
VI  - 60
IP  - 1
DP  - 2003 Oct 15
TI  - Dendritic cells in the arterial wall express C1q: potential significance in 
      atherogenesis.
PG  - 175-86
AB  - OBJECTIVE: Dendritic cells (DCs) accumulate in atherosclerotic lesions but their 
      characteristics and their role in atherogenesis are poorly understood. C1q, an 
      element of the first component of complement, is expressed by interdigitating 
      dendritic cells and follicular dendritic cells in the spleen. It has been 
      suggested that C1q is involved in capturing immune complexes in the lymphoid 
      tissue. Immune complexes are also detected in atherosclerotic lesions. The 
      present study investigated whether C1q is expressed by DCs in the arterial wall. 
      Because DCs accumulating within atherosclerotic lesions might originate from 
      monocytes that infiltrate the intima from very early stages of atherosclerosis, 
      C1q expression was also examined in monocyte-derived DCs in vitro. METHODS: 
      Specimens of the aorta, carotid, mammary, popliteal and tibial arteries were 
      obtained during operation. Expression of C1q in the arterial wall was studied by 
      immunohistochemistry. The nature of cells expressing C1q was studied in sections 
      double stained with antibodies to C1q and cell type specific markers including 
      CD1a and S-100 (for identification of DCs), CD68 (macrophages), CD3 (T-cells), 
      von Willebrand factor (endothelial cells), and smooth muscle alpha-actin (smooth 
      muscle cells). In vitro, DCs were differentiated from human peripheral blood 
      monocytes using GM-CSF and IL-4. Peripheral blood monocytes were differentiated 
      to macrophages using M-CSF. The expression of C1q in monocytes and in vitro 
      monocyte-derived DCs and macrophages was determined by RT-PCR, Western blotting, 
      immunofluorescence microscopy and flow cytometry. RESULTS: In all the arterial 
      specimens studied, DCs expressing C1q were detected. C1q was also found in 
      macrophages, macrophage foam cells and in neovascular endothelial cells in 
      atherosclerotic lesions, but no C1q expression was detected in T-cells and smooth 
      muscle cells. In vitro analysis demonstrated that monocyte-derived DCs and 
      macrophages express C1q but no C1q was detected in monocytes. CONCLUSION: C1q is 
      expressed by DCs residing in the arterial wall as well as by monocyte-derived DCs 
      in vitro. Expression of C1q occurs during differentiation of monocytes to DCs and 
      macrophages and might be important in binding and trapping immune complexes in 
      atherosclerotic lesions.
FAU - Cao, Weiping
AU  - Cao W
AD  - National University Medical Institutes, National University of Singapore, Blk 
      MD11, #02-01 10 Medical Drive, Singapore 117597, Singapore.
FAU - Bobryshev, Yuri V
AU  - Bobryshev YV
FAU - Lord, Reginald S A
AU  - Lord RS
FAU - Oakley, Reida E I
AU  - Oakley RE
FAU - Lee, Szu H
AU  - Lee SH
FAU - Lu, Jinhua
AU  - Lu J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Cardiovasc Res
JT  - Cardiovascular research
JID - 0077427
RN  - 0 (Actins)
RN  - 0 (Antigen-Antibody Complex)
RN  - 80295-33-6 (Complement C1q)
SB  - IM
MH  - Actins/analysis
MH  - *Antigen-Antibody Complex
MH  - Aorta
MH  - Arteriosclerosis/*immunology
MH  - Carotid Arteries
MH  - Cells, Cultured
MH  - Complement C1q/*analysis
MH  - Dendritic Cells/*immunology
MH  - Flow Cytometry
MH  - Foam Cells/immunology
MH  - Humans
MH  - Immunohistochemistry/methods
MH  - Macrophages/immunology
MH  - Mammary Arteries
MH  - Microscopy, Confocal
MH  - Popliteal Artery
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tibial Arteries
MH  - Tunica Intima/*immunology
EDAT- 2003/10/03 05:00
MHDA- 2003/12/16 05:00
CRDT- 2003/10/03 05:00
PHST- 2003/10/03 05:00 [pubmed]
PHST- 2003/12/16 05:00 [medline]
PHST- 2003/10/03 05:00 [entrez]
AID - S0008636303003456 [pii]
AID - 10.1016/s0008-6363(03)00345-6 [doi]
PST - ppublish
SO  - Cardiovasc Res. 2003 Oct 15;60(1):175-86. doi: 10.1016/s0008-6363(03)00345-6.