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Relationship between CCL22 Expression by Vascular Smooth Muscle Cells and Macrophage Histamine Receptors in Atherosclerosis
- Source :
- Journal of Atherosclerosis and Thrombosis
- Publication Year :
- 2018
- Publisher :
- Japan Atherosclerosis Society, 2018.
-
Abstract
- Aim: CCL22, mainly synthesized by monocyte-derived alternative (M2) macrophages, belongs to the CC family of chemokines and is involved in monocyte migration and recruitment. We have previously investigated CCL22 and histamine in atherosclerosis. Here, we investigated the hypothesis that CCL22 is involved in atherosclerosis, which is influenced by the differentiation of macrophage phenotypes via histamine. Methods: CCL22 expression was investigated in human carotid arteries and coronary arteries with bare metal stents. Ligated carotid arteries of wild-type (C57BL/6J) and apolipoprotein E-deficient mice were also used as atherosclerotic models. The localization and expression of CCL22 and classical (M1)-like and M2-like macrophages in various human and mouse atherosclerotic lesions were investigated by immunohistochemical examination and quantitative real-time polymerase chain reaction. Histamine is expressed in atherosclerosis, and it induces inflammation and immunity. Human- and mice-derived monocytes and macrophages were used to examine the role of histamine in macrophage differentiation and CCL22-expression. Macrophages derived from histamine receptor 1 (H1R)- and 2 (H2R)-knockout (KO) mice were also examined. Results: Atherosclerotic lesions showed a distribution of heterogeneous macrophage phenotypes with M1-like and M2-like macrophage dominant sites. CCL22 was distributed in sparse areas of vascular smooth muscle cells (VSMCs) and associated with M2-like macrophages. Moreover, H2R stimulation was associated with CCL22 expression via M2-like macrophage dominant differentiation. Conclusion: The expression of M1- or M2-like macrophages in atherosclerosis were observed to be dependent on the distribution of VSMCs owing to differences in causal stimuli and the switching of histamine receptors via Th1 or Th2 cytokines. These results suggest that CCL22 may control atherosclerosis.
- Subjects :
- Male
0301 basic medicine
Chemokine
Vascular smooth muscle
Macrophage
Inflammation
Muscle, Smooth, Vascular
Mice
03 medical and health sciences
chemistry.chemical_compound
Histamine receptor
Apolipoproteins E
Internal Medicine
medicine
Animals
Humans
Receptors, Histamine H2
Receptors, Histamine H1
Cells, Cultured
Chemokine CCL22
Mice, Knockout
biology
Macrophages
Monocyte
Biochemistry (medical)
Atherosclerosis
Mice, Inbred C57BL
030104 developmental biology
medicine.anatomical_structure
chemistry
Cancer research
biology.protein
Original Article
medicine.symptom
Cardiology and Cardiovascular Medicine
Biomarkers
CCL22
Histamine
Subjects
Details
- ISSN :
- 18803873 and 13403478
- Volume :
- 25
- Database :
- OpenAIRE
- Journal :
- Journal of Atherosclerosis and Thrombosis
- Accession number :
- edsair.doi.dedup.....88953d989d6685d381ceaad56eb92f56