Angiotensin-converting enzyme (CD143) is abundantly expressed by dendritic cells and discriminates human monocyte-derived dendritic cells from acute myeloid leukemia-derived dendritic cells

Danilov, Sergei M.; Sadovnikova, Elena; Scharenborg, Nicole M.; Balyasnikova, Irina V.; Svinareva, D. A.; Семикина, Е. Л.; Паровичникова, Е Н; Vg, Savchenko; Adema, Gosse J.

doi:10.1016/j.exphem.2003.08.018

Cited by 80 publications

(97 citation statements)

References 53 publications

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“…CD143 is differentially expressed in different stages of maturation or aging in many cell types. In monocytes, CD143 expression increases during differentiation toward macrophages and dendritic cells [36]. Previous studies demonstrated the presence of infiltrating monocytes and a diffuse expression of monocyte/macrophage cell markers in the damaged aortic wall of AAA patients [37], but no information is available about the pattern of monocyte subsets and tissue macrophages in AAA patients.…”

Section: Discussionmentioning

confidence: 99%

“…ACE/ CD143 influence the type of macrophage polarization probably via intracellular signaling, and this influence is independent from circulating levels of enzyme activity [50]. Experimental and observational studies suggest that monocyte CD143 is strongly linked to subsets and may be a useful marker of cell function or differentiation [36]. At the moment, CD143 expression on monocytes may be regarded as the consequence of an activation/deactivation pathway induced by milieu (e.g.…”

Section: Discussionmentioning

confidence: 99%

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CD16⁺Monocyte Subsets Are Increased in Large Abdominal Aortic Aneurysms and Are Differentially Related with Circulating and Cell-Associated Biochemical and Inflammatory Biomarkers

et al. 2013

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Proinflammatory components are present in abdominal aortic aneurysm (AAA). Circulating monocytes display heterogeneity, and three subsets have been identified, based on the differential expression for CD14 and CD16 receptors: CD14+CD16-, classical, CD14+CD16+, intermediate and CD14dimCD16+, non-classical monocytes. Increased proinflammatory CD16+monocytes with high expression of CD143 are present in CKD patients. D-dimer is increased in AAA patients, and might contribute to the pro-inflammatory response associated to circulating monocytes. We aimed to investigate the frequency of CD14+CD16+, CD14dimCD16+monocytes and monocyte CD143 expression in AAA patients, and their relationship with D-dimer, eGFR and other inflammatory parameters. Blood from 74 AAA patients and 30 healthy controls was analyzed to determine the frequency of CD14+, CD16+, CD14dimCD16+monocytes and the monocyte CD143 expression by means of flow-cytometry. AAA patients had expanded CD16+SUPsets (CD14+CD16+: 7.66 ± 0.31% vs 5.42 ± 0.27%; CD14dimCD16+: 7.43 ± 0.48% vs 5.54 ± 0.38%, AAA vs controls, mean ± SE, both p<0.05). CD14+CD16+cells were associated to D-dimer and age, and to reduced eGFR. CD14dimCD16+cells were associated to uric acid, surface CD143, and reduced count of total leukocytes and neutrophils. Within AAA patients, the two CD16+supsets and the monocyte CD143 expression display different relationships with D-dimer, parameters of renal function and circulating biochemical and inflammatory biomarkers.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

CD16⁺Monocyte Subsets Are Increased in Large Abdominal Aortic Aneurysms and Are Differentially Related with Circulating and Cell-Associated Biochemical and Inflammatory Biomarkers

et al. 2013

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“…While ACE (also referred to as CD143) expression is dramatically increased during differentiation and maturation of moncytes into macrophages or dendritic cells (38,49,125), the role of ACE in myeloid differentiation and myeloid-mediated immune responses to tumors remain largely unknown. Important advances were made toward that end by the advent of the ACE 10/10 mouse model (126,127).…”

Section: Ace and Myeloid Lineage Cellsmentioning

confidence: 99%

“…As we shall discuss further below, it is important to note that ACE and other components of the RAS are expressed in all the cell types found within the tumor microenvironment, including endothelium, monocytes, macrophages, dendritic cells, fibroblasts, and T cells (11,38,83,125). It is therefore imperative to delineate the possible role and function of ACE in these different compartments to evaluate and maximize pharmacological targeting of the RAS in cancer.…”

Section: The Tumor Microenvironmentmentioning

confidence: 99%

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Angiotensin-converting enzyme and the tumor microenvironment: mechanisms beyond angiogenesis

Okwan-Duodu

Landry

Shen

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Okwan-Duodu D, Landry J, Shen XZ, Diaz R. Angiotensin-converting enzyme and the tumor microenvironment: mechanisms beyond angiogenesis. Am J Physiol Regul Integr Comp Physiol 305: R205-R215, 2013. First published June 5, 2013 doi:10.1152/ajpregu.00544.2012.-The renin angiotensin system (RAS) is a network of enzymes and peptides that coalesce primarily on the angiotensin II type 1 receptor (AT 1R) to induce cell proliferation, angiogenesis, fibrosis, and blood pressure control. Angiotensin-converting enzyme (ACE), the key peptidase of the RAS, is promiscuous in that it cleaves other substrates such as substance P and bradykinin. Accumulating evidence implicates ACE in the pathophysiology of carcinogenesis. While the role of ACE and its peptide network in modulating angiogenesis via the AT 1R is well documented, its involvement in shaping other aspects of the tumor microenvironment remains largely unknown. Here, we review the role of ACE in modulating the immune compartment of the tumor microenvironment, which encompasses the immunosuppressive, cancer-promoting myeloidderived suppressor cells, alternatively activated tumor-associated macrophages, and T regulatory cells. We also discuss the potential roles of peptides that accumulate in the setting of chronic ACE inhibitor use, such as bradykinin, substance P, and N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), and how they may undercut the gains of anti-angiogenesis from ACE inhibition. These emerging mechanisms may harmonize the often-conflicting results on the role of ACE inhibitors and ACE polymorphisms in various cancers and call for further investigations into the potential benefit of ACE inhibitors in some neoplasms.

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Bifidobacterium adolescentis orchestrates CD143⁺ cancer‐associated fibroblasts to suppress colorectal tumorigenesis by Wnt signaling‐regulated GAS1

Chen

Fan

Lin

et al. 2023

Cancer Communications

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BackgroundThe interplay between gut microbiota and tumor microenvironment (TME) in the pathogenesis of colorectal cancer (CRC) is not well explored. Here, we elucidated the functional role of Bifidobacterium adolescentis (B.a) on CRC and investigated its possible mechanism on the manipulation of cancer‐associated fibroblasts (CAFs) in CRC.MethodsDifferent CRC animal models and various cell line models were established to explore the function of B.a on CRC. The single‐cell RNA sequencing (scRNA‐seq) or flow cytometry was used to detect the cell subsets in the TME of CRC. Western blot, quantitative real‐time polymerase chain reaction (qRT‐PCR), or immunofluorescence staining were performed to examine the activation of Wnt signaling and growth arrest specific 1 (GAS1) on CD143+ CAFs. Chromatin immunoprecipitation quantitative real‐time PCR (CHIP‐qPCR) was performed to investigate the regulation of transcription factor 4 (TCF4) on GAS1. Multi‐immunofluorescence assay examined the expression level of CD143 and GAS1 on tissue microarray.ResultsWe found that B.a abundance was significantly reduced in CRC patients from two independent cohorts and the bacteria database of GMrepo. Supplementation with B.a suppressed ApcMin/+ spontaneous or AOM/DSS‐induced tumorigenesis in mice. scRNA‐seq revealed that B.a facilitated a subset of CD143+ CAFs by inhibiting the infiltration of Th2 cells, while promoting the TNF‐alpha+ B cells in TME. CD143+ CAFs highly expressed GAS1 and exhibited tumor suppressive effect. Mechanistically, GAS1 was activated by the Wnt/β‐catenin signaling in CD143+ CAFs. B.a abundance was correlated with the expression level of CD143 and GAS1. The level of CD143+ CAFs predicted the better survival outcome in CRC patients.ConclusionsThese results highlighted that B.a induced a new subset of CD143+ CAFs by Wnt signaling‐regulated GAS1 to suppress tumorigenesis and provided a novel therapeutic target for probiotic‐based modulation of TME in CRC.

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Angiotensin-converting enzyme (CD143) is abundantly expressed by dendritic cells and discriminates human monocyte-derived dendritic cells from acute myeloid leukemia-derived dendritic cells

Cited by 80 publications

References 53 publications

CD16⁺Monocyte Subsets Are Increased in Large Abdominal Aortic Aneurysms and Are Differentially Related with Circulating and Cell-Associated Biochemical and Inflammatory Biomarkers

CD16⁺Monocyte Subsets Are Increased in Large Abdominal Aortic Aneurysms and Are Differentially Related with Circulating and Cell-Associated Biochemical and Inflammatory Biomarkers

Angiotensin-converting enzyme and the tumor microenvironment: mechanisms beyond angiogenesis

Bifidobacterium adolescentis orchestrates CD143⁺ cancer‐associated fibroblasts to suppress colorectal tumorigenesis by Wnt signaling‐regulated GAS1

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Angiotensin-converting enzyme (CD143) is abundantly expressed by dendritic cells and discriminates human monocyte-derived dendritic cells from acute myeloid leukemia-derived dendritic cells

Cited by 80 publications

References 53 publications

CD16+Monocyte Subsets Are Increased in Large Abdominal Aortic Aneurysms and Are Differentially Related with Circulating and Cell-Associated Biochemical and Inflammatory Biomarkers

CD16+Monocyte Subsets Are Increased in Large Abdominal Aortic Aneurysms and Are Differentially Related with Circulating and Cell-Associated Biochemical and Inflammatory Biomarkers

Angiotensin-converting enzyme and the tumor microenvironment: mechanisms beyond angiogenesis

Bifidobacterium adolescentis orchestrates CD143+ cancer‐associated fibroblasts to suppress colorectal tumorigenesis by Wnt signaling‐regulated GAS1

Contact Info

Product

Resources

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CD16⁺Monocyte Subsets Are Increased in Large Abdominal Aortic Aneurysms and Are Differentially Related with Circulating and Cell-Associated Biochemical and Inflammatory Biomarkers

CD16⁺Monocyte Subsets Are Increased in Large Abdominal Aortic Aneurysms and Are Differentially Related with Circulating and Cell-Associated Biochemical and Inflammatory Biomarkers

Bifidobacterium adolescentis orchestrates CD143⁺ cancer‐associated fibroblasts to suppress colorectal tumorigenesis by Wnt signaling‐regulated GAS1