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Book ; Thesis: Analysis of the role of stabilin-1 in tumour growoth and its functions in tumour-associated macrophages

Riabov, Vladimir

2011

Author's details	vorgelegt von Vladimir Riabov
Language	English
Size	112 Bl. : Ill., graph. Darst.
Publishing country	Germany
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Heidelberg, Univ., Diss., 2011
HBZ-ID	HT017174031
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: Hyperglycemia Induces Inflammatory Response of Human Macrophages to CD163-Mediated Scavenging of Hemoglobin-Haptoglobin Complexes.

Matuschik, Laura / Riabov, Vladimir / Schmuttermaier, Christina / Sevastyanova, Tatyana / Weiss, Christel / Klüter, Harald / Kzhyshkowska, Julia

International journal of molecular sciences

2022 Volume 23, Issue 3

Abstract: Hyperglycemia, a hallmark of diabetes, can induce inflammatory programming of macrophages. The macrophage scavenger receptor CD163 internalizes and degrades hemoglobin-haptoglobin (Hb-Hp) complexes built due to intravascular hemolysis. Clinical studies ... ...

Abstract	Hyperglycemia, a hallmark of diabetes, can induce inflammatory programming of macrophages. The macrophage scavenger receptor CD163 internalizes and degrades hemoglobin-haptoglobin (Hb-Hp) complexes built due to intravascular hemolysis. Clinical studies have demonstrated a correlation between impaired scavenging of Hb-Hp complexes via CD163 and diabetic vascular complications. Our aim was to identify whether hyperglycemia is able to amplify inflammation via Hb-Hp complex interactions with the immune system. M(IFNγ), M(IL-4), and control M0 macrophages were differentiated out of primary human monocytes in normo- (5 mM) and hyperglycemic (25 mM) conditions. CD163 gene expression was decreased 5.53 times in M(IFNγ) with a further decrease of 1.99 times in hyperglycemia. Hyperglycemia suppressed CD163 surface expression in M(IFNγ) (1.43 times). Flow cytometry demonstrated no impairment of Hb-Hp uptake in hyperglycemia. However, hyperglycemia induced an inflammatory response of M(IFNγ) to Hb-Hp1-1 and Hb-Hp2-2 uptake with different dynamics. Hb-Hp1-1 uptake stimulated IL-6 release (3.03 times) after 6 h but suppressed secretion (5.78 times) after 24 h. Contrarily, Hb-Hp2-2 uptake did not affect IL-6 release after 6h but increased secretion after 24 h (3.06 times). Our data show that hyperglycemia induces an inflammatory response of innate immune cells to Hb-Hp1-1 and Hb-Hp2-2 uptake, converting the silent Hb-Hp complex clearance that prevents vascular damage into an inflammatory process, hereby increasing the susceptibility of diabetic patients to vascular complications.
MeSH term(s)	Antigens, CD/metabolism ; Antigens, Differentiation, Myelomonocytic/metabolism ; Cells, Cultured ; Diabetic Angiopathies/metabolism ; Endocytosis/physiology ; Haptoglobins/metabolism ; Hemoglobins/metabolism ; Hemolysis/physiology ; Humans ; Hyperglycemia/metabolism ; Inflammation/metabolism ; Macrophages/metabolism ; Monocytes/metabolism ; Receptors, Cell Surface/metabolism ; Receptors, Scavenger/metabolism
Chemical Substances	Antigens, CD ; Antigens, Differentiation, Myelomonocytic ; CD163 antigen ; Haptoglobins ; Hemoglobins ; Receptors, Cell Surface ; Receptors, Scavenger ; haptoglobin-hemoglobin complex
Language	English
Publishing date	2022-01-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23031385
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Article ; Online: Titanium induces pro-inflammatory and tissue-destructive responses in primary human macrophages.

Gudima, Alexandru / Hesselbarth, David / Li, Guanhao / Riabov, Vladimir / Michel, Julia / Liu, Quan / Schmuttermaier, Christina / Jiao, Zhen / Sticht, Carsten / Jawhar, Ahmed / Obertacke, Udo / Klüter, Harald / Vrana, Nihal Engin / Kzhyshkowska, Julia

Journal of leukocyte biology

2024

Abstract: Implants and medical devices are efficient and practical therapeutic solutions for a multitude of pathologies. Titanium and titanium alloys are used in orthopedics, dentistry, and cardiology. Despite very good mechanical properties, and corrosion ... ...

Abstract	Implants and medical devices are efficient and practical therapeutic solutions for a multitude of pathologies. Titanium and titanium alloys are used in orthopedics, dentistry, and cardiology. Despite very good mechanical properties, and corrosion resistance titanium implants can fail due to inflammatory or tissue-degradation related complications. Macrophages are major immune cells that control acceptance of failure of the implant. In this study, for the first time, we have performed a systematic analysis of the response of differentially activated human macrophages (M(Control), M(IFNγ) and M(IL-4)) to the polished and porous titanium surfaces in order to identify the detrimental effect of titanium leading to the tissue destruction and chronic inflammation. Transcriptome analysis revealed that the highest number of differences between titanium and control settings are found in M(IL-4) that model healing type of macrophages. RT-qPCR analysis confirmed that both polished and porous titanium affected expression of cytokines, chitinases/chitinase-like proteins and matrix metalloproteinases. Titanium-induced release and activation of MMP7 by macrophages was enhanced by fibroblasts in both juxtacrine and paracrine cell interaction models. Production of titanium-induced MMPs and cytokines associated with chronic inflammation were independent of the presence of Staphylococcus aureus. MMP7, one of the most pronounced tissue-destroying factor and chitinase-like protein YKL-40 were expressed in CD68+ macrophages in peri-implant tissues of patients with orthopedic implants. In summary, we demonstrated that titanium induces pro-inflammatory and tissue-destructing responses mainly in healing macrophages, and the detrimental effects of titanium surfaces on implant-adjacent macrophages are independent on the bacterial contamination.
Language	English
Publishing date	2024-03-21
Publishing country	England
Document type	Journal Article
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1093/jleuko/qiae072
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Article ; Online: In Silico Pan-Cancer Analysis Reveals Prognostic Role of the Erythroferrone (ERFE) Gene in Human Malignancies.

Xu, Qingyu / Altrock, Eva / Schmitt, Nanni / Streuer, Alexander / Rapp, Felicitas / Nowak, Verena / Obländer, Julia / Weimer, Nadine / Palme, Iris / Göl, Melda / Hofmann, Wolf-Karsten / Nowak, Daniel / Riabov, Vladimir

International journal of molecular sciences

2023 Volume 24, Issue 2

Abstract: The erythroferrone gene ( ...

Abstract	The erythroferrone gene (
MeSH term(s)	Humans ; Prognosis ; Peptide Hormones/genetics ; Hepcidins/metabolism ; Neoplasms/genetics ; Myelodysplastic Syndromes ; Tumor Microenvironment
Chemical Substances	Peptide Hormones ; Hepcidins
Language	English
Publishing date	2023-01-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24021725
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Article: Accumulation of stabilin-1 positive macrophages in the early stage of gastric cancer is associated with short cumulative survival.

Yin, Shui-Ping / Gao, Yi / Xie, Xu-Shi / Xu, Dan-Dan / Riabov, Vladimir / Du, Wei-Dong

Oncology letters

2020 Volume 19, Issue 3, Page(s) 2404–2412

Abstract: The scavenger receptor stabilin-1 has been reported to be expressed by tumor-associated macrophages (TAMs) and to facilitate tumor growth and metastasis in mouse models of breast carcinoma and melanoma. However, to the best of our knowledge, its ... ...

Abstract	The scavenger receptor stabilin-1 has been reported to be expressed by tumor-associated macrophages (TAMs) and to facilitate tumor growth and metastasis in mouse models of breast carcinoma and melanoma. However, to the best of our knowledge, its expression and association with prognosis in human gastric cancer has not been evaluated. The present study investigated the expression of stabilin-1 and its association with clinicopathological parameters in patients with gastric cancer. The expression of stabilin-1 was evaluated by immunohistochemical staining of gastric cancer tissue samples of 371 Chinese patients with primary gastric adenocarcinoma. Confocal laser scanning microscopy was used to determine the cellular source of stabilin-1 in the gastric cancer tissues using anti-CD68, anti-CD163, anti-stabilin-1 and anti-secreted protein acidic and rich in cysteine antibodies. A higher number of stabilin-1-positive cells were observed in the cancer tissues of primary gastric adenocarcinoma compared with adjacent non-cancerous tissues of primary gastric adenocarcinoma (P<0.001); the majority of stabilin-1-positve cells were CD68
Language	English
Publishing date	2020-01-16
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2573196-8
ISSN	1792-1082 ; 1792-1074
ISSN (online)	1792-1082
ISSN	1792-1074
DOI	10.3892/ol.2020.11310
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Article ; Online: Treatment with the apoptosis inhibitor Asunercept reduces clone sizes in patients with lower risk Myelodysplastic Neoplasms.

Annals of hematology

2024 Volume 103, Issue 4, Page(s) 1221–1233

Abstract: In low-risk Myelodysplastic Neoplasms (MDS), increased activity of apoptosis-promoting factors such as tumor necrosis factor (TNFα) and pro-apoptotic Fas ligand (CD95L) have been described as possible pathomechanisms leading to impaired erythropoiesis. ... ...

Abstract	In low-risk Myelodysplastic Neoplasms (MDS), increased activity of apoptosis-promoting factors such as tumor necrosis factor (TNFα) and pro-apoptotic Fas ligand (CD95L) have been described as possible pathomechanisms leading to impaired erythropoiesis. Asunercept (APG101) is a novel therapeutic fusion protein blocking CD95, which has previously shown partial efficacy in reducing transfusion requirement in a clinical phase I trial for low-risk MDS patients (NCT01736436; 2012-11-26). In the current study we aimed to evaluate the effect of Asunercept therapy on the clonal bone marrow composition to identify potential biomarkers to predict response. Bone marrow samples of n = 12 low-risk MDS patients from the above referenced clinical trial were analyzed by serial deep whole exome sequencing in a total of n = 58 time points. We could distinguish a mean of 3.5 molecularly defined subclones per patient (range 2-6). We observed a molecular response defined as reductions of dominant clone sizes by a variant allele frequency (VAF) decrease of at least 10% (mean 20%, range: 10.5-39.2%) in dependency of Asunercept treatment in 9 of 12 (75%) patients. Most of this decline in clonal populations was observed after completion of 12 weeks treatment. Particularly early and pronounced reductions of clone sizes were found in subclones driven by mutations in genes involved in regulation of methylation (n = 1 DNMT3A, n = 1 IDH2, n = 1 TET2). Our results suggest that APG101 could be efficacious in reducing clone sizes of mutated hematopoietic cells in the bone marrow of Myelodysplastic Neoplasms, which warrants further investigation.
MeSH term(s)	Humans ; Neoplasms ; Myelodysplastic Syndromes/drug therapy ; Myelodysplastic Syndromes/genetics ; Myelodysplastic Syndromes/pathology ; Clone Cells/pathology ; Bone Marrow/pathology ; Apoptosis ; Mutation
Language	English
Publishing date	2024-02-27
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1064950-5
ISSN	1432-0584 ; 0939-5555 ; 0945-8077
ISSN (online)	1432-0584
ISSN	0939-5555 ; 0945-8077
DOI	10.1007/s00277-024-05664-5
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Article ; Online: The effect of neoadjuvant chemotherapy on the correlation of tumor-associated macrophages with CD31 and LYVE-1.

Mitrofanova, Irina / Zavyalova, Marina / Riabov, Vladimir / Cherdyntseva, Nadezhda / Kzhyshkowska, Julia

Immunobiology

2017 Volume 223, Issue 6-7, Page(s) 449–459

Abstract: Angiogenesis and lymphangiogenesis play a crucial role in tumor growth, invasion and metastasis. Tumor-associated macrophages (TAM) induce both angiogenesis and lymphangiogenesis in mouse breast cancer models and positively correlate with these processes ...

Abstract	Angiogenesis and lymphangiogenesis play a crucial role in tumor growth, invasion and metastasis. Tumor-associated macrophages (TAM) induce both angiogenesis and lymphangiogenesis in mouse breast cancer models and positively correlate with these processes in human breast cancer patients. Neoadjuvant chemotherapy (NAC) is a widely used therapeutic option for cancer treatment. However, the effect of NAC on the distribution of TAM within intratumoral compartments and their correlation with angiogenesis and lymphangiogenesis remained unknown. In the present study we analyzed the effect of NAC on the distribution of CD68+ and stabilin-1+ TAM in five functionally distinct areas of human breast cancer and their correlations with microvessel density (MVD) and lymphatic microvessel density (LMVD), identified by CD31 and LYVE1, respectively. We found that NAC enhances blood vessel density in soft fibrous stroma and in coarse fibrous stroma. Without NAC the amount of CD68+ TAM in gaps of ductal tumor structures positively correlate with CD31+ microvessel density in soft fibrous stroma. NAC had enhancing effect on the amount of CD68+ TAM but not stabilin-1+ TAM in soft fibrous stroma. However, no correlation between TAM and CD31+ microvessel density was identified after NAC. NAC did not enhance the lymphatic microvessel density. But after NAC stabilin-1 expressing subpopulation of TAM positively correlated with expression of LYVE-1. We hypothesized that CD68+ TAM can support tumor angiogenesis primarily before NAC, while stabilin-1+ TAM can contribute to the maintenance of lymphatic microvessel density after NAC.
MeSH term(s)	Adult ; Aged ; Antigens, CD/metabolism ; Antigens, Differentiation, Myelomonocytic/metabolism ; Breast Neoplasms/drug therapy ; Breast Neoplasms/immunology ; Breast Neoplasms/pathology ; Carcinoma, Ductal/drug therapy ; Carcinoma, Ductal/immunology ; Carcinoma, Ductal/pathology ; Cell Adhesion Molecules, Neuronal/metabolism ; Female ; Humans ; Macrophages/immunology ; Microvessels/pathology ; Middle Aged ; Neoadjuvant Therapy ; Neovascularization, Pathologic ; Platelet Endothelial Cell Adhesion Molecule-1/metabolism ; Receptors, Lymphocyte Homing/metabolism ; Vesicular Transport Proteins/metabolism
Chemical Substances	Antigens, CD ; Antigens, Differentiation, Myelomonocytic ; CD68 antigen, human ; Cell Adhesion Molecules, Neuronal ; LYVE1 protein, human ; Platelet Endothelial Cell Adhesion Molecule-1 ; Receptors, Lymphocyte Homing ; STAB1 protein, human ; Vesicular Transport Proteins
Language	English
Publishing date	2017-10-31
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	563292-4
ISSN	1878-3279 ; 0171-2985
ISSN (online)	1878-3279
ISSN	0171-2985
DOI	10.1016/j.imbio.2017.10.050
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Article ; Online: Reactive oxygen species (ROS) in macrophage activation and function in diabetes.

Rendra, Erika / Riabov, Vladimir / Mossel, Dieuwertje M / Sevastyanova, Tatyana / Harmsen, Martin C / Kzhyshkowska, Julia

Immunobiology

2018 Volume 224, Issue 2, Page(s) 242–253

Abstract: In a diabetic milieu high levels of reactive oxygen species (ROS) are induced. This contributes to the vascular complications of diabetes. Recent studies have shown that ROS formation is exacerbated in diabetic monocytes and macrophages due to a ... ...

Abstract	In a diabetic milieu high levels of reactive oxygen species (ROS) are induced. This contributes to the vascular complications of diabetes. Recent studies have shown that ROS formation is exacerbated in diabetic monocytes and macrophages due to a glycolytic metabolic shift. Macrophages are important players in the progression of diabetes and promote inflammation through the release of pro-inflammatory cytokines and proteases. Because ROS is an important mediator for the activation of pro-inflammatory signaling pathways, obesity and hyperglycemia-induced ROS production may favor induction of M1-like pro-inflammatory macrophages during diabetes onset and progression. ROS induces MAPK, STAT1, STAT6 and NFκB signaling, and interferes with macrophage differentiation via epigenetic (re)programming. Therefore, a comprehensive understanding of the impact of ROS on macrophage phenotype and function is needed in order to improve treatment of diabetes and its vascular complications. In the current comprehensive review, we dissect the role of ROS in macrophage polarization, and analyze how ROS production links metabolism and inflammation in diabetes and its complications. Finally, we discuss the contribution of ROS to the crosstalk between macrophages and endothelial cells in diabetic complications.
MeSH term(s)	Animals ; Diabetes Mellitus/drug therapy ; Diabetes Mellitus/etiology ; Diabetes Mellitus/metabolism ; Disease Susceptibility ; Energy Metabolism ; Humans ; Immunomodulation ; Macrophage Activation/drug effects ; Macrophage Activation/immunology ; Macrophages/drug effects ; Macrophages/immunology ; Macrophages/metabolism ; Oxidative Stress/drug effects ; Reactive Oxygen Species/metabolism ; Signal Transduction
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2018-12-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	563292-4
ISSN	1878-3279 ; 0171-2985
ISSN (online)	1878-3279
ISSN	0171-2985
DOI	10.1016/j.imbio.2018.11.010
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Article ; Online: Role of chitinase-like proteins in cancer.

Kzhyshkowska, Julia / Yin, Shuiping / Liu, Tengfei / Riabov, Vladimir / Mitrofanova, Irina

Biological chemistry

2016 Volume 397, Issue 3, Page(s) 231–247

Abstract: Chitinase-like proteins (CLPs) are lectins combining properties of cytokines and growth factors. Human CLPs include YKL-40, YKL-39 and SI-CLP that are secreted by cancer cells, macrophages, neutrophils, synoviocytes, chondrocytes and other cells. The ... ...

Abstract	Chitinase-like proteins (CLPs) are lectins combining properties of cytokines and growth factors. Human CLPs include YKL-40, YKL-39 and SI-CLP that are secreted by cancer cells, macrophages, neutrophils, synoviocytes, chondrocytes and other cells. The best investigated CLP in cancer is YKL-40. Serum and plasma levels of YKL-40 correlate with poor prognosis in breast, lung, prostate, liver, bladder, colon and other types of cancers. In combination with other circulating factors YKL-40 can be used as a predictive biomarker of cancer outcome. In experimental models YKL-40 supports tumor initiation through binding to RAGE, and is able to induce cancer cell proliferation via ERK1/2-MAPK pathway. YKL-40 supports tumor angiogenesis by interaction with syndecan-1 on endothelial cells and metastatic spread by stimulating production of pro-inflammatory and pro-invasive factors MMP9, CCL2 and CXCL2. CLPs induce production of pro- and anti-inflammatory cytokines and chemokines, and are potential modulators of inflammatory tumor microenvironment. Targeting YKL-40 using neutralizing antibodies exerts anti-cancer effect in preclinical animal models. Multifunctional role of CLPs in regulation of inflammation and intratumoral processes makes them attractive candidates for tumor therapy and immunomodulation. In this review we comprehensively analyze recent data about expression pattern, and involvement of human CLPs in cancer.
MeSH term(s)	Adipokines/chemistry ; Adipokines/genetics ; Adipokines/immunology ; Adipokines/metabolism ; Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry ; Carrier Proteins/genetics ; Carrier Proteins/immunology ; Carrier Proteins/metabolism ; Chitinase-3-Like Protein 1 ; Chitinases/chemistry ; Chitinases/genetics ; Chitinases/immunology ; Chitinases/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/metabolism ; Lectins/chemistry ; Lectins/genetics ; Lectins/immunology ; Lectins/metabolism ; Neoplasms/genetics ; Neoplasms/immunology ; Neoplasms/metabolism
Chemical Substances	Adipokines ; CHI3L1 protein, human ; CHID1 protein, human ; Carrier Proteins ; Chitinase-3-Like Protein 1 ; Lectins ; CHI3L2 protein, human (EC 3.2.1.14) ; Chitinases (EC 3.2.1.14)
Language	English
Publishing date	2016-03
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1334659-3
ISSN	1437-4315 ; 1431-6730 ; 1432-0355
ISSN (online)	1437-4315
ISSN	1431-6730 ; 1432-0355
DOI	10.1515/hsz-2015-0269
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Article ; Online: The effect of healing phenotype-inducing cytokine formulations within soft hydrogels on encapsulated monocytes and incoming immune cells.

Ščigalková, Ivana / Bystroňová, Julie / Kovářová, Lenka / Pravda, Martin / Velebný, Vladimír / Riabov, Vladimir / Klüter, Harald / Kzhyshkowska, Julia / Vrana, Nihal Engin

RSC advances

2019 Volume 9, Issue 37, Page(s) 21396–21404

Abstract: The adverse immune responses to implantable biomedical devices is a general problem with important consequences for the functionality of implants. Immunomodulatory soft hydrogel-based interfaces between the implant and the host can attenuate these ... ...

Abstract	The adverse immune responses to implantable biomedical devices is a general problem with important consequences for the functionality of implants. Immunomodulatory soft hydrogel-based interfaces between the implant and the host can attenuate these reactions. Moreover, encapsulation of the patient's own immune cells into these interfaces can lead to the personalisation of implants from the immune reaction point of view. Herein, we described a co-crosslinkable composite hydrogel (composed of gelatin and hyaluronic acid), which could be used for the encapsulation of macrophages in the presence of an anti-inflammatory phenotype-fixing cytokine cocktail. To mimick the incoming immune cells on the coating surface
Language	English
Publishing date	2019-07-10
Publishing country	England
Document type	Journal Article
ISSN	2046-2069
ISSN (online)	2046-2069
DOI	10.1039/c9ra02878a
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