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  • 1
    Online Resource
    Online Resource
    Binding and Endocytosis of Proteins Mediated by Epithelial gp330
    Wiley ; 1994
    In:  Annals of the New York Academy of Sciences Vol. 737, No. 1 ( 1994-09), p. 124-137
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 737, No. 1 ( 1994-09), p. 124-137
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    URL: Article
    DOI: 10.1111/nyas.1994.737.issue-1
    DOI: 10.1111/j.1749-6632.1994.tb44306.x
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 1994
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
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  • 2
    Online Resource
    Online Resource
    Epigenetic Silencing of LRP2 Is Associated with Dedifferentiation and Poor Survival in Multiple Solid Tumor Types
    MDPI AG ; 2023
    In:  Cancers Vol. 15, No. 6 ( 2023-03-17), p. 1830-
    Details
    In: Cancers, MDPI AG, Vol. 15, No. 6 ( 2023-03-17), p. 1830-
    Abstract: More than 80% of human cancers originate in epithelial tissues. Loss of epithelial cell characteristics are hallmarks of tumor development. Receptor-mediated endocytosis is a key function of absorptive epithelial cells with importance for cellular and organismal homeostasis. LRP2 (megalin) is the largest known endocytic membrane receptor and is essential for endocytosis of various ligands in specialized epithelia, including the proximal tubules of the kidney, the thyroid gland, and breast glandular epithelium. However, the role and regulation of LRP2 in cancers that arise from these tissues has not been delineated. Here, we examined the expression of LRP2 across 33 cancer types in The Cancer Genome Atlas. As expected, the highest levels of LRP2 were found in cancer types that arise from LRP2-expressing absorptive epithelial cells. However, in a subset of tumors from these cancer types, we observed epigenetic silencing of LRP2. LRP2 expression showed a strong inverse correlation to methylation of a specific CpG site (cg02361027) in the first intron of the LRP2 gene. Interestingly, low expression of LRP2 was associated with poor patient outcome in clear cell renal cell carcinoma, papillary renal cell carcinoma, mesothelioma, papillary thyroid carcinoma, and invasive breast carcinoma. Furthermore, loss of LRP2 expression was associated with dedifferentiated histological and molecular subtypes of these cancers. These observations now motivate further studies on the functional role of LRP2 in tumors of epithelial origin and the potential use of LRP2 as a cancer biomarker.
    Type of Medium: Online Resource
    ISSN: 2072-6694
    URL: Article
    DOI: 10.3390/cancers15061830
    Language: English
    Publisher: MDPI AG
    Publication Date: 2023
    detail.hit.zdb_id: 2527080-1
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  • 3
    Online Resource
    Online Resource
    The macrophage CD163 surface glycoprotein is an erythroblast adhesion receptor
    American Society of Hematology ; 2007
    In:  Blood Vol. 109, No. 12 ( 2007-06-15), p. 5223-5229
    Details
    In: Blood, American Society of Hematology, Vol. 109, No. 12 ( 2007-06-15), p. 5223-5229
    Abstract: Erythropoiesis occurs in erythroblastic islands, where developing erythroblasts closely interact with macrophages. The adhesion molecules that govern macrophage-erythroblast contact have only been partially defined. Our previous work has implicated the rat ED2 antigen, which is highly expressed on the surface of macrophages in erythroblastic islands, in erythroblast binding. In particular, the monoclonal antibody ED2 was found to inhibit erythroblast binding to bone marrow macrophages. Here, we identify the ED2 antigen as the rat CD163 surface glycoprotein, a member of the group B scavenger receptor cysteine-rich (SRCR) family that has previously been shown to function as a receptor for hemoglobin-haptoglobin (Hb-Hp) complexes and is believed to contribute to the clearance of free hemoglobin. CD163 transfectants and recombinant protein containing the extracellular domain of CD163 supported the adhesion of erythroblastic cells. Furthermore, we identified a 13–amino acid motif (CD163p2) corresponding to a putative interaction site within the second scavenger receptor domain of CD163 that could mediate erythroblast binding. Finally, CD163p2 promoted erythroid expansion in vitro, suggesting that it enhanced erythroid proliferation and/or survival, but did not affect differentiation. These findings identify CD163 on macrophages as an adhesion receptor for erythroblasts in erythroblastic islands, and suggest a regulatory role for CD163 during erythropoiesis.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood-2006-08-036467
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2007
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 4
    Online Resource
    Online Resource
    Obesity Alters Adipose Tissue Macrophage Iron Content and Tissue Iron Distribution
    American Diabetes Association ; 2014
    In:  Diabetes Vol. 63, No. 2 ( 2014-02-01), p. 421-432
    Details
    In: Diabetes, American Diabetes Association, Vol. 63, No. 2 ( 2014-02-01), p. 421-432
    Abstract: Adipose tissue (AT) expansion is accompanied by the infiltration and accumulation of AT macrophages (ATMs), as well as a shift in ATM polarization. Several studies have implicated recruited M1 ATMs in the metabolic consequences of obesity; however, little is known regarding the role of alternatively activated resident M2 ATMs in AT homeostasis or how their function is altered in obesity. Herein, we report the discovery of a population of alternatively activated ATMs with elevated cellular iron content and an iron-recycling gene expression profile. These iron-rich ATMs are referred to as MFehi, and the remaining ATMs are referred to as MFelo. In lean mice, ~25% of the ATMs are MFehi; this percentage decreases in obesity owing to the recruitment of MFelo macrophages. Similar to MFelo cells, MFehi ATMs undergo an inflammatory shift in obesity. In vivo, obesity reduces the iron content of MFehi ATMs and the gene expression of iron importers as well as the iron exporter, ferroportin, suggesting an impaired ability to handle iron. In vitro, exposure of primary peritoneal macrophages to saturated fatty acids also alters iron metabolism gene expression. Finally, the impaired MFehi iron handling coincides with adipocyte iron overload in obese mice. In conclusion, in obesity, iron distribution is altered both at the cellular and tissue levels, with AT playing a predominant role in this change. An increased availability of fatty acids during obesity may contribute to the observed changes in MFehi ATM phenotype and their reduced capacity to handle iron.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db13-0213
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2014
    detail.hit.zdb_id: 1501252-9
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  • 5
    Online Resource
    Online Resource
    The endocytic receptor megalin binds the iron transporting neutrophil-gelatinase-associated lipocalin with high affinity and mediates its cellular uptake
    Wiley ; 2005
    In:  FEBS Letters Vol. 579, No. 3 ( 2005-01-31), p. 773-777
    Details
    In: FEBS Letters, Wiley, Vol. 579, No. 3 ( 2005-01-31), p. 773-777
    Type of Medium: Online Resource
    ISSN: 0014-5793
    URL: Article
    DOI: 10.1016/j.febslet.2004.12.031
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2005
    detail.hit.zdb_id: 1460391-3
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Standardizing Scavenger Receptor Nomenclature
    The American Association of Immunologists ; 2014
    In:  The Journal of Immunology Vol. 192, No. 5 ( 2014-03-01), p. 1997-2006
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 192, No. 5 ( 2014-03-01), p. 1997-2006
    Abstract: Scavenger receptors constitute a large family of proteins that are structurally diverse and participate in a wide range of biological functions. These receptors are expressed predominantly by myeloid cells and recognize a variety of ligands, including endogenous and modified host-derived molecules and microbial pathogens. There are currently eight classes of scavenger receptors, many of which have multiple names, leading to inconsistencies and confusion in the literature. To address this problem, a workshop was organized by the U.S. National Institute of Allergy and Infectious Diseases, National Institutes of Health to help develop a clear definition of scavenger receptors and a standardized nomenclature based on that definition. Fifteen experts in the scavenger receptor field attended the workshop and, after extensive discussion, reached a consensus regarding the definition of scavenger receptors and a proposed scavenger receptor nomenclature. Scavenger receptors were defined as cell surface receptors that typically bind multiple ligands and promote the removal of non-self or altered-self targets. They often function by mechanisms that include endocytosis, phagocytosis, adhesion, and signaling that ultimately lead to the elimination of degraded or harmful substances. Based on this definition, nomenclature and classification of these receptors into 10 classes were proposed. The discussion and nomenclature recommendations described in this report only refer to mammalian scavenger receptors. The purpose of this article is to describe the proposed mammalian nomenclature and classification developed at the workshop and to solicit additional feedback from the broader research community.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1490003
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2014
    detail.hit.zdb_id: 1475085-5
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  • 7
    Online Resource
    Online Resource
    The class I scavenger receptor CD163 promotes internalization of ADAMTS13 by macrophages
    American Society of Hematology ; 2017
    In:  Blood Advances Vol. 1, No. 5 ( 2017-01-24), p. 293-305
    Details
    In: Blood Advances, American Society of Hematology, Vol. 1, No. 5 ( 2017-01-24), p. 293-305
    Abstract: Internalization of ADAMTS13 by macrophages may contribute to its clearance from the circulation. Here we investigated endocytic mechanisms that contribute to the uptake of ADAMTS13 by macrophages. Human monocyte-derived macrophages were used to monitor the uptake of fluorescently labeled recombinant ADAMTS13 by flow cytometry. Internalization of ADAMTS13 was blocked upon addition of the cell-permeable dynamin inhibitor dynasore. Partial blocking of ADAMTS13 uptake was observed by using mannan; however, uptake was not affected by an antibody that blocked binding to the macrophage mannose receptor CD206, which suggests that other endocytic receptors contribute to the internalization of ADAMTS13 by macrophages. A pull-down with ADAMTS13 and subsequent mass spectrometric analysis identified the class I scavenger receptor CD163 as a candidate receptor for ADAMTS13. Blocking experiments with monoclonal anti-CD163 antibody EDHu-1 resulted in decreased ADAMTS13 internalization by macrophages. Pronounced inhibition of ADAMTS13 uptake by EDHu-1 was observed in CD163 high-expressing macrophages. In agreement with these findings, CD163-expressing Chinese hamster ovary cells were capable of rapidly internalizing ADAMTS13. Surface plasmon resonance revealed binding of ADAMTS13 to scavenger receptor cysteine-rich domains 1-9 and 1-5 of CD163. Taken together, our data identify CD163 as a major endocytic receptor for ADAMTS13 on macrophages.
    Type of Medium: Online Resource
    ISSN: 2473-9529 , 2473-9537
    URL: Article
    DOI: 10.1182/bloodadvances.2016001321
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2017
    detail.hit.zdb_id: 2876449-3
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  • 8
    Online Resource
    Online Resource
    Downregulation of the Hemoglobin Scavenger Receptor in Individuals With Diabetes and the Hp 2-2 Genotype : Implications for the Response to Intraplaque Hemorrhage and Plaque Vulnerability
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Circulation Research Vol. 101, No. 1 ( 2007-07-06), p. 106-110
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 101, No. 1 ( 2007-07-06), p. 106-110
    Abstract: In individuals with diabetes mellitus (DM), the haptoglobin (Hp) genotype is a major determinant of susceptibility to myocardial infarction. We have proposed that this is because of DM and Hp genotype–dependent differences in the response to intraplaque hemorrhage. The macrophage hemoglobin scavenging receptor CD163 plays an essential role in the clearance of hemoglobin released from lysed red blood cells after intraplaque hemorrhage. We sought to test the hypothesis that expression of CD163 is DM and Hp genotype–dependent. CD163 was quantified in plaques by immunohistochemistry, on peripheral blood monocytes (PBMs) by FACS, and as soluble CD163 (sCD163) in plasma by ELISA. In DM plaques, despite an increase in macrophage infiltration, CD163 immunoreactivity was lower, resulting in a dramatic reduction in the percentage of macrophages expressing CD163 (27±2% versus 70±2%, P =0.0001). In individuals with DM as compared with individuals without DM, the percentage of PBMs expressing CD163 was reduced (3.7±0.6% versus 7.1±0.9%, P 〈 0.002) whereas soluble plasma CD163 was increased (2.6±1.1 μg/mL versus 1.6±0.8 μg/mL, P 〈 0.0005). Among DM individuals, the Hp 2-2 genotype was associated with a decrease in the percentage of PBMs expressing CD163 (2.3±0.5% versus 5.6±1.3%, P =0.01) and an increase in plasma soluble CD163 (3.0±0.2 μg/mL versus 2.3±0.2 μg/mL, P =0.04). Taken together, these results demonstrate an impaired hemoglobin clearance capacity in Hp 2-2 DM individuals and may provide the key insight explaining the increased incidence of myocardial infarction in this population.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.107.149435
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 1467838-X
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  • 9
    Online Resource
    Online Resource
    The Macrophage-Specific CD163 Is an Endocytic Receptor for Von Willebrand Factor (VWF) Cleaving Protease ADAMTS13
    American Society of Hematology ; 2016
    In:  Blood Vol. 128, No. 22 ( 2016-12-02), p. 17-17
    Details
    In: Blood, American Society of Hematology, Vol. 128, No. 22 ( 2016-12-02), p. 17-17
    Abstract: Von Willebrand Factor (VWF) cleaving protease ADAMTS13 is responsible for proteolysis of ultra large VWF multimers in the circulation. ADAMTS13 is synthesized by hepatic stellate cells in the liver. Also endothelial cells have been suggested to contribute to the synthesis of ADAMTS13. In patients with acquired thrombotic thrombocytopenic purpura auto-reactive antibodies are formed primarily against the spacer domain of ADAMTS13. Previously we have shown that monocyte-derived dendritic cells were able to endocytose ADAMTS13 via the macrophage mannose receptor and subsequently process it into peptides and present it on MHC class II. However, it is currently unclear which receptor contributes to the clearance of ADAMTS13 from the circulation. The half-life of ADAMTS13 was measured following plasma infusion in patients with congenital TTP and was found to vary between 2.1 and 3.3 days. Internalization of ADAMTS13 by tissue-resident macrophages may contribute to its clearance from the circulation. Here we investigated endocytic mechanisms contributing to the uptake of ADAMTS13 by macrophages. Human monocyte-derived macrophages (MDMs) were used to monitor the uptake of fluorescently labelled recombinant ADAMTS13 by flow cytometry. Internalization of ADAMTS13 was blocked upon addition of the cell-permeable dynamin-inhibitor dynasore. Partial blockage of ADAMTS13 internalization was observed employing mannan; uptake however was not affected by a blocking antibody directed towards the macrophage mannose receptor CD206. A pull-down with ADAMTS13 and subsequent mass spectrometric analysis identified the hemoglobin scavenger receptor CD163 as a candidate receptor for ADAMTS13. CD163 is primarily expressed by the monocyte-macrophage lineage and is highly expressed on type-2 macrophages present in the bone marrow, the red pulp of the spleen and in the liver on Kupffer cells. Blocking experiments with a monoclonal anti-CD163 antibody EDHu-1 resulted in a decreased ADAMTS13 internalization by macrophages. Pronounced inhibition of ADAMTS13 uptake by EDHu-1 was observed in macrophages in which the expression of CD163 was boosted upon incubation with IL-10. In agreement with these findings CD163-expressing CHO cells but not CHO CD163-/- cells were capable of rapidly internalizing ADAMTS13. Surface plasmon resonance revealed high affinity binding of ADAMTS13 to soluble CD163 containing scavenger receptor cysteine-rich (SRCR) domain 1-9. Our results position CD163 as a novel binding partner for ADAMTS13 and suggest that binding of ADAMTS13 to CD163 promotes its internalization by macrophages. Disclosures No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V128.22.17.17
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2016
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 10
    Online Resource
    Online Resource
    Targeting of CD163+ Macrophages in Inflammatory and Malignant Diseases
    MDPI AG ; 2020
    In:  International Journal of Molecular Sciences Vol. 21, No. 15 ( 2020-07-31), p. 5497-
    Details
    In: International Journal of Molecular Sciences, MDPI AG, Vol. 21, No. 15 ( 2020-07-31), p. 5497-
    Abstract: The macrophage is a key cell in the pro- and anti-inflammatory response including that of the inflammatory microenvironment of malignant tumors. Much current drug development in chronic inflammatory diseases and cancer therefore focuses on the macrophage as a target for immunotherapy. However, this strategy is complicated by the pleiotropic phenotype of the macrophage that is highly responsive to its microenvironment. The plasticity leads to numerous types of macrophages with rather different and, to some extent, opposing functionalities, as evident by the existence of macrophages with either stimulating or down-regulating effect on inflammation and tumor growth. The phenotypes are characterized by different surface markers and the present review describes recent progress in drug-targeting of the surface marker CD163 expressed in a subpopulation of macrophages. CD163 is an abundant endocytic receptor for multiple ligands, quantitatively important being the haptoglobin-hemoglobin complex. The microenvironment of inflammation and tumorigenesis is particular rich in CD163+ macrophages. The use of antibodies for directing anti-inflammatory (e.g., glucocorticoids) or tumoricidal (e.g., doxorubicin) drugs to CD163+ macrophages in animal models of inflammation and cancer has demonstrated a high efficacy of the conjugate drugs. This macrophage-targeting approach has a low toxicity profile that may highly improve the therapeutic window of many current drugs and drug candidates.
    Type of Medium: Online Resource
    ISSN: 1422-0067
    URL: Article
    DOI: 10.3390/ijms21155497
    Language: English
    Publisher: MDPI AG
    Publication Date: 2020
    detail.hit.zdb_id: 2019364-6
    SSG: 12
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