Anti-Galectin-2 Antibody Treatment Reduces Atherosclerotic Plaque Size and Alters Macrophage Polarity
Abstract Background Galectins have numerous cellular functions in immunity and inflammation. Short-term galectin-2 (Gal-2) blockade in ischemia-induced arteriogenesis shifts macrophages to an anti-inflammatory phenotype and improves perfusion. Gal-2 may also affect other macrophage-related cardiova...
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| Vydané v: | Thrombosis and haemostasis Ročník 122; číslo 6; s. 1047 - 1057 |
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| Hlavní autori: | , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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Rüdigerstraße 14, 70469 Stuttgart, Germany
Georg Thieme Verlag KG
01.06.2022
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| ISSN: | 0340-6245, 2567-689X, 2567-689X |
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| Abstract | Abstract
Background
Galectins have numerous cellular functions in immunity and inflammation. Short-term galectin-2 (Gal-2) blockade in ischemia-induced arteriogenesis shifts macrophages to an anti-inflammatory phenotype and improves perfusion. Gal-2 may also affect other macrophage-related cardiovascular diseases.
Objectives
This study aims to elucidate the effects of Gal-2 inhibition in atherosclerosis.
Methods
ApoE
−/−
mice were given a high-cholesterol diet (HCD) for 12 weeks. After 6 weeks of HCD, intermediate atherosclerotic plaques were present. To study the effects of anti-Gal-2 nanobody treatment on the progression of existing atherosclerosis, treatment with two llama-derived anti-Gal-2 nanobodies (clones 2H8 and 2C10), or vehicle was given for the remaining 6 weeks.
Results
Gal-2 inhibition reduced the progression of existing atherosclerosis. Atherosclerotic plaque area in the aortic root was decreased, especially so in mice treated with 2C10 nanobodies. This clone showed reduced atherosclerosis severity as reflected by a decrease in fibrous cap atheromas in addition to decreases in plaque size.
The number of plaque resident macrophages was unchanged; however, there was a significant increase in the fraction of CD206
+
macrophages. 2C10 treatment also increased plaque α-smooth muscle content, and Gal-2 may have a role in modulating the inflammatory status of smooth muscle cells. Remarkably, both treatments reduced serum cholesterol concentrations including reductions in very low-density lipoprotein, low-density lipoprotein, and high-density lipoprotein while triglyceride concentrations were unchanged.
Conclusion
Prolonged and frequent treatment with anti-Gal-2 nanobodies reduced plaque size, slowed plaque progression, and modified the phenotype of plaque macrophages toward an anti-inflammatory profile. These results hold promise for future macrophage modulating therapeutic interventions that promote arteriogenesis and reduce atherosclerosis. |
|---|---|
| AbstractList | Abstract
Background
Galectins have numerous cellular functions in immunity and inflammation. Short-term galectin-2 (Gal-2) blockade in ischemia-induced arteriogenesis shifts macrophages to an anti-inflammatory phenotype and improves perfusion. Gal-2 may also affect other macrophage-related cardiovascular diseases.
Objectives
This study aims to elucidate the effects of Gal-2 inhibition in atherosclerosis.
Methods
ApoE
−/−
mice were given a high-cholesterol diet (HCD) for 12 weeks. After 6 weeks of HCD, intermediate atherosclerotic plaques were present. To study the effects of anti-Gal-2 nanobody treatment on the progression of existing atherosclerosis, treatment with two llama-derived anti-Gal-2 nanobodies (clones 2H8 and 2C10), or vehicle was given for the remaining 6 weeks.
Results
Gal-2 inhibition reduced the progression of existing atherosclerosis. Atherosclerotic plaque area in the aortic root was decreased, especially so in mice treated with 2C10 nanobodies. This clone showed reduced atherosclerosis severity as reflected by a decrease in fibrous cap atheromas in addition to decreases in plaque size.
The number of plaque resident macrophages was unchanged; however, there was a significant increase in the fraction of CD206
+
macrophages. 2C10 treatment also increased plaque α-smooth muscle content, and Gal-2 may have a role in modulating the inflammatory status of smooth muscle cells. Remarkably, both treatments reduced serum cholesterol concentrations including reductions in very low-density lipoprotein, low-density lipoprotein, and high-density lipoprotein while triglyceride concentrations were unchanged.
Conclusion
Prolonged and frequent treatment with anti-Gal-2 nanobodies reduced plaque size, slowed plaque progression, and modified the phenotype of plaque macrophages toward an anti-inflammatory profile. These results hold promise for future macrophage modulating therapeutic interventions that promote arteriogenesis and reduce atherosclerosis. Galectins have numerous cellular functions in immunity and inflammation. Short-term galectin-2 (Gal-2) blockade in ischemia-induced arteriogenesis shifts macrophages to an anti-inflammatory phenotype and improves perfusion. Gal-2 may also affect other macrophage-related cardiovascular diseases.BACKGROUNDGalectins have numerous cellular functions in immunity and inflammation. Short-term galectin-2 (Gal-2) blockade in ischemia-induced arteriogenesis shifts macrophages to an anti-inflammatory phenotype and improves perfusion. Gal-2 may also affect other macrophage-related cardiovascular diseases.This study aims to elucidate the effects of Gal-2 inhibition in atherosclerosis.OBJECTIVESThis study aims to elucidate the effects of Gal-2 inhibition in atherosclerosis.ApoE -/- mice were given a high-cholesterol diet (HCD) for 12 weeks. After 6 weeks of HCD, intermediate atherosclerotic plaques were present. To study the effects of anti-Gal-2 nanobody treatment on the progression of existing atherosclerosis, treatment with two llama-derived anti-Gal-2 nanobodies (clones 2H8 and 2C10), or vehicle was given for the remaining 6 weeks.METHODSApoE -/- mice were given a high-cholesterol diet (HCD) for 12 weeks. After 6 weeks of HCD, intermediate atherosclerotic plaques were present. To study the effects of anti-Gal-2 nanobody treatment on the progression of existing atherosclerosis, treatment with two llama-derived anti-Gal-2 nanobodies (clones 2H8 and 2C10), or vehicle was given for the remaining 6 weeks.Gal-2 inhibition reduced the progression of existing atherosclerosis. Atherosclerotic plaque area in the aortic root was decreased, especially so in mice treated with 2C10 nanobodies. This clone showed reduced atherosclerosis severity as reflected by a decrease in fibrous cap atheromas in addition to decreases in plaque size.The number of plaque resident macrophages was unchanged; however, there was a significant increase in the fraction of CD206+ macrophages. 2C10 treatment also increased plaque α-smooth muscle content, and Gal-2 may have a role in modulating the inflammatory status of smooth muscle cells. Remarkably, both treatments reduced serum cholesterol concentrations including reductions in very low-density lipoprotein, low-density lipoprotein, and high-density lipoprotein while triglyceride concentrations were unchanged.RESULTSGal-2 inhibition reduced the progression of existing atherosclerosis. Atherosclerotic plaque area in the aortic root was decreased, especially so in mice treated with 2C10 nanobodies. This clone showed reduced atherosclerosis severity as reflected by a decrease in fibrous cap atheromas in addition to decreases in plaque size.The number of plaque resident macrophages was unchanged; however, there was a significant increase in the fraction of CD206+ macrophages. 2C10 treatment also increased plaque α-smooth muscle content, and Gal-2 may have a role in modulating the inflammatory status of smooth muscle cells. Remarkably, both treatments reduced serum cholesterol concentrations including reductions in very low-density lipoprotein, low-density lipoprotein, and high-density lipoprotein while triglyceride concentrations were unchanged.Prolonged and frequent treatment with anti-Gal-2 nanobodies reduced plaque size, slowed plaque progression, and modified the phenotype of plaque macrophages toward an anti-inflammatory profile. These results hold promise for future macrophage modulating therapeutic interventions that promote arteriogenesis and reduce atherosclerosis.CONCLUSIONProlonged and frequent treatment with anti-Gal-2 nanobodies reduced plaque size, slowed plaque progression, and modified the phenotype of plaque macrophages toward an anti-inflammatory profile. These results hold promise for future macrophage modulating therapeutic interventions that promote arteriogenesis and reduce atherosclerosis. Galectins have numerous cellular functions in immunity and inflammation. Short-term galectin-2 (Gal-2) blockade in ischemia-induced arteriogenesis shifts macrophages to an anti-inflammatory phenotype and improves perfusion. Gal-2 may also affect other macrophage-related cardiovascular diseases. This study aims to elucidate the effects of Gal-2 inhibition in atherosclerosis. mice were given a high-cholesterol diet (HCD) for 12 weeks. After 6 weeks of HCD, intermediate atherosclerotic plaques were present. To study the effects of anti-Gal-2 nanobody treatment on the progression of existing atherosclerosis, treatment with two llama-derived anti-Gal-2 nanobodies (clones 2H8 and 2C10), or vehicle was given for the remaining 6 weeks. Gal-2 inhibition reduced the progression of existing atherosclerosis. Atherosclerotic plaque area in the aortic root was decreased, especially so in mice treated with 2C10 nanobodies. This clone showed reduced atherosclerosis severity as reflected by a decrease in fibrous cap atheromas in addition to decreases in plaque size.The number of plaque resident macrophages was unchanged; however, there was a significant increase in the fraction of CD206 macrophages. 2C10 treatment also increased plaque α-smooth muscle content, and Gal-2 may have a role in modulating the inflammatory status of smooth muscle cells. Remarkably, both treatments reduced serum cholesterol concentrations including reductions in very low-density lipoprotein, low-density lipoprotein, and high-density lipoprotein while triglyceride concentrations were unchanged. Prolonged and frequent treatment with anti-Gal-2 nanobodies reduced plaque size, slowed plaque progression, and modified the phenotype of plaque macrophages toward an anti-inflammatory profile. These results hold promise for future macrophage modulating therapeutic interventions that promote arteriogenesis and reduce atherosclerosis. |
| Author | Eringa, Ed Gijbels, Marion Vries, Carlie J. de Zelcer, Noam Bosmans, Laura A. Jansen, Matthijs Beckers, Linda Hendrix, Sebastian Tiel, Claudia van Kane, Jamie Horrevoets, Anton J. Royen, Niels van Lutgens, Esther von Hundelshausen, Philipp Vervloet, Marc |
| Author_xml | – sequence: 1 givenname: Jamie surname: Kane fullname: Kane, Jamie organization: Department of Physiology, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centre, Amsterdam, The Netherlands – sequence: 2 givenname: Matthijs surname: Jansen fullname: Jansen, Matthijs organization: Department of Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centre, Amsterdam, The Netherlands – sequence: 3 givenname: Sebastian surname: Hendrix fullname: Hendrix, Sebastian organization: Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centre, Amsterdam, The Netherlands – sequence: 4 givenname: Laura A. surname: Bosmans fullname: Bosmans, Laura A. organization: Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centre, Amsterdam, The Netherlands – sequence: 5 givenname: Linda surname: Beckers fullname: Beckers, Linda organization: Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centre, Amsterdam, The Netherlands – sequence: 6 givenname: Claudia van surname: Tiel fullname: Tiel, Claudia van organization: Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centre, Amsterdam, The Netherlands – sequence: 7 givenname: Marion surname: Gijbels fullname: Gijbels, Marion organization: Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), GROW-School for Oncology and Developmental Biology, Maastricht University, Maastricht, The Netherlands – sequence: 8 givenname: Noam surname: Zelcer fullname: Zelcer, Noam organization: Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centre, Amsterdam, The Netherlands – sequence: 9 givenname: Carlie J. de surname: Vries fullname: Vries, Carlie J. de organization: Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centre, Amsterdam, The Netherlands – sequence: 10 givenname: Philipp orcidid: 0000-0001-7474-9370 surname: von Hundelshausen fullname: von Hundelshausen, Philipp organization: Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximillian's University, Munich, Germany – sequence: 11 givenname: Marc surname: Vervloet fullname: Vervloet, Marc organization: Department of Nephrology, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centre, Amsterdam, The Netherlands – sequence: 12 givenname: Ed surname: Eringa fullname: Eringa, Ed organization: Department of Physiology, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centre, Amsterdam, The Netherlands – sequence: 13 givenname: Anton J. surname: Horrevoets fullname: Horrevoets, Anton J. organization: Department of Molecular Cell Biology and Immunology, Amsterdam University Medical Centre, Amsterdam, The Netherlands – sequence: 14 givenname: Niels van surname: Royen fullname: Royen, Niels van organization: Department of Cardiology, Radboud University Medical Centre, Nijmegen, The Netherlands – sequence: 15 givenname: Esther surname: Lutgens fullname: Lutgens, Esther email: e.lutgens@amsterdamumc.nl organization: Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam University Medical Centre |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34852377$$D View this record in MEDLINE/PubMed |
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Background
Galectins have numerous cellular functions in immunity and inflammation. Short-term galectin-2 (Gal-2) blockade in ischemia-induced... Galectins have numerous cellular functions in immunity and inflammation. Short-term galectin-2 (Gal-2) blockade in ischemia-induced arteriogenesis shifts... |
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| SubjectTerms | Atherosclerosis and Ischaemic Disease |
| Title | Anti-Galectin-2 Antibody Treatment Reduces Atherosclerotic Plaque Size and Alters Macrophage Polarity |
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