Methionine Aminopeptidase 2 (MetAP2) Inhibitor BL6 Attenuates Inflammation in Cultured Microglia and in a Mouse Model of Alzheimer’s Disease

Methionine aminopeptidase 2 (MetAP2) plays an important role in the regulation of protein synthesis and post-translational processing. Preclinical/clinical applications of MetAP2 inhibitors for the treatment of various diseases have been explored because of their antiangiogenic, anticancer, antiobes...

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Main Authors: Xiuli Zhang, Shivakumar Subbanna, Colin R. O. Williams, Stefanie Canals-Baker, Audrey Hashim, Donald A. Wilson, Louis M. Weiss, Srushti Shukla, Parthiban Chokkalingam, Sasmita Das, Bhaskar C. Das, Mariko Saito
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Language:English
Published: MDPI AG 2025-01-01
Series:Molecules
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Online Access:https://www.mdpi.com/1420-3049/30/3/620
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author Xiuli Zhang
Shivakumar Subbanna
Colin R. O. Williams
Stefanie Canals-Baker
Audrey Hashim
Donald A. Wilson
Louis M. Weiss
Srushti Shukla
Parthiban Chokkalingam
Sasmita Das
Bhaskar C. Das
Mariko Saito
author_facet Xiuli Zhang
Shivakumar Subbanna
Colin R. O. Williams
Stefanie Canals-Baker
Audrey Hashim
Donald A. Wilson
Louis M. Weiss
Srushti Shukla
Parthiban Chokkalingam
Sasmita Das
Bhaskar C. Das
Mariko Saito
author_sort Xiuli Zhang
collection DOAJ
description Methionine aminopeptidase 2 (MetAP2) plays an important role in the regulation of protein synthesis and post-translational processing. Preclinical/clinical applications of MetAP2 inhibitors for the treatment of various diseases have been explored because of their antiangiogenic, anticancer, antiobesity, antidiabetic, and immunosuppressive properties. However, the effects of MetAP2 inhibitors on CNS diseases are rarely examined despite the abundant presence of MetAP2 in the brain. Previously, we synthesized a novel boron-containing MetAP2 inhibitor, BL6, and found that it suppressed angiogenesis and adipogenesis yet improved glucose uptake. Here, we studied the anti-inflammatory effects of BL6 in SIM-A9 microglia and in a mouse model of Alzheimer’s disease generated by the intracerebroventricular (icv) injection of streptozotocin (STZ). We found that BL6 reduced proinflammatory molecules, such as nitric oxide, iNOS, IL-1β, and IL-6, together with phospho-Akt and phospho-NF-κB p65, which were elevated in lipopolysaccharide (LPS)-activated microglial SIM-A9 cells. However, the LPS-induced reduction in Arg-1 and CD206 was attenuated by BL6, suggesting that BL6 promotes microglial M1 to M2 polarization. BL6 also decreased glial activation along with a reduction in phospho-tau and an elevation in synaptophysin in the icv-STZ mouse model. Thus, our experiments demonstrate an anti-neuroinflammatory action of BL6, suggesting possible clinical applications of MetAP2 inhibitors for brain disorders in which neuroinflammation is involved.
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spelling doaj-art-37e5d7fbdad6452aa5dc85b962d9937b2025-08-20T02:48:07ZengMDPI AGMolecules1420-30492025-01-0130362010.3390/molecules30030620Methionine Aminopeptidase 2 (MetAP2) Inhibitor BL6 Attenuates Inflammation in Cultured Microglia and in a Mouse Model of Alzheimer’s DiseaseXiuli Zhang0Shivakumar Subbanna1Colin R. O. Williams2Stefanie Canals-Baker3Audrey Hashim4Donald A. Wilson5Louis M. Weiss6Srushti Shukla7Parthiban Chokkalingam8Sasmita Das9Bhaskar C. Das10Mariko Saito11Division of Neurochemistry, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USADivision of Neurochemistry, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USAEmotional Brain Institute, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USADivision of Neurochemistry, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USADivision of Neurochemistry, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USAEmotional Brain Institute, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USADepartment of Pathology/Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USASchool of Pharmacy and Pharmaceutical Sciences, University at Buffalo, The State University of New York, Buffalo, NY 14201, USASchool of Pharmacy and Pharmaceutical Sciences, University at Buffalo, The State University of New York, Buffalo, NY 14201, USASchool of Pharmacy and Pharmaceutical Sciences, University at Buffalo, The State University of New York, Buffalo, NY 14201, USASchool of Pharmacy and Pharmaceutical Sciences, University at Buffalo, The State University of New York, Buffalo, NY 14201, USADivision of Neurochemistry, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USAMethionine aminopeptidase 2 (MetAP2) plays an important role in the regulation of protein synthesis and post-translational processing. Preclinical/clinical applications of MetAP2 inhibitors for the treatment of various diseases have been explored because of their antiangiogenic, anticancer, antiobesity, antidiabetic, and immunosuppressive properties. However, the effects of MetAP2 inhibitors on CNS diseases are rarely examined despite the abundant presence of MetAP2 in the brain. Previously, we synthesized a novel boron-containing MetAP2 inhibitor, BL6, and found that it suppressed angiogenesis and adipogenesis yet improved glucose uptake. Here, we studied the anti-inflammatory effects of BL6 in SIM-A9 microglia and in a mouse model of Alzheimer’s disease generated by the intracerebroventricular (icv) injection of streptozotocin (STZ). We found that BL6 reduced proinflammatory molecules, such as nitric oxide, iNOS, IL-1β, and IL-6, together with phospho-Akt and phospho-NF-κB p65, which were elevated in lipopolysaccharide (LPS)-activated microglial SIM-A9 cells. However, the LPS-induced reduction in Arg-1 and CD206 was attenuated by BL6, suggesting that BL6 promotes microglial M1 to M2 polarization. BL6 also decreased glial activation along with a reduction in phospho-tau and an elevation in synaptophysin in the icv-STZ mouse model. Thus, our experiments demonstrate an anti-neuroinflammatory action of BL6, suggesting possible clinical applications of MetAP2 inhibitors for brain disorders in which neuroinflammation is involved.https://www.mdpi.com/1420-3049/30/3/620MetAP2 inhibitorsmicroglianeuroinflammationSIM-A9icv-STZAlzheimer’s disease
spellingShingle Xiuli Zhang
Shivakumar Subbanna
Colin R. O. Williams
Stefanie Canals-Baker
Audrey Hashim
Donald A. Wilson
Louis M. Weiss
Srushti Shukla
Parthiban Chokkalingam
Sasmita Das
Bhaskar C. Das
Mariko Saito
Methionine Aminopeptidase 2 (MetAP2) Inhibitor BL6 Attenuates Inflammation in Cultured Microglia and in a Mouse Model of Alzheimer’s Disease
Molecules
MetAP2 inhibitors
microglia
neuroinflammation
SIM-A9
icv-STZ
Alzheimer’s disease
title Methionine Aminopeptidase 2 (MetAP2) Inhibitor BL6 Attenuates Inflammation in Cultured Microglia and in a Mouse Model of Alzheimer’s Disease
title_full Methionine Aminopeptidase 2 (MetAP2) Inhibitor BL6 Attenuates Inflammation in Cultured Microglia and in a Mouse Model of Alzheimer’s Disease
title_fullStr Methionine Aminopeptidase 2 (MetAP2) Inhibitor BL6 Attenuates Inflammation in Cultured Microglia and in a Mouse Model of Alzheimer’s Disease
title_full_unstemmed Methionine Aminopeptidase 2 (MetAP2) Inhibitor BL6 Attenuates Inflammation in Cultured Microglia and in a Mouse Model of Alzheimer’s Disease
title_short Methionine Aminopeptidase 2 (MetAP2) Inhibitor BL6 Attenuates Inflammation in Cultured Microglia and in a Mouse Model of Alzheimer’s Disease
title_sort methionine aminopeptidase 2 metap2 inhibitor bl6 attenuates inflammation in cultured microglia and in a mouse model of alzheimer s disease
topic MetAP2 inhibitors
microglia
neuroinflammation
SIM-A9
icv-STZ
Alzheimer’s disease
url https://www.mdpi.com/1420-3049/30/3/620
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