Eraysy Machín-Martínez
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Eraysy Machín-Martínez has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Abiel Roche-Lima
Center for Collaborative Research in Health Disparities, RCMI Program, Medical Science Campus, University of Puerto Rico, San Juan, PR 00936-5067, USA
1 shared publication - Eduardo L. Tosado Rodriguez
Integrated Informatics Services, Research Capacity Core, Center for Collaborative Research in Health Disparities (CCRHD), Academic Affairs Deanship, University of Puerto Rico-Medical Sciences Campus, San Juan, PR 00936, USA
1 shared publication - Kelvin Carrasquillo-Carrion
Integrated Informatics Services, Research Capacity Core, Center for Collaborative Research in Health Disparities (CCRHD), Academic Affairs Deanship, University of Puerto Rico-Medical Sciences Campus, San Juan, PR 00936, USA
1 shared publication - Loyda M. Melendez
Department of Microbiology and Medical Zoology, University of Puerto Rico-Medical Sciences Campus, San Juan, PR 00936, USA
1 shared publication - Manuel E. Álvarez-Ríos
Department of Biology, University of Puerto Rico, Río Piedras Campus, San Juan, PR 00921, USA
1 shared publication - Omar Vélez López
Department of Microbiology and Medical Zoology, University of Puerto Rico, Medical Sciences Campus, San Juan, PR 00936, USA
1 shared publication
Latest Publications
- Open Access
- 23 August 2024
- Published by MDPI AG in Biomedicines
- Vol. 12 (9) , 1934
Analysis of Sigma-1 Receptor Antagonist BD1047 Effect on Upregulating Proteins in HIV-1-Infected Macrophages Exposed to Cocaine Using Quantitative Proteomics
HIV-1 infects monocyte-derived macrophages (MDM) that migrate into the brain and secrete virus and neurotoxic molecules, including cathepsin B (CATB), causing cognitive dysfunction. Cocaine potentiates CATB secretion and neurotoxicity in HIV-infected MDM. Pretreatment with BD1047, a sigma-1 receptor antagonist, before cocaine exposure reduces HIV-1, CATB secretion, and neuronal apoptosis. We aimed to elucidate the intracellular pathways modulated by BD1047 in HIV-infected MDM exposed to cocaine. We hypothesized that the Sig1R antagonist BD1047, prior to cocaine, significantly deregulates proteins and pathways involved in HIV-1 replication and CATB secretion that lead to neurotoxicity. MDM culture lysates from HIV-1-infected women treated with BD1047 before cocaine were compared with untreated controls using TMT quantitative proteomics, bioinformatics, Lima statistics, and pathway analyses. Results demonstrate that pretreatment with BD1047 before cocaine dysregulated eighty (80) proteins when compared with the infected cocaine group. We found fifteen (15) proteins related to HIV-1 infection, CATB, and mitochondrial function. Upregulated proteins were related to oxidative phosphorylation (SLC25A-31), mitochondria (ATP5PD), ion transport (VDAC2–3), endoplasmic reticulum transport (PHB, TMED10, CANX), and cytoskeleton remodeling (TUB1A-C, ANXA1). BD1047 treatment protects HIV-1-infected MDM exposed to cocaine by upregulating proteins that reduce mitochondrial damage, ER transport, and exocytosis associated with CATB-induced neurotoxicity.
- 23 August 2024
- Published by MDPI AG in Biomedicines
- Vol. 12 (9) , 1934
Open AccessAnalysis of Sigma-1 Receptor Antagonist BD1047 Effect on Upregulating Proteins in HIV-1-Infected Macrophages Exposed to Cocaine Using Quantitative Proteomics
HIV-1 infects monocyte-derived macrophages (MDM) that migrate into the brain and secrete virus and neurotoxic molecules, including cathepsin B (CATB), causing cognitive dysfunction. Cocaine potentiates CATB secretion and neurotoxicity in HIV-infected MDM. Pretreatment with BD1047, a sigma-1 receptor antagonist, before cocaine exposure reduces HIV-1, CATB secretion, and neuronal apoptosis. We aimed to elucidate the intracellular pathways modulated by BD1047 in HIV-infected MDM exposed to cocaine. We hypothesized that the Sig1R antagonist BD1047, prior to cocaine, significantly deregulates proteins and pathways involved in HIV-1 replication and CATB secretion that lead to neurotoxicity. MDM culture lysates from HIV-1-infected women treated with BD1047 before cocaine were compared with untreated controls using TMT quantitative proteomics, bioinformatics, Lima statistics, and pathway analyses. Results demonstrate that pretreatment with BD1047 before cocaine dysregulated eighty (80) proteins when compared with the infected cocaine group. We found fifteen (15) proteins related to HIV-1 infection, CATB, and mitochondrial function. Upregulated proteins were related to oxidative phosphorylation (SLC25A-31), mitochondria (ATP5PD), ion transport (VDAC2–3), endoplasmic reticulum transport (PHB, TMED10, CANX), and cytoskeleton remodeling (TUB1A-C, ANXA1). BD1047 treatment protects HIV-1-infected MDM exposed to cocaine by upregulating proteins that reduce mitochondrial damage, ER transport, and exocytosis associated with CATB-induced neurotoxicity.