Integrated Proteomics Reveals Apoptosis-related Mechanisms Associated with Placental Malaria*

Kawahara, Rebeca; Rosa-Fernandes, Lívia; Santos, Ancély Ferreira dos; Bandeira, Carla Letícia; Dombrowski, Jamille Gregório; Souza, Rodrigo Medeiros de; Fonseca, Micaella Pereira da; Festuccia, William T.; Labriola, Letícia; Larsen, Martin R.; Marinho, Cláudio Romero Farias; Palmisano, Giuseppe

doi:10.1074/mcp.ra118.000907

Cited by 16 publications

(13 citation statements)

References 67 publications

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“…Tryptic glycopeptides obtained from microsomal membrane proteins were enriched using HILIC SPE as previously described 26,27 . Briefly, dried peptides were reconstituted in 100 μL loading and washing buffer containing ACN 80% (v/v) in TFA 1% (v/v).…”

Section: Glycopeptide Enrichment and Pngase F Deglycosylationmentioning

confidence: 99%

SARS-CoV-2 activates ER stress and Unfolded protein response

Rosa-Fernandes

Macedo-da-Silvia

et al. 2021

Preprint

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Coronavirus disease-2019 (COVID-19) pandemic caused by the SARS-CoV-2 coronavirus infection is a major global public health concern affecting millions of people worldwide. The scientific community has joint efforts to provide effective and rapid solutions to this disease. Knowing the molecular, transmission and clinical features of this disease is of paramount importance to develop effective therapeutic and diagnostic tools. Here, we provide evidence that SARS-CoV-2 hijacks the glycosylation biosynthetic, ER-stress and UPR machineries for viral replication using a time-resolved (0-48 hours post infection, hpi) total, membrane as well as glycoproteome mapping and orthogonal validation. We found that SARS-CoV-2 induces ER stress and UPR is observed in Vero and Calu-3 cell lines with activation of the PERK-eIF2α-ATF4-CHOP signaling pathway. ER-associated protein upregulation was detected in lung biopsies of COVID-19 patients and associated with survival. At later time points, cell death mechanisms are triggered. The data show that ER stress and UPR pathways are required for SARS-CoV-2 infection, therefore representing a potential target to develop/implement anti-CoVID-19 drugs.

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Section: Glycopeptide Enrichment and Pngase F Deglycosylationmentioning

confidence: 99%

SARS-CoV-2 activates ER stress and Unfolded protein response

Rosa-Fernandes

Macedo-da-Silvia

et al. 2021

Preprint

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“…These data show that congenital malaria transmission can affect the newborn’s immune system and directly impact the patient’s clinical outcome. Kawahara et.al, 2019 [ 124 ] performed a label-based and label-free quantitative proteomic analysis using a P. berghei -infected mouse model of placental malaria in parallel to the analysis of placentas collected from pregnant women with past-infection placental malaria. Regulated proteins involved in protein metabolism, intracellular transport, generation of precursor metabolites and energy were among the common enriched pathways in infected mouse and human cohort compared with uninfected ones.…”

Section: Malaria: Congenital Malaria Is Defined When the Parasite mentioning

confidence: 99%

“…Moreover, in the same study, the authors applied a comprehensive TMT-labeled phosphoproteome and glycoproteome analysis of human past-infected placentas and control placentas, showing AKT and ERK pathways activation, increased expression of BAX and cleaved caspase-3 and decreased BCL2 and HSPB1. All the results together feature the occurrence of oxidative stress and apoptotic processes that may be related to adverse fetal outcomes [ 124 ].…”

Section: Malaria: Congenital Malaria Is Defined When the Parasite mentioning

confidence: 99%

Lights and Shadows of TORCH Infection Proteomics

Macedo-da-Silva

Marinho

Palmisano

et al. 2020

Genes

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Congenital abnormalities cause serious fetal consequences. The term TORCH is used to designate the most common perinatal infections, where: (T) refers to toxoplasmosis, (O) means "others" and includes syphilis, varicella-zoster, parvovirus B19, zika virus (ZIKV), and malaria among others, (R) refers to rubella, (C) relates to cytomegalovirus infection, and (H) to herpes simplex virus infections. Among the main abnormalities identified in neonates exposed to congenital infections are central nervous system (CNS) damage, microcephaly, hearing loss, and ophthalmological impairment, all requiring regular follow-up to monitor its progression. Protein changes such as mutations, post-translational modifications, abundance, structure, and function may indicate a pathological condition before the onset of the first symptoms, allowing early diagnosis and understanding of a particular disease or infection. The term “proteomics” is defined as the science that studies the proteome, which consists of the total protein content of a cell, tissue or organism in a given space and time, including post-translational modifications (PTMs) and interactions between proteins. Currently, quantitative bottom-up proteomic strategies allow rapid and high throughput characterization of complex biological mixtures. Investigating proteome modulation during host–pathogen interaction helps in elucidating the mechanisms of infection and in predicting disease progression. This “molecular battle” between host and pathogen is a key to identify drug targets and diagnostic markers. Here, we conducted a survey on proteomic techniques applied to congenital diseases classified in the terminology “TORCH”, including toxoplasmosis, ZIKV, malaria, syphilis, human immunodeficiency virus (HIV), herpes simplex virus (HSV) and human cytomegalovirus (HCVM). We have highlighted proteins and/or protein complexes actively involved in the infection. Most of the proteomic studies reported have been performed in cell line models, and the evaluation of tissues (brain, muscle, and placenta) and biofluids (plasma, serum and urine) in animal models is still underexplored. Moreover, there are a plethora of studies focusing on the pathogen or the host without considering the triad mother-fetus-pathogen as a dynamic and interconnected system.

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“…HIV 1 virus evades macrophage apoptosis by transcription of prosurvival genes via MAP2K1/ERK2 pathway 44 . Placental malaria usually complicated by poor neonatal outcome due to growth retardation is related to apoptosis-related mechanism 45 . Hepatitis B and C viruses cause chronic liver disease and parenchymal damage by escaping viral clearance by apoptosis 46 .…”

Section: Apoptosis and Infectionsmentioning

confidence: 99%

Apoptosis: Dual Role in Aetiology and Cure

Wynn

Myint

Mya

2019

BJMS

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Apoptosis is a programmed cell death which occurs following a variety of stimuli. Physiologically the process is important for morphogenesis of organs and homeostasis of different types of cells. Apoptotic cell death is responsible for a variety of pathologic states such as elimination of cell death in mutated cells, infected cells, tumour cells and transplant rejection well as the pathological atrophy. In this review, there is discussion about the control of apoptosis, detection methods of apoptosis, its association with infectious and non-communicable diseases. Intracellular microorganisms survive through inhibition of host cell apoptosis as well as they destroy the parenchymal cells causing impaired functions. It plays important role in tumourigenesis. There are possible therapeutic roles of drugs that modify apoptosis in human diseases.

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Integrated Proteomics Reveals Apoptosis-related Mechanisms Associated with Placental Malaria*

Cited by 16 publications

References 67 publications

SARS-CoV-2 activates ER stress and Unfolded protein response

SARS-CoV-2 activates ER stress and Unfolded protein response

Lights and Shadows of TORCH Infection Proteomics

Apoptosis: Dual Role in Aetiology and Cure

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