Different profiles of apoptosis and activation in children with progressive or static HIV-related encephalopathy

Almudena Blanco, Roberta Nardacci, Franca Del Nonno, Francesco Callea, Paola Francalanci, Mauro Piacentini, Ma Ángeles Muñoz Fernández

Research output: Contribution to journalArticle

Abstract

To analyze neurodegeneration in brain cortex samples from human immunodeficiency virus (HIV)-vertically-infected children diagnosed with progressive or static HIV-encephalopathy. We performed a descriptive retrospective and cross-sectional study on 15 HIV-infected children. Eight children were diagnosed with progressive-encephalopathy (EP) and seven with static-EP. Autopsy samples of the frontal cortex from the 15 children were studied. Apoptotic analysis was performed by an assay, which detects apoptotic cells by labeling the fragmentation of DNA by TdT - mediated dUTP nick end labeling (TUNEL) assay. The presence of phosphorylated p53 (p53Ser46P) indicates the beginning of the cell death process. Glial fibrillary acidic protein a marker for glial cells, and p53Ser46P were detected by immunohistochemical assays. All samples from the 15 HIV-infected children showed positive results using TUNEL and showed an increase in p53Ser46P. However, the number of apoptotic cells was higher in samples from children with progressive-EP and was comprised of a higher number of dying neurons than dying glial cells. In contrast, glial cells were more affected in children with static-EP. We observed gliosis (abnormal proliferation of astrocytes in damaged areas of the brain) in all samples, but in the static-EP samples, gliosis was observed in areas close to blood vessels, and it was more pronounced than in progressive-EP samples. Our results suggest that depending whether the diagnosis is progressive-EP or static-EP, neural affliction activates programmed cell death in brain tissue of HIV-infected children. Moreover, there are differences in the type of cellular population affected as well as in the level of glial cell activation.

Original languageEnglish
Pages (from-to)367-373
Number of pages7
JournalJournal of Pediatric Infectious Diseases
Volume4
Issue number4
DOIs
Publication statusPublished - 2009

Fingerprint

Brain Diseases
HIV
Apoptosis
Neuroglia
Gliosis
Brain
Cell Death
Glial Fibrillary Acidic Protein
Frontal Lobe
DNA Fragmentation
Astrocytes
Blood Vessels
Autopsy
Cell Count
Cross-Sectional Studies
Neurons

Keywords

  • Apoptosis
  • Central nervous system
  • Children
  • Glial activation
  • HIV-encephalopathy
  • p53

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Infectious Diseases

Cite this

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title = "Different profiles of apoptosis and activation in children with progressive or static HIV-related encephalopathy",
abstract = "To analyze neurodegeneration in brain cortex samples from human immunodeficiency virus (HIV)-vertically-infected children diagnosed with progressive or static HIV-encephalopathy. We performed a descriptive retrospective and cross-sectional study on 15 HIV-infected children. Eight children were diagnosed with progressive-encephalopathy (EP) and seven with static-EP. Autopsy samples of the frontal cortex from the 15 children were studied. Apoptotic analysis was performed by an assay, which detects apoptotic cells by labeling the fragmentation of DNA by TdT - mediated dUTP nick end labeling (TUNEL) assay. The presence of phosphorylated p53 (p53Ser46P) indicates the beginning of the cell death process. Glial fibrillary acidic protein a marker for glial cells, and p53Ser46P were detected by immunohistochemical assays. All samples from the 15 HIV-infected children showed positive results using TUNEL and showed an increase in p53Ser46P. However, the number of apoptotic cells was higher in samples from children with progressive-EP and was comprised of a higher number of dying neurons than dying glial cells. In contrast, glial cells were more affected in children with static-EP. We observed gliosis (abnormal proliferation of astrocytes in damaged areas of the brain) in all samples, but in the static-EP samples, gliosis was observed in areas close to blood vessels, and it was more pronounced than in progressive-EP samples. Our results suggest that depending whether the diagnosis is progressive-EP or static-EP, neural affliction activates programmed cell death in brain tissue of HIV-infected children. Moreover, there are differences in the type of cellular population affected as well as in the level of glial cell activation.",
keywords = "Apoptosis, Central nervous system, Children, Glial activation, HIV-encephalopathy, p53",
author = "Almudena Blanco and Roberta Nardacci and {Del Nonno}, Franca and Francesco Callea and Paola Francalanci and Mauro Piacentini and Fern{\'a}ndez, {Ma {\'A}ngeles Mu{\~n}oz}",
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T1 - Different profiles of apoptosis and activation in children with progressive or static HIV-related encephalopathy

AU - Blanco, Almudena

AU - Nardacci, Roberta

AU - Del Nonno, Franca

AU - Callea, Francesco

AU - Francalanci, Paola

AU - Piacentini, Mauro

AU - Fernández, Ma Ángeles Muñoz

PY - 2009

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N2 - To analyze neurodegeneration in brain cortex samples from human immunodeficiency virus (HIV)-vertically-infected children diagnosed with progressive or static HIV-encephalopathy. We performed a descriptive retrospective and cross-sectional study on 15 HIV-infected children. Eight children were diagnosed with progressive-encephalopathy (EP) and seven with static-EP. Autopsy samples of the frontal cortex from the 15 children were studied. Apoptotic analysis was performed by an assay, which detects apoptotic cells by labeling the fragmentation of DNA by TdT - mediated dUTP nick end labeling (TUNEL) assay. The presence of phosphorylated p53 (p53Ser46P) indicates the beginning of the cell death process. Glial fibrillary acidic protein a marker for glial cells, and p53Ser46P were detected by immunohistochemical assays. All samples from the 15 HIV-infected children showed positive results using TUNEL and showed an increase in p53Ser46P. However, the number of apoptotic cells was higher in samples from children with progressive-EP and was comprised of a higher number of dying neurons than dying glial cells. In contrast, glial cells were more affected in children with static-EP. We observed gliosis (abnormal proliferation of astrocytes in damaged areas of the brain) in all samples, but in the static-EP samples, gliosis was observed in areas close to blood vessels, and it was more pronounced than in progressive-EP samples. Our results suggest that depending whether the diagnosis is progressive-EP or static-EP, neural affliction activates programmed cell death in brain tissue of HIV-infected children. Moreover, there are differences in the type of cellular population affected as well as in the level of glial cell activation.

AB - To analyze neurodegeneration in brain cortex samples from human immunodeficiency virus (HIV)-vertically-infected children diagnosed with progressive or static HIV-encephalopathy. We performed a descriptive retrospective and cross-sectional study on 15 HIV-infected children. Eight children were diagnosed with progressive-encephalopathy (EP) and seven with static-EP. Autopsy samples of the frontal cortex from the 15 children were studied. Apoptotic analysis was performed by an assay, which detects apoptotic cells by labeling the fragmentation of DNA by TdT - mediated dUTP nick end labeling (TUNEL) assay. The presence of phosphorylated p53 (p53Ser46P) indicates the beginning of the cell death process. Glial fibrillary acidic protein a marker for glial cells, and p53Ser46P were detected by immunohistochemical assays. All samples from the 15 HIV-infected children showed positive results using TUNEL and showed an increase in p53Ser46P. However, the number of apoptotic cells was higher in samples from children with progressive-EP and was comprised of a higher number of dying neurons than dying glial cells. In contrast, glial cells were more affected in children with static-EP. We observed gliosis (abnormal proliferation of astrocytes in damaged areas of the brain) in all samples, but in the static-EP samples, gliosis was observed in areas close to blood vessels, and it was more pronounced than in progressive-EP samples. Our results suggest that depending whether the diagnosis is progressive-EP or static-EP, neural affliction activates programmed cell death in brain tissue of HIV-infected children. Moreover, there are differences in the type of cellular population affected as well as in the level of glial cell activation.

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