Human tuberculosis brain promotes neuronal apoptosis but not in astrocytes with high expression of vascular endothelial growth factor

The present study aimed to investigate the involvement of the angiogenic marker vascular endothelia growth factor (VEGF) and apoptotic markers of Bcl-2 and Bax in the neurons and astrocytes in the brain infected by Mycobacterium tuberculosis. The immunohistochemistry staining was performed to analyz...

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Veröffentlicht in:Tuberculosis (Edinburgh, Scotland) Scotland), 2018-09, Vol.112, p.45-51
Hauptverfasser: Othman, Fatihah N., Muthuraju, Sangu, Noor, Siti Suraiya M., Abdullah, Sarimah, Mohd Yusoff, Abdul Aziz, Tharakan, John, Bhaskar, Shalini, Mahmood, Mohd Shah, Kassim, Fauziah, Rafia, Hanip, Mohd Haspani, Mohd Saffari, Alias, Azmi, Pando, Rogelio H., Abdullah, Jafri M., Jaafar, Hasnan
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container_title Tuberculosis (Edinburgh, Scotland)
container_volume 112
creator Othman, Fatihah N.
Muthuraju, Sangu
Noor, Siti Suraiya M.
Abdullah, Sarimah
Mohd Yusoff, Abdul Aziz
Tharakan, John
Bhaskar, Shalini
Mahmood, Mohd Shah
Kassim, Fauziah
Rafia, Hanip
Mohd Haspani, Mohd Saffari
Alias, Azmi
Pando, Rogelio H.
Abdullah, Jafri M.
Jaafar, Hasnan
description The present study aimed to investigate the involvement of the angiogenic marker vascular endothelia growth factor (VEGF) and apoptotic markers of Bcl-2 and Bax in the neurons and astrocytes in the brain infected by Mycobacterium tuberculosis. The immunohistochemistry staining was performed to analyze the expression of the VEGF, Bcl-2 and Bax in the astrocytes and neurons. The expression of VEGF was high in neurons and astrocytes in both the infected brain and control tissues with no difference of angiogenic activity (p = 0.40). Higher Bcl-2 expression was seen in astrocytes of infected brain tissues compared to the control tissues (p = 0.004) promoted a higher anti-apoptotic activity in astrocytes. The neurons expressed strong Bax expression in the infected brain tissues compared to the control tissues (p 
doi_str_mv 10.1016/j.tube.2018.07.007
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The immunohistochemistry staining was performed to analyze the expression of the VEGF, Bcl-2 and Bax in the astrocytes and neurons. The expression of VEGF was high in neurons and astrocytes in both the infected brain and control tissues with no difference of angiogenic activity (p = 0.40). Higher Bcl-2 expression was seen in astrocytes of infected brain tissues compared to the control tissues (p = 0.004) promoted a higher anti-apoptotic activity in astrocytes. The neurons expressed strong Bax expression in the infected brain tissues compared to the control tissues (p &lt; 0.001), which indicated more apoptosis in neurons. Thus, neuronal death and survival of infected astrocytes together with high expression of VEGF might be associated with formation of brain tuberculosis. 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The immunohistochemistry staining was performed to analyze the expression of the VEGF, Bcl-2 and Bax in the astrocytes and neurons. The expression of VEGF was high in neurons and astrocytes in both the infected brain and control tissues with no difference of angiogenic activity (p = 0.40). Higher Bcl-2 expression was seen in astrocytes of infected brain tissues compared to the control tissues (p = 0.004) promoted a higher anti-apoptotic activity in astrocytes. The neurons expressed strong Bax expression in the infected brain tissues compared to the control tissues (p &lt; 0.001), which indicated more apoptosis in neurons. Thus, neuronal death and survival of infected astrocytes together with high expression of VEGF might be associated with formation of brain tuberculosis. In conclusion, neurons could be more vulnerable than astrocytes in human tuberculosis brain with high expression of VEGF.</description><subject>Angiogenesis</subject><subject>Apoptosis</subject><subject>Astrocyte</subject><subject>Astrocytes</subject><subject>Astrocytes - metabolism</subject><subject>Astrocytes - microbiology</subject><subject>Astrocytes - pathology</subject><subject>Bacteria</subject><subject>Bcl-2 protein</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Bcl2 and Bax</subject><subject>Brain</subject><subject>Case-Control Studies</subject><subject>Growth factors</subject><subject>Human brain tuberculosis</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Mycobacterium tuberculosis - pathogenicity</subject><subject>Neurons</subject><subject>Neurons - metabolism</subject><subject>Neurons - microbiology</subject><subject>Neurons - pathology</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Signal Transduction</subject><subject>Tissues</subject><subject>Tuberculosis</subject><subject>Tuberculosis, Central Nervous System - metabolism</subject><subject>Tuberculosis, Central Nervous System - microbiology</subject><subject>Tuberculosis, Central Nervous System - pathology</subject><subject>Up-Regulation</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>VEGF</subject><issn>1472-9792</issn><issn>1873-281X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kbFuFDEURS0EIiHJD1AgSzQ0M7E9u2tbokEREKRIaVLQWW_s56xXM-PB9iTkA_hvPNpAQUHlV5x7JN9LyFvOWs747vLQlqXHVjCuWiZbxuQLcsqV7Bqh-PeX9d5I0WipxQl5k_OB1RBT7DU56ZhgW71Tp-TX9TLCRFdRsssQc8i0TxAmOqc4xoKZTrikOMFAYY5zORJLoVMstGKQS4r2aQUfQ9nTfbjfU_w5J8w5xIlGTx8gVzUkipOLZY9DqLL7FB8r7sGWmM7JKw9Dxovn94zcffl8d3Xd3Nx-_Xb16aaxndqUxknfdwCw5dwpgeC133QekTsp7FZ2W7fxoJ1WDDT3HNmOWcCeS-hhx7E7Ix-O2vq3HwvmYsaQLQ4DTBiXbARnQnPFVVfR9_-gh7ik2sJKca07qbWolDhSNsWcE3ozpzBCejKcmXUjczBrtWbdyDBp6kY19O5ZvfQjur-RP6NU4OMRwFrFQ8Bksg04WXQhoS3GxfA__2835KdJ</recordid><startdate>201809</startdate><enddate>201809</enddate><creator>Othman, Fatihah N.</creator><creator>Muthuraju, Sangu</creator><creator>Noor, Siti Suraiya M.</creator><creator>Abdullah, Sarimah</creator><creator>Mohd Yusoff, Abdul Aziz</creator><creator>Tharakan, John</creator><creator>Bhaskar, Shalini</creator><creator>Mahmood, Mohd Shah</creator><creator>Kassim, Fauziah</creator><creator>Rafia, Hanip</creator><creator>Mohd Haspani, Mohd Saffari</creator><creator>Alias, Azmi</creator><creator>Pando, Rogelio H.</creator><creator>Abdullah, Jafri M.</creator><creator>Jaafar, Hasnan</creator><general>Elsevier Ltd</general><general>Elsevier Science Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>C1K</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-0258-7410</orcidid></search><sort><creationdate>201809</creationdate><title>Human tuberculosis brain promotes neuronal apoptosis but not in astrocytes with high expression of vascular endothelial growth factor</title><author>Othman, Fatihah N. ; 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The immunohistochemistry staining was performed to analyze the expression of the VEGF, Bcl-2 and Bax in the astrocytes and neurons. The expression of VEGF was high in neurons and astrocytes in both the infected brain and control tissues with no difference of angiogenic activity (p = 0.40). Higher Bcl-2 expression was seen in astrocytes of infected brain tissues compared to the control tissues (p = 0.004) promoted a higher anti-apoptotic activity in astrocytes. The neurons expressed strong Bax expression in the infected brain tissues compared to the control tissues (p &lt; 0.001), which indicated more apoptosis in neurons. Thus, neuronal death and survival of infected astrocytes together with high expression of VEGF might be associated with formation of brain tuberculosis. 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subjects Angiogenesis
Apoptosis
Astrocyte
Astrocytes
Astrocytes - metabolism
Astrocytes - microbiology
Astrocytes - pathology
Bacteria
Bcl-2 protein
bcl-2-Associated X Protein - metabolism
Bcl2 and Bax
Brain
Case-Control Studies
Growth factors
Human brain tuberculosis
Humans
Immunohistochemistry
Mycobacterium tuberculosis - pathogenicity
Neurons
Neurons - metabolism
Neurons - microbiology
Neurons - pathology
Proto-Oncogene Proteins c-bcl-2 - metabolism
Signal Transduction
Tissues
Tuberculosis
Tuberculosis, Central Nervous System - metabolism
Tuberculosis, Central Nervous System - microbiology
Tuberculosis, Central Nervous System - pathology
Up-Regulation
Vascular endothelial growth factor
Vascular Endothelial Growth Factor A - metabolism
VEGF
title Human tuberculosis brain promotes neuronal apoptosis but not in astrocytes with high expression of vascular endothelial growth factor
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