Cited by 11Neuroinflammation and Neurodegeneration MechanismsNuclear Receptors and SignalingEstrogen and related hormone effects

Alteration in nuclear factor-kappaB pathway and functionality of estrogen via receptors promote neuroinflammation in frontal cortex after 1-Methyl-4-Phenyl-1,2,3,6-tetrahydropyridine treatment

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Mitra, Soham, Ghosh, Nabanita, Sinha, Priyobrata, Chakrabarti, Nilkanta, Bhattacharyya, Arindam·2015·Scientific Reports

Abstract

The MPTP mediated neurodegeneration in substantia nigra has been well studied, but not the status of frontal cortex. The novelty of the present study is to explore the sex difference of frontal cortex during MPTP intoxication and to investigate the role of estrogen and its receptors in presence of glial cells in a time chase experiment; to identify which pathway of NF-kappaB exist to proceed the neuroinflammation; to investigate the estrogen binding with its nuclear or cytosolic receptors and whether any direct relation exists between estrogen receptor (ER) -beta and NF-kappaB molecules p65 and RelB. The progression of neurodegeneration occurred with the association of glial cells and functional (via its nuclear and cytosolic receptors) estrogen level. Both the canonical and/or non canonical pathways of NF-kappaB exist in frontal cortex of both the sexes after MPTP treatment. The homodimeric or heterodimeric form of ER-beta binds with NF-kappaB molecules p65 and RelB differently, but the canonical or non canonical pathways of NF-kappaB molecules could not be stopped or may be promoted. The changes in the molecular and cellular pattern in frontal cortex of both sexes during MPTP intoxication depends on the estrogen function via its nuclear or cytosolic estrogen receptors.

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  1. Aoki E., Yano R., Yokoyama H., Kato H. & Araki T. Role of nuclear transcription factor kappa B (NF-kappaB) for MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahyropyridine)-induced apoptosis in nigral neurons of mice. Exp. Mol. Pathol. 86, 57– 64 (2009). 19027004
  2. Flood P. M. et al. Transcriptional Factor NF-κB as a Target for Therapy in Parkinson’s Disease. Parkinsons Dis. 2011, 216298 (2011). 21603248 PMC3095232

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Authors
Mitra, S., Ghosh, N., Sinha, P., Chakrabarti, N., & Bhattacharyya, A.
Affiliations
University of Calcutta (IN)
Corresponding author
Bhattacharyya, Arindam
Venue
Scientific Reports
Published
2015-09-14
Volume
5
Issue
1
Pages
13949-13949
ISSN
2045-2322 (ISSN-L)
OpenAlex
W2394639973
Cited by
11
References
51
Citations by year
2025: 2 · 2022: 1 · 2020: 2 · 2019: 2 · 2018: 3 · 2016: 1
FWCI
0.71
Type
journal article
Language
en
Open access
Locations
  • Scientific Reports (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • Department of Biotechnology, Ministry of Science and Technology, India
  • Indian Council of Medical Research (5/8/4-4)
  • Council of Scientific and Industrial Research, India (09/028, 09/028 (0896)/2012-EMR-1)
  • University Grants Commission
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
Keywords
MPTP, neuroinflammation, frontal cortex, estrogen receptor beta, NF-κB signaling, RelB, NF-κB p65, glial cells, sex differences, neurodegeneration, Parkinson's disease model
MeSH terms
Animals, Aromatase, Calcium-Binding Proteins, Enzyme-Linked Immunosorbent Assay, Estrogens, Female, Frontal Lobe, Glial Fibrillary Acidic Protein, Immunohistochemistry, Inflammation, Male, Microfilament Proteins, Neuroglia, Protein Binding, Tamoxifen, Tumor Necrosis Factor-alpha, NF-kappa B, MPTP Poisoning, Estrogen Receptor alpha, Estrogen Receptor beta, Mice, Transcription Factor RelB, Transcription Factor RelA, Transcriptome

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