Complement component 1q subcomponent binding protein in the brain of the rat
Open accessAbstract
Complement component 1q subcomponent binding protein (C1qbp) is a multifunctional protein involved in immune response, energy homeostasis of cells as a plasma membrane receptor, and a nuclear, cytoplasmic or mitochondrial protein. Recent reports suggested its neuronal function, too, possibly in axon maintenance, synaptic function, and neuroplasticity. Therefore, we addressed to identify C1qbp in the rat brain using in situ hybridization histochemistry and immunolabelling at light and electron microscopic level. C1qbp has a topographical distribution in the brain established by the same pattern of C1qbp mRNA-expressing and protein-containing neurons with the highest abundance in the cerebral cortex, anterodorsal thalamic nucleus, hypothalamic paraventricular (PVN) and arcuate nuclei, spinal trigeminal nucleus. Double labelling of C1qbp with the neuronal marker NeuN, with the astrocyte marker S100, and the microglia marker Iba1 demonstrated the presence of C1qbp in neurons but not in glial cells in the normal brain, while C1qbp appeared in microglia following their activation induced by focal ischemic lesion. Only restricted neurons expressed C1qbp, for example, in the PVN, magnocellular neurons selectively contained C1qbp. Further double labelling by using the mitochondria marker Idh3a antibody suggested the mitochondrial localization of C1qbp in the brain, confirmed by correlated light and electron microscopy at 3 different brain regions. Post-embedding immunoelectron microscopy also suggested uneven C1qbp content of mitochondria in different brain areas but also heterogeneity within single neurons. These data suggest a specific function of C1qbp in the brain related to mitochondria, such as the regulation of local energy supply in neuronal cells.
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p32 predominantly localizes in mitochondria and is a recognized RNA-binding protein within the mitochondrial context.
“p32, a well-conserved eukaryotic protein that predominantly localizes in mitochondria (Barna et al, 2019; Gotoh et al, 2018), serves as a recognized RNA-binding protein within the mitochondrial context.”
From The mitochondrial long non-coding RNA lncMtloop regulates mitochondrial transcription and suppresses Alzheimer’s disease (2024) · cites this paper as Barna et al, 2019
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References 72 · Cited by 26
- Authors
- Barna, J., Dimén, D., Puska, G., Kovács, D., Csikós, V., Oláh, S., Udvari, E. B., Pál, G., & Dobolyi, Á.
- Affiliations
- Semmelweis University (HU)
- Eötvös Loránd University (HU)
- Corresponding author
- Dobolyi, Árpád
- Venue
- Scientific Reports
- Published
- 2019-03-14
- Volume
- 9
- Issue
- 1
- Pages
- 4597-4597
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC6418184
- OpenAlex
- W2922529586
- Cited by
- 26
- References
- 72
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 6 · 2023: 2 · 2022: 4 · 2021: 2 · 2020: 3 · 2019: 2
- FWCI
- 1.10
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- ELTE Digital Institutional Repository (EDIT) (Eötvös Loránd University) (submittedVersion, other-oa)
- Funders
- Semmelweis Egyetem
- Hungarian Scientific Research Fund (NKFIH OTKA K116538, K116538)
- Magyar Tudományos Akadémia (NKFIH OTKA K116538)
- Emberi Eroforrások Minisztériuma (783-3/2018/FEKUTSRAT))
- Eötvös Loránd Tudományegyetem (783 3/2018/FEKUTSRAT, VEKOP-2, VEKOP-2.3.3-15-2016-00007)
- Nemzeti Kutatási Fejlesztési és Innovációs Hivatal (NKFIH-2920-1/2016-VEKOP-2.3, NKFIH-4300-1/2017-NKP_17, NKFIH-6785-1/2016-VEKOP-2.3.3-15, VEKOP-2.3.3-15-2016-00007)
- National Research, Development and Innovation Office (VEKOP-2.3.3-15-2016-00007, 783-3/2018/FEKUTSRAT)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- C1QBP, brain, mitochondrial localization, neuronal energy metabolism, microglial activation, focal cerebral ischemia, paraventricular nucleus, magnocellular neurons, cerebral cortex, thalamus, hypothalamus, spinal trigeminal nucleus, neurometabolism
- MeSH terms
- Animals, Brain, Cerebral Cortex, Fluorescent Antibody Technique, Immunohistochemistry, Mitochondria, RNA, Messenger, Gene Expression, Protein Transport, Mitochondrial Proteins, Rats
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