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Expression of complement C1qB and C4 mRNAs during rat brain development
S A Johnson1, G M Pasinetti, C E Finch
1Neurogerontology Division, Andrus Gerontology Center, University of Southern California, Los Angeles 90089-0191.
Insights
Complement C1qB and C4 messenger RNAs are present throughout rat brain development, particularly in microglia and neurons, suggesting novel roles beyond programmed cell death.
Area of Science:
- Neuroscience
- Immunology
- Developmental Biology
Background:
- The complement system plays a role in immune responses.
- Its function during brain development is not fully understood.
Purpose of the Study:
- To investigate the distribution and expression patterns of complement C1qB and C4 messenger RNAs (mRNAs) during rat brain development.
- To explore the potential role of complement components in neurodevelopment and programmed cell death.
Main Methods:
- Northern blot analysis
- In situ hybridization
- Analysis of gene expression during embryonic and postnatal development
Main Results:
- Complement C1qB and C4 mRNAs were detected from embryonic day 14 (E14) and remained abundant through six weeks postnatal.
- C1qB mRNA was highly expressed in microglia/macrophages in specific brain regions, while C4 mRNA showed broader distribution in putative neurons.
- mRNA levels did not correlate with apoptotic profiles, suggesting complement is not involved in programmed cell death during this period.
Conclusions:
- Complement C1q and C4 components are widely distributed and consistently expressed during rat brain development.
- Their presence suggests novel, non-cytotoxic roles in brain development, distinct from the classical complement cascade's typical functions.
Abstract:
This study examined the distribution of complement C1qB and C4 mRNAs during rat brain development by northern blot and in situ hybridization. Both C1q and C4 mRNAs were already present at embryonic day 14 (E14) and showed little change in abundance through six weeks postnatal. At E16, C1qB mRNA was present at high abundance in putative microglia/macrophages in cortical marginal and intermediate zones, and hippocampal analge, but not in the neurogenic ventricular or sub-ventricular zones. C4 mRNA had a broadly similar regional distribution, but was present at lower abundance in a larger number of cells, putatively neurons. The distribution pattern for C1qB and C4 mRNAs did not change appreciably as brain development proceeded. The lower prevalence of C mRNAs in neuroepithelial or subventricular zones suggests an inverse relationship of C mRNA to cell proliferation. The frequency of apoptotic nuclear profiles, which was as much as ten-fold higher at P7 vs. E17, did not correlate anatomically with C1qB or C4 mRNA levels. Thus, the widespread distribution and consistent presence of each C mRNA during development argues against a role for C in programmed cell death during brain development. We suggest that C1q and C4 components have novel roles during brain development that may be unrelated to normal cytotoxic actions of the activated classical C cascade.