The nervous system serves as the core of the complex control and coordination mechanisms crucial for sustaining vital life activities in the human body. Recent studies have indicated a significant regulatory role of connective tissue growth factor (CTGF) in the nervous system, participating in the pathogenesis of various neurological diseases.
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Distribution and Expression of CTGF in the Nervous System
Through immunohistochemical staining and in situ hybridization techniques, researchers have identified positive signals of CTGF protein in neurons and astrocytes, with varying expression levels in different brain regions. Specifically, high expression is observed in the cerebral cortex VI b layer, dorsal endopiriform nucleus (DEPN), olfactory bulb, and deep regions of accessory olfactory bulb. This distribution pattern provides crucial insights into the functional role of CTGF in the nervous system.
The Role of CTGF in Neural Development
In terms of neural development, studies suggest that CTGF may regulate neuronal density and dendritic branching. Conditional knockout of CTGF in excitatory neurons of the cerebral cortex VI b layer resulted in increased neuronal density, indicating a potential autocrine or paracrine role of CTGF in regulating local neuronal density. Furthermore, the knockout affected the complexity of dendritic branching in VI b layer neurons, highlighting a specific role of CTGF in dendritic branching regulation. These findings shed new light on the mechanisms of CTGF in neural morphological development.
CTGF in Neurodegenerative Diseases
CTGF's involvement in neurodegenerative diseases has garnered significant attention. In models of Alzheimer's disease and amyotrophic lateral sclerosis (ALS), CTGF expression is upregulated. Observations in Alzheimer's mouse models suggest a potential neuroprotective role of CTGF related to the degradation of amyloid beta. In ALS models, CTGF is distributed in spinal cord motor neurons and muscles, indicating a complex regulation between neurons and glial cells. These findings underscore the intricate role of CTGF in neurodegenerative diseases.
Research on CTGF in Depression and Epilepsy
Despite being distinct neurological conditions, both depression and epilepsy exhibit involvement of CTGF. Postmortem analysis of depressed patients' brains revealed increased expression of CTGF in the amygdala. Similarly, in rats displaying anxiety and depression-like behaviors, CTGF expression in the dentate gyrus is elevated. Experimental evidence supporting the antidepressant effects of CTGF inhibition implies a novel therapeutic target for depression.
In epilepsy, the knockout of CTGF in mice did not significantly impact the severity and latency of seizures but delayed seizure onset. This suggests a potential therapeutic role in inhibiting CTGF function in preventing epileptic seizures. Notably, DEPN, a crucial nucleus in epilepsy, exhibits high CTGF expression, indicating a close relationship between CTGF and neural pathways associated with DEPN. Understanding the interplay of CTGF in depression and epilepsy is essential for preventing further deterioration in these conditions.
In the future, further in-depth research is warranted to elucidate the precise mechanisms of CTGF in the nervous system, particularly its role in neural development and morphological changes. The study of CTGF in the nervous system provides a novel perspective for understanding normal neurological function and the pathogenesis of neurological diseases.
References
- Fu M.; et al. Multifunctional regulatory protein connective tissue growth factor (CTGF): a potential therapeutic target for diverse diseases. Acta Pharmaceutica Sinica B. 2022, 12(4): 1740-1760.
- Gonzalez D.; Brandan E. CTGF/CCN2 from skeletal muscle to nervous system: impact on neurodegenerative diseases. Molecular Neurobiology. 2019, 56: 5911-5916.
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