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TGF-beta1 expression is reduced in hydrocephalic H-Tx rat brain
X Cai1, J V Pattisapu, R W Tarnuzzer
1Wade's Center for Hydrocephalus Research, Orlando Regional Health Research Institute, FL 32806, USA.
Summary
Transforming growth factor-beta1 (TGF-beta1) levels are significantly lower in hydrocephalic H-Tx rats compared to controls. This reduction in TGF-beta1 may be a result, not a cause, of congenital hydrocephalus.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Transforming growth factor-beta1 (TGF-beta1) is a cytokine with diverse biological functions.
- Previous studies indicated TGF-beta1 overexpression can induce hydrocephalus in mice.
- Congenital hydrocephalus is a complex neurological disorder characterized by excessive cerebrospinal fluid accumulation in the brain.
Purpose of the Study:
- To investigate TGF-beta1 expression levels in the H-Tx rat, a model for congenital hydrocephalus.
- To determine if TGF-beta1 levels are altered in hydrocephalic rats compared to their normal siblings and control rats.
- To explore the potential role of TGF-beta1 in the pathogenesis of congenital hydrocephalus.
Main Methods:
- Quantitative RT-PCR was employed to measure TGF-beta1 gene expression in rat brain tissue.
- H-Tx rats at 3, 10, and 21 days of age were compared with their normal littermates and Sprague-Dawley (SD) control rats.
- Expression levels of epidermal growth factor were also assessed.
Main Results:
- Hydrocephalic H-Tx rats exhibited significantly lower TGF-beta1 levels at 3 and 10 days compared to normal siblings (p < 0.01).
- This difference in TGF-beta1 levels between hydrocephalic and normal H-Tx rats diminished by 21 days.
- Both hydrocephalic and normal H-Tx rats showed significantly lower TGF-beta1 levels than SD controls across all age groups (p < 0.01).
- A similar reduction in epidermal growth factor expression was observed, suggesting the TGF-beta1 change is not unique to hydrocephalus in this model.
Conclusions:
- TGF-beta1 expression is significantly reduced in the H-Tx rat model of congenital hydrocephalus, contrary to findings in other models.
- The decreased TGF-beta1 levels are unlikely to be the primary cause of hydrocephalus in H-Tx rats.
- It is hypothesized that reduced TGF-beta1 may be a downstream effect, possibly due to feedback inhibition from genes it regulates, such as extracellular matrix components.