Research reportβ-amyloid increases neurocan expression through regulating Sox9 in astrocytes: A potential relationship between Sox9 and chondroitin sulfate proteoglycans in Alzheimer's disease

- β-amyloid increased cell viability and proliferation in astrocytes.
- β-amyloid simultaneously increased the expression of neurocan and Sox9.
- Neurocan expression was also inhibited after Sox9 silencing.
- β-amyloid could increase neurocan expression in a Sox9 dependent manner.

ObjectiveThis study aimed to investigate whether β-amyloid (Aβ) was able to enhance neurocan expression in a Sox9 dependent manner in astrocytes.Methods and materialsAstrocytes were incubated with Aβ at different concentrations, the expression of Sox9 and neurocan was detected by Western blot assay. Meanwhile, the viability and proliferation of astrocytes were assessed by MTT assay. Then, the Sox9 expression was silenced, and the expression of Sox9 and neurocan was examined.ResultsAfter incubation with Aβ, the viability of astrocytes was increased regardless silencing of Sox9 (all P<0.05). The proliferation of astrocytes was also gradually increased with the increase in the time of Aβ incubation (all P<0.05). With the increase in Aβ concentration, the expression of Sox9 and neurocan was also increased (all P<0.05). However, after silencing of Sox9 expression, the neurocan expression was significantly reduced as compared to control group and scra-siRNA group (all P<0.05).ConclusionOur study shows the viability and proliferation of astrocytes are significantly increased by Aβ in a dose dependent manner. Moreover, Aβ may effectively up-regulate the neurocan expression via regulating Sox9.