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Differentiation of the SH-SY5Y Human Neuroblastoma Cell Line
Published on: February 17, 2016
Cadmium inhibits neurite outgrowth in differentiating human SH-SY5Y neuroblastoma cells
Eun Joo Pak1, Gi Dong Son1, Byung Sun Yoo2
1Department of Life Science, Kyonggi University, Suwon, Republic of Korea.
Abstract:
Cadmium, a highly ubiquitous heavy metal, is well known to induce neurotoxicity. However, the underlying mechanism of cadmium-mediated neurotoxicity remains unclear. We have studied cadmium inhibition of neurite outgrowth using human SH-SY5Y neuroblastoma cells induced to differentiate by all-trans-retinoic acid (RA). Cadmium, at a concentration of 3 μmol/L, had no significant effect on the viability of differentiating SH-SY5Y cells. However, the neurite outgrowth of the differentiating SH-SY5Y cells 48 hours after cadmium treatment (1-3 μmol/L cadmium) was significantly inhibited in a dose-dependent manner. Treatment of RA-stimulated differentiating SH-SY5Y cells with 1 to 3 μmol/L cadmium resulted in decreased level of cross-reactivities with 43-kDa growth-associated protein (GAP-43) in a dose-dependent manner. The reactive oxygen species (ROS) scavenger, NAC (N-acetyl-l-cysteine), recovered the expression of GAP-43 in cadmium-treated cells. The results indicate that cadmium is able to inhibit neurite outgrowth of differentiating SH-SY5Y cells and that this effect might result from ROS generation by cadmium.
Insights
Cadmium exposure inhibits nerve cell growth by reducing growth-associated protein 43 (GAP-43) levels. This neurotoxic effect is linked to reactive oxygen species (ROS) generation.
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Cadmium is a pervasive heavy metal known to cause neurotoxicity.
- The precise mechanisms behind cadmium-induced neurotoxicity are not fully understood.
Purpose of the Study:
- To investigate how cadmium affects neurite outgrowth in differentiating human neuroblastoma cells.
- To explore the role of reactive oxygen species (ROS) in cadmium's neurotoxic effects.
Main Methods:
- Human SH-SY5Y neuroblastoma cells were differentiated using all-trans-retinoic acid (RA).
- Cells were treated with varying concentrations of cadmium (1-3 μmol/L).
- The expression of growth-associated protein 43 (GAP-43) and the impact of N-acetyl-l-cysteine (NAC) were assessed.
Main Results:
- Cadmium (1-3 μmol/L) significantly inhibited neurite outgrowth in a dose-dependent manner without affecting cell viability.
- Cadmium treatment led to a dose-dependent decrease in GAP-43 levels.
- The ROS scavenger NAC restored GAP-43 expression in cadmium-treated cells.
Conclusions:
- Cadmium inhibits neurite outgrowth in differentiating SH-SY5Y cells.
- This inhibition may be mediated by cadmium-induced generation of reactive oxygen species (ROS).
- GAP-43 downregulation appears to be a key factor in cadmium neurotoxicity.
