Disruption of calreticulin-mediated cellular adhesion signaling in the cadmium-induced omphalocele in the chick model
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Administration of cadmium (Cd) causes omphalocele in the chick embryo. The earliest histological changes in the chick Cd model are the breakdown of adherens junctions (AJs). Calreticulin (CRT) plays a key role in Ca2+ signaling and cell adhesion. Ca2+ signaling in the Cd chick model is known to be altered. The calcium-dependent adhesion molecule, E-cadherin, and its associate, β-catenin, are key components of AJs regulated by CRT. CRT knockouts display omphalocele. We hypothesized that CRT, E-cadherin and β-catenin are downregulated during early embryogenesis in the Cd chick model.
After 60 h (H) incubation, chicks were harvested 1H, 4H, and 8H post treatment with saline or Cd and divided into controls and Cd. RT-PCR was performed to evaluate mRNA levels of CRT, E-cadherin and β-catenin in the Cd chick model.
The mRNA levels of CRT were significantly decreased in the Cd group at 1H compared to controls (p < 0.05). The mRNA levels of E-cadherin and β-catenin were significantly decreased at 4H in the Cd group compared to controls (p < 0.05). There were no significant differences at 8H.
Downregulation of CRT, E-cadherin and β-catenin genes may cause omphalocele in the Cd chick model by disrupting CRT-mediated Ca2+ signaling and AJs.
KeywordsCalreticulin E-Cadherin β-Catenin Cadmium Omphalocele
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