Induction of innate immune gene expression following methyl methanesulfonate-induced DNA damage in sea urchins.
Helena C ReinardyJ ChapmanA G BodnarPublished in: Biology letters (2016)
Sea urchins are noted for the absence of neoplastic disease and represent a novel model to investigate cellular and systemic cancer protection mechanisms. Following intracoelomic injection of the DNA alkylating agent methyl methanesulfonate, DNA damage was detected in sea urchin cells and tissues (coelomocytes, muscle, oesophagus, ampullae and gonad) by the alkaline unwinding, fast micromethod. Gene expression analyses of the coelomocytes indicated upregulation of innate immune markers, including genes involved in NF-κB signalling. Results suggest that activation of the innate immune system following DNA damage may contribute to the naturally occurring resistance to neoplastic disease observed in sea urchins.
Keyphrases
- dna damage
- innate immune
- gene expression
- oxidative stress
- dna repair
- dna methylation
- induced apoptosis
- signaling pathway
- immune response
- skeletal muscle
- circulating tumor
- cell proliferation
- cell free
- squamous cell carcinoma
- high glucose
- drug induced
- lps induced
- inflammatory response
- pi k akt
- young adults
- endothelial cells
- cell death
- circulating tumor cells