Viability and gene expression responses to polymeric nanoparticles in human and rat cells

Autor: Alain Le Faou, Mosaad A. Abdel-Wahhab, Bertrand H. Rihn, Jérôme Chevrier, Olivier Joubert, Justine Paoli, Roudayna Diab, Carole Ronzani, Ramia Safar
Přispěvatelé: Cibles thérapeutiques, formulation et expertise pré-clinique du médicament (CITHEFOR), Université de Lorraine (UL), Faculté de Médecine [Nancy], National Research Center (NRC), National Research Center
Jazyk: angličtina
Rok vydání: 2014
Předmět:
Zdroj: Cell Biology and Toxicology
Cell Biology and Toxicology, Springer Verlag, 2014, 30 (3), pp.137-46. ⟨10.1007/s10565-014-9275-4⟩
ISSN: 0742-2091
1573-6822
DOI: 10.1007/s10565-014-9275-4⟩
Popis: International audience; Applications of polymeric nanoparticles (NP) in medical fields are rapidly expanding. However, the influence of polymeric NP on cell growth and functions is widely underestimated. Therefore, we have studied cell and polymeric NP interactions by addressing two cell types with two endpoints (viability and gene expressions). Rat NR8383 and human THP-1 monocytic cell lines were exposed to 6 to 200 μg/mL of Eudragit(R) RL NP for 24 h, and cellular viability was estimated using MTT, WST-1, and trypan blue tests. A decrease of viability was observed with NR8383 cells (down to 70% for 200 μg/mL), and on the contrary, an increase with THP-1 cells (up to 140% for 200 μg/mL). Differential expression of genes involved in oxidative damage (NCF1), inflammation (NFKB, TNFA, IL6, IL1B), autophagy (ATG16L), and apoptotic balance (PDCD4, BCL2, CASP8) was analyzed. ATG16L, BCL2, and TNFA were up-regulated in NR8383 cells, which are consistent with an induction of autophagy and inflammation. On the other hand, NCF1, NFKB, and IL1B were down-regulated in THP-1 cells, which may contribute to explain the increase of cellular viability. Our results show that (1) the toxic potency of NP is dependent on the cellular model used and (2) mechanistic toxicology should be the corner stone for the evaluation of NP hazard.
Databáze: OpenAIRE