TY  - JOUR
TI  - The natural compound sanguinarine perturbs the regenerative capabilities of planarians
AU  - Balestrini, Linda
AU  - Di Donfrancesco, Alessia
AU  - Rossi, Leonardo
AU  - Marracci, Silvia
AU  - Isolani, MariaE.
AU  - Bianucci, AnnaM.
AU  - Batistoni, Renata
T2  - The International Journal of Developmental Biology
AB  - The natural alkaloid sanguinarine has remarkable therapeutic properties and has been used for centuries as a folk remedy.  This compound exhibits interesting anticancer properties and is currently receiving attention as a potential chemotherapeutic agent. Nevertheless, limited information exists regarding its safety for developing organisms. Planarians are an animal model known for their extraordinary stem cell-based regenerative capabilities and are increasingly used for toxicological and pharmacological studies. Here, we report that sanguinarine, at micromolar concentrations, perturbs the regeneration process in the planarian Dugesia japonica. We show that sanguinarine exposure causes defects during anterior regeneration and visual system recovery, as well as anomalous remodelling of pre-existing structures. Investigating the effects of sanguinarine on stem cells, we found that sanguinarine perturbs the transcriptional profile of early and late stem cell progeny markers. Our results indicate that sanguinarine exposure alters cell dynamics and induces apoptosis without affecting cell proliferation. Finally, sanguinarine exposure influences the expression level of H+, K+-ATPase α subunit, a gene of the P-type-ATPase pump family which plays a crucial role during anterior regeneration in planaria. On the whole, our data reveal that sanguinarine perturbs multiple mechanisms which regulate regeneration dynamics and contribute to a better understanding of the safety profile of this alkaloid in developing organisms.
PY  - 2017
DO  - 10.1387/ijdb.160169rb
VL  - 61
IS  - 1-2
SP  - 43
EP  - 52
J2  - Int. J. Dev. Biol.
LA  - en
SN  - 0214-6282
SN  - 1696-3547
UR  - https://ijdb.ehu.eus/article/160169rb
Y2  - 2024/11/05/11:25:16
ER  -