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10.1038/srep12425 http://scihub22266oqcxt.onion/10.1038/srep12425 C4515638!4515638 !26213355     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26213355 &cmd=llinks): Failed to open stream: HTTP request failed! 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Parallel damage in mitochondrial and lysosomal compartments promotes efficient cell death with autophagy: The case of the pentacyclic triterpenoids |pdf=|usr=}}{{26213355 }} gab.com Text Parallel damage in mitochondrial and lysosomal compartments promotes efficient cell death with autophagy: The case of the pentacyclic triterpenoids JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26213355 #FOAvip The role of autophagy in cell death is still controversial and a lot of debate has concerned the transition from its pro-survival to its pro-death roles. The similar structure of the triterpenoids Betulinic (BA) and Oleanolic (OA) acids allowed us to prove that this transition involves parallel damage in mitochondria and lysosome. After treating immortalized human skin keratinocytes (HaCaT) with either BA or OA, we evaluated cell viability, proliferation and mechanism of cell death, function and morphology of mitochondria and lysosomes, and the status of the autophagy flux. We also quantified the interactions of BA and OA with membrane mimics, both in-vitro and in-silico. Essentially, OA caused mitochondrial damage that relied on autophagy to rescue cellular homeostasis, which failed upon lysosomal inhibition by Chloroquine or Bafilomycin-A1. BA caused parallel damage on mitochondria and lysosome, turning autophagy into a destructive process. The higher cytotoxicity of BA correlated with its stronger efficiency in damaging membrane mimics. Based on these findings, we underlined the concept that autophagy will turn into a destructive outcome when there is parallel damage in mitochondrial and lysosomal membranes. We trust that this concept will help the development of new drugs against aggressive cancers. Twit Text FOAVip Parallel damage in mitochondrial and lysosomal compartments promotes efficient cell death with autophagy: The case of the pentacyclic triterpenoids ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26213355 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26213355 #FOAvip English Wikipedia <ref>{{Cite pmid|26213355 }}</ref> Parallel damage in mitochondrial and lysosomal compartments promotes efficient cell death with autophagy: The case of the pentacyclic triterpenoids #MMPMID26213355 Martins WK ; Costa ÉT ; Cruz MC ; Stolf BS ; Miotto R ; Cordeiro RM ; Baptista MS Sci Rep 2015[Jul]; 5 (ä): 12425 PMID26213355 show ga The role of autophagy in cell death is still controversial and a lot of debate has concerned the transition from its pro-survival to its pro-death roles. The similar structure of the triterpenoids Betulinic (BA) and Oleanolic (OA) acids allowed us to prove that this transition involves parallel damage in mitochondria and lysosome. After treating immortalized human skin keratinocytes (HaCaT) with either BA or OA, we evaluated cell viability, proliferation and mechanism of cell death, function and morphology of mitochondria and lysosomes, and the status of the autophagy flux. We also quantified the interactions of BA and OA with membrane mimics, both in-vitro and in-silico. Essentially, OA caused mitochondrial damage that relied on autophagy to rescue cellular homeostasis, which failed upon lysosomal inhibition by Chloroquine or Bafilomycin-A1. BA caused parallel damage on mitochondria and lysosome, turning autophagy into a destructive process. The higher cytotoxicity of BA correlated with its stronger efficiency in damaging membrane mimics. Based on these findings, we underlined the concept that autophagy will turn into a destructive outcome when there is parallel damage in mitochondrial and lysosomal membranes. We trust that this concept will help the development of new drugs against aggressive cancers. |Apoptosis/drug effects/*physiology [MESH] |Autophagy/drug effects/*physiology [MESH] |Cell Proliferation/drug effects/physiology [MESH] |Cells, Cultured [MESH] |Dose-Response Relationship, Drug [MESH] |Humans [MESH] |Keratinocytes/cytology/drug effects/*physiology [MESH] |Lysosomes/drug effects/*physiology/ultrastructure [MESH] |Mitochondria/drug effects/*physiology/ultrastructure [MESH]Parallel damage in mitochondrial and lysosomal compartments promotes e(epmc).pdf DeepDyve Pubget Overpricing