Liposomal temocene (m-THPPo) photodynamic treatment induces cell death by mitochondria-independent apoptosis

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Liposomal temocene (m-THPPo) photodynamic treatment induces cell death by mitochondria-independent apoptosis. / Soriano, Jorge; Garcia-Diaz, Maria; Mora, Margarita; Sagristá, Maria Lluïsa; Nonell, Santi; Villanueva, Angeles; Stockert, Juan Carlos; Cañete, Magdalena.

In: BBA General Subjects, Vol. 1830, No. 10, 28.05.2013, p. 4611-4620.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Soriano, J, Garcia-Diaz, M, Mora, M, Sagristá, ML, Nonell, S, Villanueva, A, Stockert, JC & Cañete, M 2013, 'Liposomal temocene (m-THPPo) photodynamic treatment induces cell death by mitochondria-independent apoptosis', BBA General Subjects, vol. 1830, no. 10, pp. 4611-4620. https://doi.org/10.1016/j.bbagen.2013.05.021

APA

Soriano, J., Garcia-Diaz, M., Mora, M., Sagristá, M. L., Nonell, S., Villanueva, A., Stockert, J. C., & Cañete, M. (2013). Liposomal temocene (m-THPPo) photodynamic treatment induces cell death by mitochondria-independent apoptosis. BBA General Subjects, 1830(10), 4611-4620. https://doi.org/10.1016/j.bbagen.2013.05.021

Vancouver

Soriano J, Garcia-Diaz M, Mora M, Sagristá ML, Nonell S, Villanueva A et al. Liposomal temocene (m-THPPo) photodynamic treatment induces cell death by mitochondria-independent apoptosis. BBA General Subjects. 2013 May 28;1830(10):4611-4620. https://doi.org/10.1016/j.bbagen.2013.05.021

Author

Soriano, Jorge ; Garcia-Diaz, Maria ; Mora, Margarita ; Sagristá, Maria Lluïsa ; Nonell, Santi ; Villanueva, Angeles ; Stockert, Juan Carlos ; Cañete, Magdalena. / Liposomal temocene (m-THPPo) photodynamic treatment induces cell death by mitochondria-independent apoptosis. In: BBA General Subjects. 2013 ; Vol. 1830, No. 10. pp. 4611-4620.

Bibtex

@article{79565cda184e4fa0bb41b9b680d0eb6e,
title = "Liposomal temocene (m-THPPo) photodynamic treatment induces cell death by mitochondria-independent apoptosis",
abstract = "BACKGROUND: The cell death pathway activated after photodynamic therapy (PDT) is controlled by a variety of parameters including the chemical structure of the photosensitizer, its subcellular localization, and the photodynamic damage induced. The present study aims to characterize a suitable m-THPPo liposomal formulation, to determine its subcellular localization in HeLa cells and to establish the cell death mechanisms that are activated after photodynamic treatments. METHODS: Liposomes containing m-THPPo were prepared from a mixture of DPPC and DMPG at a 9:1 molar ratio. In order to procure the best encapsulation efficiency, the m-THPPo/lipid molar ratio was considered. HeLa cells were incubated with liposomal m-THPPo and the subcellular localization of m-THPPo was studied. Several assays such as TUNEL, annexin V/propidium iodide and Hoechst-33258 staining were performed after photodynamic treatments. The apoptotic initiation was assessed by cytochrome c and caspase-2 immunofluorescence. RESULTS: m-THPPo encapsulated in liposomes showed a decrease of the fluorescence and singlet oxygen quantum yields, compared to those of m-THPPo dissolved in tetrahydrofuran. Liposomal m-THPPo showed colocalization with LysoTracker{\textregistered} and it induced photoinactivation of HeLa cells by an apoptotic mechanism. In apoptotic cells no relocalization of cytochrome c could be detected, but caspase-2 was positive immediately after photosensitizing treatments. CONCLUSIONS: Photodynamic treatment with liposomal m-THPPo leads to a significant percentage of apoptotic morphology of HeLa cells. The activation of caspase-2, without the relocalization of cytochrome c, indicates a mitochondrial-independent apoptotic mechanism. GENERAL SIGNIFICANCE: These results provide a better understanding of the cell death mechanism induced after liposomal m-THPPo photodynamic treatment.",
keywords = "Former Faculty of Pharmaceutical Sciences, apoptosis, liposome, photosensitizer, temocene",
author = "Jorge Soriano and Maria Garcia-Diaz and Margarita Mora and Sagrist{\'a}, {Maria Llu{\"i}sa} and Santi Nonell and Angeles Villanueva and Stockert, {Juan Carlos} and Magdalena Ca{\~n}ete",
note = "Copyright {\textcopyright} 2013 Elsevier B.V. All rights reserved.",
year = "2013",
month = may,
day = "28",
doi = "10.1016/j.bbagen.2013.05.021",
language = "English",
volume = "1830",
pages = "4611--4620",
journal = "B B A - General Subjects",
issn = "0304-4165",
publisher = "Elsevier",
number = "10",

}

RIS

TY - JOUR

T1 - Liposomal temocene (m-THPPo) photodynamic treatment induces cell death by mitochondria-independent apoptosis

AU - Soriano, Jorge

AU - Garcia-Diaz, Maria

AU - Mora, Margarita

AU - Sagristá, Maria Lluïsa

AU - Nonell, Santi

AU - Villanueva, Angeles

AU - Stockert, Juan Carlos

AU - Cañete, Magdalena

N1 - Copyright © 2013 Elsevier B.V. All rights reserved.

PY - 2013/5/28

Y1 - 2013/5/28

N2 - BACKGROUND: The cell death pathway activated after photodynamic therapy (PDT) is controlled by a variety of parameters including the chemical structure of the photosensitizer, its subcellular localization, and the photodynamic damage induced. The present study aims to characterize a suitable m-THPPo liposomal formulation, to determine its subcellular localization in HeLa cells and to establish the cell death mechanisms that are activated after photodynamic treatments. METHODS: Liposomes containing m-THPPo were prepared from a mixture of DPPC and DMPG at a 9:1 molar ratio. In order to procure the best encapsulation efficiency, the m-THPPo/lipid molar ratio was considered. HeLa cells were incubated with liposomal m-THPPo and the subcellular localization of m-THPPo was studied. Several assays such as TUNEL, annexin V/propidium iodide and Hoechst-33258 staining were performed after photodynamic treatments. The apoptotic initiation was assessed by cytochrome c and caspase-2 immunofluorescence. RESULTS: m-THPPo encapsulated in liposomes showed a decrease of the fluorescence and singlet oxygen quantum yields, compared to those of m-THPPo dissolved in tetrahydrofuran. Liposomal m-THPPo showed colocalization with LysoTracker® and it induced photoinactivation of HeLa cells by an apoptotic mechanism. In apoptotic cells no relocalization of cytochrome c could be detected, but caspase-2 was positive immediately after photosensitizing treatments. CONCLUSIONS: Photodynamic treatment with liposomal m-THPPo leads to a significant percentage of apoptotic morphology of HeLa cells. The activation of caspase-2, without the relocalization of cytochrome c, indicates a mitochondrial-independent apoptotic mechanism. GENERAL SIGNIFICANCE: These results provide a better understanding of the cell death mechanism induced after liposomal m-THPPo photodynamic treatment.

AB - BACKGROUND: The cell death pathway activated after photodynamic therapy (PDT) is controlled by a variety of parameters including the chemical structure of the photosensitizer, its subcellular localization, and the photodynamic damage induced. The present study aims to characterize a suitable m-THPPo liposomal formulation, to determine its subcellular localization in HeLa cells and to establish the cell death mechanisms that are activated after photodynamic treatments. METHODS: Liposomes containing m-THPPo were prepared from a mixture of DPPC and DMPG at a 9:1 molar ratio. In order to procure the best encapsulation efficiency, the m-THPPo/lipid molar ratio was considered. HeLa cells were incubated with liposomal m-THPPo and the subcellular localization of m-THPPo was studied. Several assays such as TUNEL, annexin V/propidium iodide and Hoechst-33258 staining were performed after photodynamic treatments. The apoptotic initiation was assessed by cytochrome c and caspase-2 immunofluorescence. RESULTS: m-THPPo encapsulated in liposomes showed a decrease of the fluorescence and singlet oxygen quantum yields, compared to those of m-THPPo dissolved in tetrahydrofuran. Liposomal m-THPPo showed colocalization with LysoTracker® and it induced photoinactivation of HeLa cells by an apoptotic mechanism. In apoptotic cells no relocalization of cytochrome c could be detected, but caspase-2 was positive immediately after photosensitizing treatments. CONCLUSIONS: Photodynamic treatment with liposomal m-THPPo leads to a significant percentage of apoptotic morphology of HeLa cells. The activation of caspase-2, without the relocalization of cytochrome c, indicates a mitochondrial-independent apoptotic mechanism. GENERAL SIGNIFICANCE: These results provide a better understanding of the cell death mechanism induced after liposomal m-THPPo photodynamic treatment.

KW - Former Faculty of Pharmaceutical Sciences

KW - apoptosis

KW - liposome

KW - photosensitizer

KW - temocene

U2 - 10.1016/j.bbagen.2013.05.021

DO - 10.1016/j.bbagen.2013.05.021

M3 - Journal article

C2 - 23721802

VL - 1830

SP - 4611

EP - 4620

JO - B B A - General Subjects

JF - B B A - General Subjects

SN - 0304-4165

IS - 10

ER -

ID: 46458725