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Radiation-induced "Nanopores" Facili...

Ferranti, Charles Stephen.

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Radiation-induced "Nanopores" Facilitate Calcium-mediated Apoptosis via Asmase Activity.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Radiation-induced "Nanopores" Facilitate Calcium-mediated Apoptosis via Asmase Activity./
作者:	Ferranti, Charles Stephen.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2019,
面頁冊數:	141 p.
附註:	Source: Dissertations Abstracts International, Volume: 80-11, Section: B.
Contained By:	Dissertations Abstracts International80-11B.
標題:	Biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=13812216
ISBN:	9781392135693

Radiation-induced "Nanopores" Facilitate Calcium-mediated Apoptosis via Asmase Activity.
Ferranti, Charles Stephen.

Radiation-induced "Nanopores" Facilitate Calcium-mediated Apoptosis via Asmase Activity. - Ann Arbor : ProQuest Dissertations & Theses, 2019 - 141 p.

Source: Dissertations Abstracts International, Volume: 80-11, Section: B.

Thesis (Ph.D.)--Weill Medical College of Cornell University, 2019.

This item must not be added to any third party search indexes.

Diverse stresses, including reactive oxygen species (ROS), ionizing radiation, mechanical stress, and ultraviolet light activate acid sphingomyelinase (ASMase) and generate the second messenger ceramide at the plasma membrane to trigger apoptosis in specific cell types, such as hematopoietic cells and endothelium. In this pathway, ceramide elevation above a cell type-specific threshold drives local reorganization of the bilayer into ceramide-rich platforms, macrodomains (0.5 - 5 µm diameter) that transmit the apoptotic death signal. An unresolved issue in this cascade is how ASMase, which resides intracellularly within lysosomes, is released extracellularly in seconds to hydrolyze sphingomyelin preferentially localized to the outer leaflet of the plasma membrane (PM) in all mammalian cells. Here we show that physical damage to PM by ionizing radiation and ROS induces a full thickness PM disruption that allows local calcium influx, lysosome fusion with PMs, and ASMase release. Further, using electron microscopy we detect a "nanopore-like" structure that forms within seconds in PMs due to lipid peroxidation, which allows calcium entry to initiate lysosome fusion. We posit the extent of upstream physical injury to mammalian membrane, calibrated by incidence and severity of nanopore-mediated local calcium influx for lysosome fusion, represents a biophysical mechanism for induction of cell death.

ISBN: 9781392135693Subjects--Topical Terms:

522710
Biology.

Radiation-induced "Nanopores" Facilitate Calcium-mediated Apoptosis via Asmase Activity.
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520 $a Diverse stresses, including reactive oxygen species (ROS), ionizing radiation, mechanical stress, and ultraviolet light activate acid sphingomyelinase (ASMase) and generate the second messenger ceramide at the plasma membrane to trigger apoptosis in specific cell types, such as hematopoietic cells and endothelium. In this pathway, ceramide elevation above a cell type-specific threshold drives local reorganization of the bilayer into ceramide-rich platforms, macrodomains (0.5 - 5 µm diameter) that transmit the apoptotic death signal. An unresolved issue in this cascade is how ASMase, which resides intracellularly within lysosomes, is released extracellularly in seconds to hydrolyze sphingomyelin preferentially localized to the outer leaflet of the plasma membrane (PM) in all mammalian cells. Here we show that physical damage to PM by ionizing radiation and ROS induces a full thickness PM disruption that allows local calcium influx, lysosome fusion with PMs, and ASMase release. Further, using electron microscopy we detect a "nanopore-like" structure that forms within seconds in PMs due to lipid peroxidation, which allows calcium entry to initiate lysosome fusion. We posit the extent of upstream physical injury to mammalian membrane, calibrated by incidence and severity of nanopore-mediated local calcium influx for lysosome fusion, represents a biophysical mechanism for induction of cell death.
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