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Live Imaging of Mitochondrial BAX Re...

Maes, Margaret E.

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Live Imaging of Mitochondrial BAX Recruitment.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Live Imaging of Mitochondrial BAX Recruitment./
作者:	Maes, Margaret E.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2017,
面頁冊數:	325 p.
附註:	Source: Dissertation Abstracts International, Volume: 78-10(E), Section: B.
Contained By:	Dissertation Abstracts International78-10B(E).
標題:	Cellular biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10281337
ISBN:	9781369767421

Live Imaging of Mitochondrial BAX Recruitment.
Maes, Margaret E.

Live Imaging of Mitochondrial BAX Recruitment. - Ann Arbor : ProQuest Dissertations & Theses, 2017 - 325 p.

Source: Dissertation Abstracts International, Volume: 78-10(E), Section: B.

Thesis (Ph.D.)--The University of Wisconsin - Madison, 2017.

Glaucoma is an optic neuropathy characterized by retinal ganglion cell (RGC) death. One of the most common risk factors for the disease is an increase in intraocular pressure (IOP), which creates chronic stress at the optic nerve head, the region where RGC axons converge. It is thought that this damage is the causative factor for RGC death, consequently almost all treatments for glaucoma patients are focused on IOP-lowering strategies. Reducing the IOP alone, however, does not prevent loss of RGCs that have already been exposed to damaging effects; therefore it would be beneficial to combine IOP-lowering treatments with RGC protective strategies.

ISBN: 9781369767421Subjects--Topical Terms:

3172791
Cellular biology.

Live Imaging of Mitochondrial BAX Recruitment.
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300 $a 325 p.
500 $a Source: Dissertation Abstracts International, Volume: 78-10(E), Section: B.
500 $a Adviser: Robert Nickells.
502 $a Thesis (Ph.D.)--The University of Wisconsin - Madison, 2017.
520 $a Glaucoma is an optic neuropathy characterized by retinal ganglion cell (RGC) death. One of the most common risk factors for the disease is an increase in intraocular pressure (IOP), which creates chronic stress at the optic nerve head, the region where RGC axons converge. It is thought that this damage is the causative factor for RGC death, consequently almost all treatments for glaucoma patients are focused on IOP-lowering strategies. Reducing the IOP alone, however, does not prevent loss of RGCs that have already been exposed to damaging effects; therefore it would be beneficial to combine IOP-lowering treatments with RGC protective strategies.
520 $a Optic nerve damage causes retinal ganglion cells (RGCs) to undergo BAX-dependent intrinsic apoptosis. To date, the only long-term neuroprotective strategy for mouse RGCs after optic nerve injury has been genetic deletion of Bax. BAX is a pro-apoptotic member of the BCL2 gene family that mediates a cell's commitment to the apoptotic program, which highlights BAX as an attractive target for developing neuroprotective strategies in RGCs.
520 $a To target BAX for therapeutic intervention, it is imperative to understand its mechanisms of activation and recruitment. A method to quantify BAX recruitment in living cells was developed and applied to time-lapse imaging of immortalized tissue culture cells and to ex vivo live imaging of RGCs in mouse retina. Regardless of cell type, apoptotic stimulus, or time of BAX initiation, individual cells exhibited variable BAX recruitment rates. Differences in the time of BAX initiation after staurosporine addition among cell types suggested that each cell type may have intrinsic properties contributing to the time to BAX activation after apoptotic stimulus. Most strikingly, RGCs showed a significantly slower rate of BAX recruitment and exhibited a BAX retro-translocation phenomenon, highlighting a likely role of the complex tissue environment in providing pro-survival support to RGCs and potentially altering the internal mechanism of BAX recruitment.
520 $a BAX has also been demonstrated to play an integral role in the process of mitochondrial dynamics, both in steady-state conditions and during apoptosis, however its requirement during the latter had not been directly tested. It was found that completion of the BAX recruitment process coincided with rapid mitochondrial fragmentation during apoptosis. Furthermore, this process did not occur in the presence of a BAX mutant that was unable to participate in the MOM integration step of BAX recruitment, demonstrating that mitochondrial fragmentation during apoptosis required BAX.
520 $a These studies critically evaluated the BAX recruitment process to dissect key differences in the initiation of BAX activation, the rate of BAX recruitment, and the events of BAX recruitment completion and mitochondrial fragmentation. A retro-translocation event in RGCs after BAX activation was also identified. Understanding the mechanism controlling this phenomenon could provide additional targets for the development of therapeutic strategies.
590 $a School code: 0262.
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650 4 $a Ophthalmology. $3 862704
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710 2 $a The University of Wisconsin - Madison. $b Cellular and Molecular Pathology. $3 3194061
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