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Abstract During apoptosis, the process of mitochondrial outer membrane permeabilization MOMP represents a point-of-no-return as it commits the cell to death.
Here we have assessed the role of caspases, Bcl-2 family members and the mitochondrial permeability transition pore on ER stress-induced MOMP and subsequent cell death.
Induction of ER stress leads to upregulation of several genes such as Grp78, Edem1, Erp72, Atf4, Wars, Herp, p58ipk, and ERdj4 and leads to caspase activation, release of mitochondrial intermembrane proteins and dissipation of mitochondrial transmembrane potential m.
Mouse embryonic fibroblasts MEFs from caspase-9, -2 and, -3 knock-out mice were resistant to ER stress-induced apoptosis which correlated with decreased processing of pro-caspase-3 and Furthermore, pretreatment of cells with caspase inhibitors Boc-D.
However, only deficiency of caspase-9 and -2 could prevent ER stress-mediated loss of m. Bcl-2 overexpression or pretreatment of cells with the cell permeable BH4 domain BH4-Tat or the mitochondrial permeability transition pore inhibitors, bongkrekic acid or cyclosporine A, attenuated the ER stress-induced loss of m.
These data suggest a role for caspase-9 and -2, Bcl-2 family members and the mitochondrial permeability transition pore in loss of mitochondrial membrane potential during ER stress-induced apoptosis. Introduction The endoplasmic reticulum ER is a cytosolic membrane bound network connected to the nucleus, mitochondria, and the plasma membrane.
Membrane and secreted proteins are targeted to the ER for folding and posttranslational modification [ 12 ]. In addition, the ER is the primary storage organelle for intracellularthereby the main regulator of cellular homeostasis.
Given its central role in protein folding and its influence on -mediated signaling pathways, disruption of the ER homeostasis, also called ER stress, has severe consequences for the cell [ 12 ].
A number of pathophysiological conditions are associated with ER stress, including stroke, ischemia, hyperhomocystinemia, diabetes, viral infections, and mutations that impair protein folding [ 34 ]. To combat the deleterious effects of ER stress, the cell has evolved a variety of protective strategies collectively known as the Unfolded Protein Response UPR.
However, unresolved ER stress results in the activation of apoptosis. The exact mechanism involved in transition of the UPR from a protective to an apoptotic response is not clearly understood, but it does appear to be dependent on cysteinyl aspartate proteases of the caspase family and the proteins of Bcl-2 family [ 67 ].
Several studies have reported the involvement of initiator caspase-2, -8, and -9 [ 89 ] and effector caspase-3 and -7 in ER stress-induced apoptosis [ 10 ].
It has also been suggested that caspase acts as an initiator caspase during ER stress-induced apoptosis [ 1112 ]. However, a significant role for caspase in ER stress-induced apoptosis has not been supported by the majority of the literature reviewed in [ 13 ].
For example, caspasedeficient murine P19 embryonic carcinoma cells do not exhibit altered levels of tunicamycin-induced DNA fragmentation [ 8 ]. Furthermore, in humans, a single nucleotide polymorphism in caspase results in the synthesis of a truncated protein, lacking enzymatic activity [ 16 ].
Recent reports implicate the involvement of mitochondria in ER stress-induced apoptosis [ 10 ].
Release of cytochrome c from mitochondria during ER stress-induced apoptosis has been suggested to be mediated by mitochondrial permeability transition MPT [ 1718 ]. The molecular mechanism of the mitochondrial membrane depolarisation and the release of cytochrome c are well studied in various types of cellular stresses, and two mechanistically different models have been proposed [ 19 ].
The first one is controlled by proteins of the Bcl-2 family, while the second one involves a high conductance ion channel, the permeability transition pore PTP [ 20 ]. The role of the Bcl-2 family in ER stress-induced apoptosis is emphasized by concurrent repression of Bcl-2 and upregulation of Bim by the transcription factor, CHOP, a key determinant of ER stress-induced apoptosis [ 2122 ].
Bcl-2 family members are known to localize both to the ER and the mitochondria, where they may act to regulate the signaling pathways that promote the opening of the PTP [ 1924 ]. On the other hand, when the death antagonists, such as Bcl-2 and Bcl-xL bind to the PTP, they prevent the opening of the channel in response to many apoptotic signals [ 19 ].
The two models of cytochrome c release are not independent. The cytochrome c-dependent apoptotic pathway activated by ER-mitochondria crosstalk seems to play an essential role in the ER stress-mediated cell death [ 26 ].
The ER and mitochondria are in close contact which supports communication between these two organelles, including synthesis and transfer of lipids, and the exchange ofthat regulates ER chaperones, mitochondrial ATP production and apoptosis [ 27 ].
Here we have determined the role of caspases, Bcl-2 family members, and PTP on the mitochondrial changes associated with ER-induced apoptosis.
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