Both intrinsic and extrinsic pathways can trigger activation of caspase 3.21 Activation of caspase through cell death receptors is regulated by a subset of the TNF receptor superfamily, which includes Fas/CD95, TNF receptor (TNFR)-1, and death receptor-3.8 Release of cytochrome c from mitochondria through stress stimuli, induces activation of caspase 9
, which in turn leads to activation of caspase 3 enzyme.
The Caspase 9
activities were significantly increased in 1.6 mg/l of the PFOS single exposure group, 0.8 mg/l of the PFOS co-treatment and 1.6 mg/l of the PFOS co-treatment groups as compared to the control (Figure 4b).
Morrell, "Pyroptosis as a regulated form of necrosis: PI+/annexin V-/high caspase 1/low caspase 9
activity in cells = pyroptosis?," Circulation Research, vol.
The caspase activity in treated MCF-7 revealed that FAA increased the activation of caspases 8 and 6 in all three used concentrations, while in only one concentration it increased caspase 9
(only in IC75) and caspase 3 (only in IC25) activities.
Caspase-3 and caspase 9
are in the pivotal junctions in apoptosis signaling pathways.
The primary antibodies were p53 (monoclonal mouse anti-human p53 protein clone DO-7), Bcl-2 (monoclonal mouse anti-human Bcl-2 oncoprotein clone 124), Caspase 8 (monoclonal mouse anti-human Caspase 8 clone Caspase 8), and Caspase 9
(monoclonal mouse anti-human Caspase 9
clone Caspase 9
Activation of P53 death signals lead to Caspases activation and thus can induce apoptosis through release of mitochondrial Cytochrome c into the cytoplasm which then facilitates activation of Caspase 9
, leading to activation of Caspase 3 and other effector caspases.
The mitochondria participated in the process by stimulating the intrinsic pathway via caspase 9
with a reduction in mitochondrial membrane potential (MMP) and an increase in cytochrome c release.
Moreover, in order to assess the pathway of apoptosis, we carry out an analysis of caspase 9
expression (which is an intrinsic pathway marker) and caspase 8 (which is a mediator of the extrinsic way of apoptosis).
In this study, the activity of caspase-3 and caspase 9
increased significantly (P < 0.05) with time in ZER-and ZER-NLC-treated cells.
This can result from decreased proliferation or increased cell death, which is why the investigators also looked at caspase 8 and caspase 9
. The former was activated by BPS alone and when combined with estradiol, but caspase 9
was less affected, consistent with an increase in apoptosis.
Apoptosis is initiated in OLG concomitant with a rapid decline in phosphatidylinositol-3 kinase (PI3-K) activity and Bcl-2 mRNA expression, a gradual increase in caspase 3 mRNA, and the eventual release of cytochrome c and activation of caspase 9