Final answer:
The extrinsic apoptosis pathway is triggered by cellular trauma, leading to the release of factor III and subsequent signaling cascades. Disruption in extracellular matrix interactions and release of cytochrome C from mitochondria due to Bcl2 proteins Bak and Bax are key aspects.
Step-by-step explanation:
The extrinsic apoptosis pathway is initiated when there is damage to cells and tissues, which typically can result from trauma. This trauma causes cells extrinsic to the bloodstream to release factor III (also known as thromboplastin).
Subsequently, this activates a cascade that involves calcium (Ca²+) ions. In the context of apoptosis, external signaling can initiate the cell death process. For example, disruption of interactions between the cell and the extracellular matrix can trigger apoptosis, helping to control potentially harmful proliferations, such as tumor cells that metastasize.
Specific receptors on the cell surface interact with the extracellular matrix to initiate intracellular signaling cascades that are vital for cell survival. If distancing from the extracellular matrix occurs, these signals halt, leading the cell to undergo apoptosis.
Furthermore, proteins like Bak and Bax, which are part of the Bcl2 protein family, form channels in the mitochondrial membrane that permit the release of cytochrome C, leading towards the apoptosis pathway.
Another external signaling example is during T-cell development, where cells that inappropriately bind to self-proteins are induced to undergo apoptosis, to prevent autoimmune responses.