Answer Posted / sonai raja
Apoptosis
Apoptosis, or programmed cell death, is a normal component
of the development and health of multicellular organisms.
Cells die in response to a variety of stimuli and during
apoptosis they do so in a controlled, regulated fashion.
This makes apoptosis distinct from another form of cell
death called necrosis in which uncontrolled cell death
leads to lysis of cells, inflammatory responses and,
potentially, to serious health problems. Apoptosis, by
contrast, is a process in which cells play an active role
in their own death (which is why apoptosis is often
referred to as cell suicide).
Upon receiving specific signals instructing the cells to
undergo apoptosis a number of distinctive changes occur in
the cell. A family of proteins known as caspases are
typically activated in the early stages of apoptosis. These
proteins breakdown or cleave key cellular components that
are required for normal cellular function including
structural proteins in the cytoskeleton and nuclear
proteins such as DNA repair enzymes. The caspases can also
activate other degradative enzymes such as DNases, which
begin to cleave the DNA in the nucleus.
Apoptotic cells display distinctive morphology during the
apoptotic process. This can be seen in the image below
which shows a trophoblast cell undergoing apoptosis.
Typically, the cell begins to shrink following the cleavage
of lamins and actin filaments in the cytoskeleton (A). The
breakdown of chromatin in the nucleus often leads to
nuclear condensation and in many cases the nuclei of
apoptotic cells take on a "horse-shoe" like appearance (B).
Cells continue to shrink (C), packaging themselves into a
form that allows for their removal by macrophages. These
phagocytic cells are responsible for clearing the apoptotic
cells from tissues in a clean and tidy fashion that avoids
many of the problems associated with necrotic cell death.
In order to promote their phagocytosis by macrophages,
apoptotic cells often ungergo plasma membrane changes that
trigger the macrophage response. One such change is the
translocation of phosphatidylserine from the inside of the
cell to the outer surface. The end stages of apoptosis are
often characterised by the appearance of membrane blebs (D)
or blisters process. Small vesicles called apoptotic bodies
are also sometimes observed (D, arrow).
The apoptotic process can also be seen in a video which can
be viewed by clicking here.
There are a number of mechanisms through which apoptosis
can be induced in cells. The sensitivity of cells to any of
these stimuli can vary depending on a number of factors
such as the expression of pro- and anti-apoptotic proteins
(eg. the Bcl-2 proteins or the Inhibitor of Apoptosis
Proteins), the severity of the stimulus and the stage of
the cell cycle. Some of the major stimuli that can induce
apoptosis are outlined in the illustration below.
In some cases the apoptotic stimuli comprise extrinsic
signals such as the binding of death inducing ligands to
cell surface receptors called death receptors. These
ligands can either be soluble factors or can be expressed
on the surface of cells such as cytotoxic T lymphocytes.
The latter occurs when T-cells recognise damaged or virus
infected cells and initiate apoptosis in order to prevent
damaged cells from becoming neoplastic (cancerous) or virus-
infected cells from spreading the infection. Apoptosis can
also be induced by cytotoxic T-lymphocytes using the enzyme
granzyme.
In other cases apoptosis can be initiated following
intrinsic signals that are produced following cellular
stress. Cellular stress may occur from exposure to
radiation or chemicals or to viral infection. It might also
be a consequence of growth factor deprivation or oxidative
stress caused by free radicals. In general intrinsic
signals initiate apoptosis via the involvement of the
mitochondria. The relative ratios of the various bcl-2
proteins can often determine how much cellular stress is
necessary to induce apoptosis.
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