EMD Millipore eBook - 6

Analyzing Cell Death * So Many Ways to Die

understanding of the molecular pathways associated
with cell death modalities has both broadened and
defined our understandjing of the way cells die.
For example, what was first described in 1973
as "Type III" cell death is now known to include
death, necrosis, and pathways of apoptosis which
originate from stimuli either intrinsic or extrinsic
to the cell (cell death glossary and Figure 1).
Cell Death: A Glossary
Anoikis: adherent-cell apoptosis that occurs on
the loss of matrix interactions. Believed to be a
major tumor-suppressive mechanism.
Apoptosis, extrinsic: programmed cell death
induced by extracellular signals initiated by
ligation of transmembrane receptors such as FAS
Apoptosis, intrinsic: Caspase-dependent
or -independent programmed cell death
altering mitochondrial membrane potential
Autophagic cell death: induced cytoplasmic
vacuolization with catabolism of bulk
cytoplasmic contents
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Ferroptosis: Cysteine uptake-triggered, irondependent, nonapoptotic, oxidative cell death
Necroptosis: TNFR1 signaling via RIP1 in the
presence of Caspase-8 inhibition
Necrosis: passive cell death, often resulting
from infection or injury
Parthanatos: -depletion of ATP and NAD+ by
excessive polymerase activity
Partial demolition/cornification: Permanent
alteration of cell function that is frequently
caspase-dependent. Examples include erythrocyte
enucleation, lens fiber formation, and skin cell
keratinization.
Pyroptosis: caspase-1 mediated apoptosis
associated with inflammation-responsible
for loss of T cells in HIV
Secondary necrosis: necrosis as sequelae of
apoptosis, often observed in cell culture.

The importance of determining the mode of
cell death was explained in the recent seminar
"The Many Roads to Cell Death" by Dr. John
Abrams of UT Southwestern Medical Center,
whose lab uses multiple descriptive and functional
criteria to characterize cellular demise and to understand the key molecular networks that regulate it.
One of the earliest instances of the use of flow
cytometric methods to assess cell health parameters
such as apoptosis can be traced to 1986, when
Umansky and Pechatnikov et al. used a cytometer
built in their lab to study the effects of gamma
irradiation on rat thymocytes, splenocytes, and
bone marrow cells. Six years later, William Telford
et al. used light-scattering properties along with a
fluorescent DNA marker to obtain quantitative
apoptosis data from individual cells. Now the head
of the Flow Cytometry Core Facility at the Center
for Cancer Research at the National Institutes of
Health, Dr. Telford stresses the importance of
using multiparametric assays that rely not only on
immunodetection but also examine biochemical
and biophysical features to characterize cell death,
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