Cell renewal, cell death and apoptosis Flashcards
the balance between the production of new cells and cell death that maintains the appropriate number of cells in a tissue.
homeostasis
What are reversible functional and structural responses to physiologic stresses; hypertrophy, hyperplasia, atrophy, metaplasia
adaptation
What is the state where cells are no longer able to adapt; ATP depletion, cell swelling, alterations in intracellular organelles, such as mitochondria and the cytoskeleton
cell injury
the end result of progressive and irreversible cell injury. Cells die by one of two mechanisms; necrosis or apoptosis
cell death
Apoptosis and necrosis have different characteristics; What are the differences
differ in their morphology, mechanisms, and roles in physiology and diseases.
What is an
Accidental cell death from acute injury by external factors. It is the ungoverned, irreversible, and premature death of cells and living tissues.
Necrosis (detrimental, not natural)
What is a
Programmed cell death (cell-suicide program).
It is carefully regulated.
It balances cell proliferation and maintains constant cell numbers.
It eliminates “non-functioning, unwanted, damaged, or potentially dangerous” cells.
apoptosis (beneficial, natural)
These are causes of: Pathological conditions Trauma; injury, burns, shock Lack of blood flow; hernia, cancer, hypoxia, stroke, myocardial infarction Infection; viruses to tapeworms Chemicals; poisons Inflammation; Nutritional imbalances;
necrosis
o
Physiological conditions to cause (blank):
The programmed destruction of cells during embryogenesis. For example, during development of a limb, tissue present between the digits must be removed. This occurs through localized apoptosis.
Normal cell loss in proliferating cell populations.
Involution of hormone-dependent tissues upon hormone withdrawal.
apoptosis
What condition can undergo apoptosis or necrosis?
myocardial infarction
o Pathophysiological conditions to cause (blank):
DNA damage; anticancer drugs, radiation, and hypoxia.
Accumulation of misfolded proteins leading to endoplasmic reticulum (ER) stress.
Cell death in certain infections, particularly viral infections.
Pathologic atrophy of organs and tissues as a result of stimuli removal.
Cytotoxic T cell-induced cell death.
Cell death that occurs in heart diseases.
apoptosis
When cells are stressed it causes (blank)
If cell injury is irreversible what happens to the cell?
This happens in what type of cell death?
reversible or irreversible injury
Swelling, complete dissolution of nucleus, plasma membrane disrupted, enzymatic digestion of cell contents
Necrosis
Apoptosis results in what happening to the cell?
shrinkage, chromatin condensation + fragmentation + become apoptopic bodies, PM remains intact, cellular contents may be released in apoptopic bodies.
apoptotic bodies contain what?
fragmented nucleus
apoptotic cells express (blank) signals which recruit and are recognized by (blank).
eat me.
Phagocytes
What are some notable eat me signals of apoptotic cells?
- “Flipped-out” phosphatidylserine which is restricted to the inner leaflet of the plasma membrane.
- Thrombospondin
- An adhesive glycoprotein
- Natural antibodies and proteins of the complement system, notably C1q
- Soluble factors
This process of phagocytosis of apoptotic cells is (blank) , often within minutes, and inflammation is (blank).
efficient
absent.
(blank) cells swell and lyse; the contents are released into the extracellular space and cause inflammation.
Necrotic
Apoptotic signaling pathways:
(blank) are the effectors of apoptosis
Caspases
Activation of what molecular will lead to a cascade and eventual apoptosis? i.e the ultimate executioner of apoptosis
caspase
Initiation of apoptosis occurs principally by signals from two distinct pathways
Intrinsic or mitochondrial pathway
Extrinsic or death receptor–initiated pathway
(blank) have cysteine (C) residues at their active sites and cleave after aspartic acid (Asp) residues in their substrate proteins.
Cleave nearly 100 different cell target proteins.
Caspases
What are four different targets of caspases?
- ICAD inhibitor of DNAse, (frag of DNA)
- Nuclear lamins (frag of nucleus)
- Cytoskeletal proteins actin, myosin, alph-actinin, tubulin, vimentin (frag of membrane)
- Golgi matrix proteins (frag of golig)
(blank) act as either initiators or effectors of apoptosis
caspases
In normal cells, caspase is typically (blank)
inactive
What is the caspase pathway?
- Each caspase is initially made as an inactive proenzyme (procaspase). Some procaspases are activated by proteolytic cleavage by an activated caspase: two cleaved fragments from each of two procaspase molecules associate to form an active caspase, which is a tetramer of two small and two large subunits; the prodomains are usually discarded, as indicated.
- The first procaspases activated are called initiator procaspases, which then cleave and activate many executioner procaspase molecules, producing an amplifying chain reaction (a proteolytic caspase cascade). The executioner caspases then cleave a variety of key proteins in the cell.
What are the initiator caspases?
2,8,9,10
What are the executioner caspases?
3,6,7
What does the intrinsic or mitochondrial pathway of initation of aptosis consist of?
Members of the Bcl-2 family act at the mitochondria.
Cytochrome c released from mitochondria triggers caspase activation.
Bcl-2 family members regulate the intrinsic pathway
by controlling mitochondrial release of (blank)
cytochrome c
(blank) domain mediates a direct binding interaction between one pro-apoptotic protein and one anti-apoptotic protein to form heterodimers.
The BH3
(blank) often acquire mutations that allow them to alter the balance between pro- and anti-apoptotic proteins, making it less likely for them to commit suicide even under conditions when normal cells would
Cancer cells
(blank) is the only domain shared by all BCL-2 families.
BH3
Bcl-2 family proteins regulate the intrinsic pathway
by controlling mitochondrial release of (blank)
anti-IAP proteins
