Apoptosis

Cell proliferation

The process of producing new cells through cell division

Cell death

The removal of cells when they are no longer needed

G0 phase

A resting state where cells stop proliferating but may re-enter the cell cycle (fibroblasts remain here)

PDGF

Stimulates fibroblast proliferation migration and collagen release during wound healing

VEGF

Stimulates endothelial cell proliferation and formation of new blood vessels if a tissue is not getting enough oxygen

Fibroblasts

Cells that produce collagen and help repair damaged tissue

Endothelial cells

Cells lining blood vessels that proliferate in response to VEGF and create new vessels

Stem cells

Cells capable of:

• self-renewal (one daughter cells gets differentiated and the other will remain a stem cell)

• Producing differentiated cells

Self-renewal

The ability of stem cells to produce another stem cell during division (the other is a daughter cell that will differentiate)

Transient amplifying cells

Stem cell descendants that rapidly proliferate before differentiating

Pluripotent

Able to differentiate into any cell type

Embryonic stem cells

Pluripotent cells isolated from an embryo

Somatic cell nuclear transfer

Replacing an egg nucleus with the nucleus of an adult somatic cell

• Advantages: cells come from patient, no rejection

• Disadvantage: ethical concerns over the generation and destruction of an embryo and possibility of cloning a human

Therapeutic cloning

Producing patient-specific cells for transplantation therapy

Induced pluripotent stem cells (iPSCs)

Adult somatic cells reprogrammed into pluripotent stem cells (no embryos required)

Oct4

Sox2 and Nanog

Transdifferentiation

Direct conversion of one differentiated somatic cell into another

Apoptosis

Programmed cell death that removes unwanted or damaged cells

Necrosis

Uncontrolled cell death involving cell damage and release of cellular contents

Apoptotic bodies

Membrane-bound fragments formed when an apoptotic cell breaks apart

DNA fragmentation

Breakdown of DNA into approximately 200 base pair fragments during apoptosis

Phosphatidylserine

Membrane lipid that flips to the outer leaflet as an eat me signal

Scramblase

Enzyme that moves phosphatidylserine to the outer membrane leaflet

Caspases

Proteases that cleave proteins and carry out apoptosis

Procaspase

Inactive precursor form of a caspase

Initiator caspases

Caspases activated by apoptotic signals that activate effector caspases

Effector caspases

Caspases that digest proteins necessary for apoptosis

Ced-3

C. elegans gene encoding a caspase required for apoptosis

Ced-4

Positive regulator of apoptosis in C. elegans

Ced-9

Negative regulator of apoptosis in C. elegans

Bcl-2

Mammalian equivalent of Ced-9 that inhibits apoptosis

Bcl-2 family

Proteins divided into antiapoptotic regulators proapoptotic regulators and proapoptotic effectors

Antiapoptotic proteins

Proteins that inhibit cell death

Proapoptotic proteins

Proteins that promote programmed cell death

Bax and Bak

Proapoptotic effectors that form pores in the mitochondrial membrane

Cytochrome c

Mitochondrial protein released during apoptosis that helps activate the apoptosome

Apoptosome

Protein complex that activates caspase-9

Caspase-9

Initiator caspase activated by the mitochondrial pathway

Intrinsic pathway

Apoptosis triggered by internal stress such as DNA damage or growth factor deprivation

Extrinsic pathway

Apoptosis triggered by signals from other cells binding to specific receptors

p53

Protein that responds to DNA damage and can trigger cell cycle arrest or apoptosis

Caspase-8

Initiator caspase activated by the extrinsic pathway

TNF family

Signal molecules involved in triggering extrinsic apoptosis

Autophagy

Gradual breakdown and recycling of cell components that promotes survival during nutrient deprivation

Necroptosis

Programmed cell death involving disruption of the plasma membrane and release of cell contents

Pyroptosis

An alternative pathway of programmed cell death