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October, 2006
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Apoptosis: One of the mechanisms by which Cell death occurs (compare with Necrosis and Autophagocytosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (Dna fragmentation); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.

Real Time Detection of In Vitro Tumor Cell Apoptosis Induced by CD8+ T Cells to Study Immune Suppressive Functions of Tumor-infiltrating Myeloid Cells

1Royal (Dick) School of Veterinary Studies and Roslin Institute, University of Edinburgh, 2MRC Centre for Reproductive Health, University of Edinburgh, 3Edinburgh Phenotypic Assay Centre, University of Edinburgh, 4Cancer Research UK Edinburgh Centre, MRC Institute of Genetics, Molecular Medicine, University of Edinburgh

JoVE 58841

 Cancer Research

An Introduction to Cell Death

JoVE 5649

Necrosis, apoptosis, and autophagic cell death are all manners in which cells can die, and these mechanisms can be induced by different stimuli, such as cell injury, low nutrient levels, or signaling proteins. Whereas necrosis is considered to be an “accidental” or unexpected form of cell death, evidence exists that apoptosis and autophagy are both programmed…

 Cell Biology

Annexin V and Propidium Iodide Labeling

JoVE 5650

Staining with annexin V and propidium iodide (PI) provides researchers with a way to identify different types of cell death—either necrosis or apoptosis. This technique relies on two components. The first, annexin V, is a protein that binds certain phospholipids called phosphatidylserines, which normally occur only in the inner, cytoplasm-facing leaflet of a…

 Cell Biology

The TUNEL Assay

JoVE 5651

One of the hallmarks of apoptosis is the nuclear DNA fragmentation by nucleases. These enzymes are activated by caspases, the family of proteins that execute the cell death program. TUNEL assay is a method that takes advantage of this feature to detect apoptotic cells. In this assay, an enzyme called terminal deoxynucleotidyl transferase catalyzes the addition of dUTP…

 Cell Biology

Adult Stem Cells

JoVE 10810

Stem cells are undifferentiated cells that divide and produce more stem cells or progenitor cells that differentiate into mature, specialized cell types. All the cells in the body are generated from stem cells in the early embryo, but small populations of stem cells are also present in many adult tissues including the bone marrow, brain, skin, and gut. These adult stem cells typically produce the various cell types found in that tissue—to replace cells that are damaged or to continuously renew the tissue. The epithelium lining the small intestine is continuously renewed by adult stem cells. It is the most rapidly replaced tissue in the human body, with most cells being replaced within 3-5 days. The intestinal epithelium consists of thousands of villi that protrude into the interior of the small intestine—increasing its surface area to aid in the absorption of nutrients. Intestinal stem cells are located at the base of invaginations called crypts that lie between the villi. They divide to produce new stem cells, as well as daughter cells (called transit amplifying cells) that divide rapidly, move up the villi and differentiate into all the cell types in the intestinal epithelium, including absorptive, goblet, enteroendocrine, and Paneth cells. These mature cells continue to move up the villi as they carry out their functions, except Paneth cell

 Core: Biotechnology

Bone Remodeling

JoVE 10866

Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.

Parathyroid hormone (PTH) maintains homeostatic control of blood calcium levels by regulating bone resorption. PTH is released from the parathyroid glands in response to low levels of calcium in the blood. It stimulates osteoblasts to produce immune molecules that promote the differentiation of precursor cells into osteoclasts. Activation of osteoclasts promotes bone resorption, causing the mineralized bone matrix to break down and release calcium into the blood. When blood calcium levels are restored, a negative-feedback loop prevents further release of PTH. Osteoporosis is a disease in which bone resorption exceeds bone formation, resulting in reduced bone density. Osteoporosis is more prevalent in women, especially after menopause. This is due to the critical role played by the female sex hormone—estrogen—in bone remodeling. Estrogen limits the formation of osteoclasts and promotes their destruction via apoptosis. This ensures that bone formation is higher than bone resorption. However, estrogen levels decli

 Core: Musculoskeletal System

Negative Regulator Molecules

JoVE 10764

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.

Three of the best-understood negative regulators are p53, p21, and retinoblastoma protein (Rb). The regulatory roles of each of these proteins were discovered after faulty copies were found in cells with uncontrolled replication (i.e., cancer). These proteins exert most of their regulatory effects at the G1 checkpoint early in the cell cycle. P53 strongly influences a cell’s commitment to divide. It responds to DNA damage by discontinuing the cell cycle and summoning enzymes to repair the damage. If the DNA damage is irreparable, p53 can prevent the cell from proceeding through the cell cycle by inducing apoptosis, or cell death. An increase in p53 triggers the production of p21. P21 prevents the cell from transitioning from the G1 to the S phase of the cell cycle by binding to CDK/cyclin complexes, inhibiting their positive regulatory actions. Rb negatively regulates the cell cycle by acting on different positive regulators, mainly in response to cell size. Active (dephosphorylated) Rb binds to transcription factors, preventing them from initiating gene tran

 Core: Cell Cycle and Division
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