Culture of Human Skin Fibroblasts  

Cellular Senescence
 
Cellular senescence is the phenomenon where normal differentiated diploid cells lose the ability to divide. This phenomenon is also known as replicative senescence. Senescence or irreversible proliferate arrest of cells can also be caused by various stresses including oxidative damage. In vitro cellular aging is generally known as the Hayflick phenomenon and the limited division potential of normal cells is called the Hayflick limit after its discoverer Len Hayflick. The whole period of serial passaging is considered as cellular aging and begins with a long period of growth and cell proliferation. The end-stage of aging is replicative senescence, involving processes that eventually lead to metabolic inactivation and cell death. The process of aging causes cell morphology changes throughout the life span of e.g. normal skin fibroblasts. Young fibroblasts form very confluent adherent monolayers of long and thin cells. Middle-aged fibroblasts form less confluent monolayers of enlarged cells. In a population of old fibroblasts there is almost no cell proliferation going on and nearly all cells are enlarged. Serially passaged cells accumulate long actin rods within their cell bodies due to perturbations in actin polymerization.  

Cellular Aging
 
Cellular aging in general is characterized by a stochastic accumulation of molecular damage in nucleic acids, proteins and lipids causing a progressive failure of homeodynamics. Molecular damage of the homeodynamic components is essentially recovered but accumulation of damage occurs when a certain damage threshold is exceeded. Some important components of the homeodynamic machinery consist of the multiple pathways of repair including nuclear and mitochondrial DNA repair as well as pathways of protein turnover and repair. The main mechanistic hypotheses for explaining the accumulation of molecular damage and thus failure of homeodynamics are: altered gene regulation, somatic mutation accumulation, protein errors and modifications, and free radical-induced damage.  

Inspired by Suresh I. S. Rattan.