An analysis of telomere and telomerase hypothesis

January by Vince Giuliano A new study reported in the press this week looks at the relationship of exercise to expression of telomerase and telomere lengths in athletes and non-athletes. Other studies on the same topic have appeared in the last year or so.

An analysis of telomere and telomerase hypothesis

Contact Cellular Senescence Because cells are the fundamental building blocks of our bodies, it is logical to assume that cellular changes contribute to the aging process. In this essay I review the methods used to study cellular aging in vitro, in particular replicative senescence, and debate whether these findings could be related to organismal aging.

Phase I is the primary culture, when cells from the explant multiply to cover the surface of the culture flask--most cell types grow in the lab attached to a solid surface.

The Hayflick Limit

Phase II represents the period when cells divide in culture. Briefly, once cells cover a flask's surface, they stop multiplying. For cell growth to continue, the cells must be subcultivated. To do so, one removes the culture's medium and adds a digestive enzyme called trypsin that dissolves the substances binding cells together.

An analysis of telomere and telomerase hypothesis

After adding growth medium and pipetting one obtains the cells in a homogeneous suspension that are then divided by two--or more--new flasks. Cells then attach to the new flasks' surface and start dividing once again until a new subcultivation is required.

Most cells divide vigorously and can often be subcultivated in a matter of a few days. After several months, however, cells start dividing slower, which marks the beginning of Phase III.

Hayflick and Moorhead noticed that cultures stopped dividing after an average of 50 cumulative population doublings CPDs --splitting one flask of cells into two new flasks of the same size increases the CPDs by one, splitting by four flasks increases the CPDs by two and so on.

This phenomenon of growth arrest after a period of apparently normal cell proliferation is known as the Hayflick limit, Phase III phenomenon, or, as it will be called herein, replicative senescence RS. Hayflick and Moorhead worked with fibroblasts, a cell type found in connective tissue widely used in research, but RS has been found in other cell types: In addition, RS is observed in cells derived from embryonic tissues, in cells from adults of all ages, and in cells taken from many animals: The number of CPDs cells undergo in culture varies considerably between cell types and species.

Early results suggested a relation between CPDs cells could endure and the longevity of the species from which the cells were derived.

For example, cells from the Galapagos tortoise, which--as described --can live over a century, divide about times Goldstein,while mouse cells divide roughly 15 times Stanley et al.

In addition, cells taken from patients with progeroid syndromes such as Werner syndrome WS -- described elsewhere --endure far fewer CPDs than normal cells Salk et al.

Exceptions exist and certain cell lines can divide indefinitely without reaching RS. These are said to be "immortal" and include embryonic germ cells and most cell lines derived from tumors, such as HeLa cells Brunmark et al.

An analysis of telomere and telomerase hypothesis

Some types of rat cells have also been claimed as capable of evading RS Mathon et al. Biomarkers of Cell Senescence The discovery of RS sparked considerable interest and the phenotype of cell senescence in human fibroblasts has been characterized by a series of features, termed biomarkers d'Adda di Fagagna, The most obvious biomarker is growth arrest, i.

Even vigorously dividing cultures are heterogeneous and contain a percentage of growth-arrested cells; this percentage progressively increases until all cells in the population are quiescent, that is, they have stopped dividing Cristofalo and Sharf, ; Smith and Whitney, ; interestingly, the percentage of growth-arrested cells is higher in cells from patients with progeroid syndromes, such as WS cells, when compared with normal cells at the same CPD Kill et Lara Pizzorno, MDiv, MA, LMT with Barry Wheeler, ND Treating the sequelae of andropause, the age- and stress-related decline in hormones in the adult male, with bio-identical hormone replacement (BHRT) can restore more youthful hormone levels and significantly alleviate symptoms associated with “normal” aging, optimizing health, happiness and quality of life.

The prediction of clinical behavior, response to therapy, and outcome of infiltrative glioma is challenging. On the basis of previous studies of tumor biology, we defined five glioma molecular. By Vince Giuliano In past blog entries and in my treatise I have explained how I was an early adapter at taking telomerase extenders like astrogaloside4 and cycloastragenol, and why, later as a result of following much research, I stopped Continue reading →.

Telomere biology has the potential to extend human life span, to dramatically lower rates of the great remaining killer diseases: heart disease, stroke, and Alzheimer’s.

All three diseases increase exponentially with age, and their toll will be slashed as we we learn how to address the body’s aging clocks. You would think that the Nobel Prize might have done more to raise the profile. Stone et al. () mapped the mouse homolog of the human retinoblastoma gene, symbolized Rb1, to chromosome 14 by analysis of somatic cell hybrids.

In recombinant inbred strains, the findings suggested close linkage of Rb1 and Es10, which appears to be the mouse homolog of ESD ().By in situ hybridization, Ono and Yoshida () assigned the RB1 gene to mouse 14D3 and the rat homolog to . Origin of Life • Precellular, Cellular • Testing hypotheses –A priori assumptions (often not stated) may themselves be tested –Hypotheses must make falsifiable "predictions" •"Null" hypothesis: chance alone is responsible –Predictions are confirmed (consistent with) or refuted by data –"Parsimony" distinguishes between alternative, unfalsified, working.

Équipe Paul HOFMAN