Dr. Mar?a A. Blasco's team found that functional cells differentiated by pluripotent stem cells also carry long telomeres and are healthier.

Bypassing the traditional molecular operation, telomeres are extended only by in vitro cultivation of pluripotent stem cells.
this is good news for scientists working on whether long telomeres benefit health and extend life.
, however, whether these cells actually slow aging and reduce the prevalence has not been proven.
recently, Dr. Mar?a A. Blasco's team from Spain's National Cancer Research Center (CNIO) proved its advantage in mice.
even more surprising, functional cells that are differentiated by these pluripotent stem cells also carry long telomeres.
mouse models with these special cells have been shown to have healthier bodies, including fewer DNA damage, slow molecular aging, and a reduced risk of cancer.
related research published in the journal Nature Communications.
stem cells carrying extra-long telomeres: open hanging? As the "life clock", telomeres have always been the focus of life scientists' research, and they are closely related to life span, DNA damage, cancer and other diseases.
scientists have also been trying to crack the link to the source of health and longevity.
back in 2009, the Blasco team shunned traditional genetic manipulation and succeeded in prolonging their chromosomal telomeres through in vitro culture induced pluripotent stem cells (iPSCs) and embryonic stem cells (ESCs).
, this telomere extension did not alter the telomerase gene.
these cells have the structure and function to build normal adult organs.
although over time, the telomeres will shrink at a certain rate.
but at the same age, cells carrying extra-long telomeres will have their telomerelengthies longer than normal telomeres.
it's easy to understand because the starting line is different.
now, the Blasco team injected these cells into mice to build a model of mice carrying long telomeres.
selected mouse tissue seamounts (0), 1, 6, and 12 months ago found that although telomeres shortened at normal frequencies over time, these cells, which had the advantage of length, still had longer telomeres than normal cells.
, these long telomeres have less DNA damage accumulation and greater damage repair ability. In addition, the prevalence of tumors in animal models was significantly lower than in wild mice,
.
chimeric mice carrying cells with this innate advantage were found to have relatively few cells containing short telomeres in their bodies, decreased cell DNA loss and had a relatively low expression level of p53.
this means that the signs of aging in the chimeric mice decrease and the prevalence decreases.
Blasco says their research shows that in vitro culture produces iPSCs that carry long telomeres, and that functional cells that differentiate the stem cells also contain long telomeres, which exhibit better life performance.
next, the Blasco team will test more of the unknown by building a mouse model with twice as long telomeres: Does double-long telomeres mean longer lives? Does nature determine the longevity of genetically similar species by the length of telomeres? What is the probability of cancer in this new species? Telomere-related information: Elizabeth Blackburn of the University of California, San Francisco, Carol Greider of the John Hopkin School of Medicine in Baltimore, Jack Szostak of Harvard Medical School, and the Howard Hughes Institute of Medicine were awarded the award for discovering the mechanisms of telomeres and telomerase protection chromosomes.
Karolinska Medical School, the trio "solved a major biological problem" of how chromosomes are fully copied and protected from degradation when cells divide.
all the mysteries lie in telomeres and telomerase.
telomerase, made from the root of chromosomes, is a natural falloff of chromosomes that can cause aging and cancer.
telomeres are also known to scientists as the "life clock".
in new cells, the telomeres are shortened every time the cells divide.
when the telomeres can no longer be shortened, cells cannot continue to divide and die.
Elizabeth, The Telomerase they found in Blackburn, played an important role in the growth of some out-of-control malignant cells. about 90 percent of cancer cells in the
have growing telomeres and relatively large numbers of telomerase.
Elizabeth Black was born in Australia in 1948 and received her Ph.D. from the University of Cambridge in 1975 after completing a university course at the University of Melbourne, Australia.
Carol Grad, American.
was born in California in 1961 and studied at the University of California, Santa Barbara and Berkeley, and received her Ph.D. in 1987, under the bet of Elizabeth Blackburn.
Jack Shostak, American.
was born in London in 1952 and grew up in Canada.
he attended McGill University in Canada and Cornell University in the United States, where he received his Ph.D. in 1977.
has taught at Harvard Medical School since 1979 and is now a professor of genetics at Massachusetts General Hospital, where he also serves at the Howard Hughes Institute of Medicine.
Telomere Introduction: Telomeres are short, multi-repeated non-transcription sequences (TTAGGG) and some binding proteins to form a special structure, in addition to providing buffers of non-transcription DNA, it can also protect the ends of chromosomes from fusion and degradation, in chromosome positioning, replication, protection and control of cell growth and life, and closely related to apoptosis, cell transformation and eternal life.
when cells divide once, the telomeres on each chromosome become shorter. about 50 to 200 nucleotides in the genes that make up part of the telomeres
, which cannot be fully replicated (lost) due to multiple cell divisions, so that the cells stop dividing at the end of their function.
, the severely shortened telomeres are a sign of cell aging.
in some cells that require an infinite replication cycle, the length of the telomeres is preserved by the specific DNA polymerase-telomerase that can synthesize the telomeres after each cell divides.
telomere DNA is composed of a simple DNA highly repeatable sequence, telomerase can be used to give endogenous DNA tailings, DNA molecules each time the division replication, telomeres shorten a little (such as Okazaki fragments), once the telomeres are exhausted, the cells will immediately activate the apoptosis mechanism, that is, the cell towards apoptosis.
historical scientists searching for genes that cause cell death have discovered a substance called telomeres that exist at the top of chromosomes.
telomeres themselves do not have any password function, it is like a high hat placed on the head of the chromosome.
in a new cell, the telomeres at the top of the chromosome are shortened once each time the cells divide, and when the telomeres can no longer be shortened, the cells cannot continue to divide.
this time the cells reached the most widely accepted 100-times-splitting limit and began to die.
, telomeres are considered "life clocks" by scientists.
scientists began to study how chromosomal telomeres in sperm and cancer cells are not shortened for long periods of time.
1984, molecular biologists studied single-celled organisms and discovered a telomerase that maintains telomere length and revealed its peculiar role in the human body: telomerase does not work on almost all other cells except human reproductive cells and some somatic cells, but it maintains the length of the telomeres of cancer cells, allowing it to expand indefinitely.
as early as the 1930s, Muller and Meclintock discovered the existence of telomere structures.
1978, the telomere structure of the tetra-diaphragm was first determined.
1990, Calvin Harley has linked telomeres to human aging: first, the older the cells, the shorter the telomeres;
some telomeres in senescent cells lose most of the telomere repeat sequences.
ageing occurs when the function of the cell's telomeres is impaired, and when the telomeres are shortened to a critical length, aging accelerates and approaches death.
second, normal cell telomeres are shorter.
cell division causes the telomeres to be shorter, split once, and shorten a little, just like a worn iron, and when only one residue is worn, the cells are close to aging.
cells divide their telomeres once with the loss of DNA of about 30 to 200 bp (base pairs).
third, the study found that there is an enzyme in the cell, which synthesizes telomeres.
telomere replication cannot be catalyzed by a classic DNA polymerase, but by a special reverse transcriptase, telomerase.
cannot detect telomerase in normal human cells.
some benign lesions cells, in vitro cultured fibroblasts also can not measure telomerase activity.
but this enzyme is positive in reproductive cells, testicles, ovaries, placenta, and fetal cells.
remarkable discovery is that malignant tumor cells have high activity of telomerase, telomerase-positive tumors include carnage cancer, lymphoma, acute leukemia, breast cancer, colon cancer, lung cancer and so on.
, high-level telomeraseendoenzyme as a target for tumor treatment, is one of the hot spots of current concern.
other life-span-related genes are also being discovered in a similar way to telomeres.
scientists hope not only to find all the life clocks in the human body, but also to find a way to dial the clock.
at present, many planttes telomerase has been extracted, many countries are engaged in research on related topics.
argue that even if a drug that protects telomeres from degradation in division is invented, the significance of life evergreens is debatable, because the acceptance of an elderly person's body after being implanted into a young telomere is still a question.
, with the results of "Discovering How Telomeres and Telomerase Protect Chromosomes," has solved the mysteries of human aging and serious diseases such as cancer (Elizabeth Blackburn of the University of California, San Francisco, Usain, And Sauerger, Johns Hopkins School of Medicine in Baltimore, USA; and Jack Szastak of Harvard Medical School in the United States).
) won the 2009 Nobel Prize in Physiology or Medicine.
Source: Decoding Medicine, Sohu.com.