Prostate Restored
Prostate Restored
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The development of highlander syndrome in human patients suggests that humans might possess the genes that enable the property of eternal youth. The actualization of eternal youth is a long-held dream, and numerous studies have been performed to elucidate the mechanisms of aging and to achieve eternal youth.
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Read More »The actualization of eternal youth is a long-held dream, and numerous studies have been performed to elucidate the mechanisms of aging and to achieve eternal youth. Consequently, recent studies have partially elucidated the process of aging and proposed several anti-aging or rejuvenation procedures; however, the studies are currently in the middle stage, and the key elements of the aging process have yet to be elucidated. The purpose of this chapter is to present an overview of the recent topics on cellular aging and rejuvenation to provide an outline of the content in this book. This chapter also complements the chapters that follow; in which researchers introduce topics related to aging and rejuvenation. Certain creatures possess the properties of eternal youth and deathlessness. These include Turritopsis (a species of small jellyfish) and planarians. Old Turritopsis starts a degeneration to transform into polyps and thereby achieves a perpetual life cycle [ 1 ]. The old cells contained in an old imago change into young cells when the imago transforms into a polyp. The polyp then starts to grow until it reaches the imago stage. As the Turritopsis can repeat this cycle forever, it can be considered to exist in a state of deathlessness. Planarians possess a special property of not growing older. They contain numerous stem cells throughout their bodies and every portion of their body can reproduce [ 2 ]. Planarians may therefore be an ageless organism. The property of agelessness is also present in humans. The case of Brooke Greenberg, an American woman who could not grow older after developing highlander syndrome, was the subject of a number of news reports in Japan a few years ago [ 3 ]. Moreover, there are several reported cases of female patients who developed highlander syndrome; however, the veracity of these reports is unclear, and the gene that causes the syndrome has not been elucidated. The development of highlander syndrome in human patients suggests that humans might possess the genes that enable the property of eternal youth. The other remarkable premature senility syndrome is Hutchinson–Gilford progeria syndrome (HGPS), which is caused by partial loss of the lamin A protein [ 22 ]. HGPS patients are normal at birth. HGPS develops at 6–18 months of age; the average life span of an HGPS patient is 13 years. Lamin A exists inside a nuclear membrane and supports the structure of the membrane. It is changed to a farnesylated version to perform nuclear translocation, and farnesylated lamin A is related to both the replication and transcription of DNA and signal transduction. The unusual farnesylated lamin A that is found in HGPS patients is called “progerin” [ 23 ]. Progerin accumulates and inhibits translocation, and the inhibition causes the aging of cells. In normal individuals, progerin gradually accumulates in the skin cells due to aging. Progerin is therefore a target of treatments to delay the aging process. Information that is important for elucidating the aging process in humans can be obtained from the genes that cause premature senility syndrome. Five types of helicases (RecQL1, BLM, WRN RecQL4/RTS, and RecQL5) that untangle DNA chains exist in humans. The change of the proteins to abnormal sequences causes premature senility syndromes [ 20 ]. Werner, Bloom, and Rothmund–Thomson syndromes are caused by abnormal structures of the WRN, BLM, and RecQL4/RT proteins, respectively. The WRN protein, which is related to the replication, restoration, transcription, and stabilization of DNA or telomeres, is remarkable. In the case of patients of Werner syndrome, the onset of symptoms occurs after patients stop growing at approximately 10 years of age. In Werner syndrome, the aging process advances much faster than in normal individuals. Patients show normal nerve and immune systems but possess unusual chromosomes. The WRN gene was expected to become a target of aging in normal individuals, because with the exception of the speed at which aging advances, the symptoms are similar to the normal aging process. However, WRN knockout mice do not show premature senility syndrome, whereas WRN and TERC knockout mice do [ 21 ]. Further investigation is necessary to improve our understanding of the relationship between WRN and the aging process. Studies using both old cells (M1 period) and young cells (Low PDL) have suggested other causes of the aging. When cell fusion occurs between a young cell and an old cell from which the nucleus has been removed, the cell division of the fused cell is inhibited. However, when old cells that were previously treated with a protein synthesis inhibitor are used, growth is not inhibited. Moreover, when the cell membrane of old cells or mRNAs of cells stopped at the Go period, respectively, are injected into younger cells, cell division stops or DNA replication is inhibited. These results suggest that some proteins, mRNAs and/or cell membranes that are present in older cells gradually accumulate with every cell division and promote the aging process. The genes corresponding to such compounds have also been screened [ 16 , 17 ]. Some genes (gas, gadd, mot1, and hic-5) have been cloned. Unfortunately, they were not the most important genes for controlling the aging process. Recently screening has been performed using RNA, and some promising genes have been identified [ 18 , 19 ]. Recent studies have suggested an interaction between mitochondrial dysfunction and telomere shortening because of the following process [ 12 , 14 , 15 ]. The shortening of telomeres causes the activation of the p53 protein, the activation of which inhibits the activities of PGC-1α and β, which induce the activation of mitochondria. This inhibition finally causes a decrease in many important mitochondrial activities and the progression of the aging process. On the contrary, an increase in the level of active oxygen species due to mitochondrial dysfunction often causes the oxidation of telomeres; the numerous guanine repeats on telomeres cause them to react easily with oxygen. In telomere DNA, oxidation disturbs the combination of TRF2 with telomere DNAs and the normal T-rope structure, which is the first signal that cell division cannot proceed. Thus, under high concentrations oxygen, the telomeres in human cells are rapidly shortened and cell growth is inhibited.
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Read More »Mitochondria also have a role in the aging process [ 11 , 12 ]. Mitochondria produce ATP using the electron transport chain pathway where reactive oxygen species (hydrogen peroxide, hydroxyl radical and hydroperoxyl radical) are produced. Reactive oxygen species are often leaked through the mitochondrial inner membrane, damage DNA, proteins, and lipids. It has been confirmed by the experiments with nematodes [ 13 ] that reactive oxygen species promote aging. For instance, the mutation of the mev-1 gene in nematodes was found to result in a shorter life span, because the gene disruption caused a defect in the electron transport chain and an increase in the level of reactive oxygen species. Conversely, a mutation of the age-1 gene in nematodes caused the enhancement of catalase activity which degraded hydrogen peroxide and resulted in a prolonged life span. The pathway from telomere shortening to the cessation of cell division has also been elucidated [ 7 ]. A telomere is formed by both double-stranded DNA, which is made by repeated sequences (“TTAGGG” in the mammals), and single-strand DNA (G-tail) of similar sequences that exist at the terminal portion. A telomere has to construct the T-rope structure to avoid degradation by DNA degrading enzymes. This structure gives the first signal to initiate the progression of cell division. The shortening of telomeres causes the obstruction of the T-rope structure and signals certain proteins, including telomeric repeat-binding factor 2 (TRF2), AMP kinase and histone deacetylase, to delay or stop cell division. The detection of the signal by AMP kinase activates p53 and/or p21 proteins and inhibits the work of the cyclin-dependent kinase (CDK) complex. Finally, the inhibition of the CDK complex causes cell division to stop at the Go period, because CDK is a control switch that determines whether cell division should be promoted. RNA primer is degraded and exchanged to DNA with DNA polymerase I followed by replication with DNA polymerase III. However, the RNA primer present at the terminal portion of telomeres cannot be exchanged to DNA. As a result, approximately 100 sequence bases are shortened in every replication. The shortening of telomeres acts as a fuse and decides the limit of cell division. The length limit (M1 period) in human fibroblasts is approximately 5 kb, but most cells in elderly humans do not reach the M1 period [ 9 ]. Moreover, mouse telomeres are of sufficient length, even in old mice, due to the expression of telomerase. Otherwise, cells in the M1 period can continue to undergo cell division by transforming with T antigen [ 10 ]. In such cells, the shortening of telomeres continues, and cell division is finally stopped again by the fusion of mutual terminals (the M2 period) or apoptosis. Telomeres are therefore protected from further shortening by a safe limit (the M1 period). Cultured human cells become older through repeated cell division. Cells eventually stop dividing when they reach the critical passage number, the Hayflick limit [ 4 ]. Blackburn [ 5 ] and Greider discovered that the telomeres function as a clock by marking the passage of time in cells. The molecular mechanism of aging, which is described below [ 6 – 8 ], was elucidated through this discovery.
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