"Longevity Protein" Research Upgrades to Primates to Provide an Important Model System for Studying Stunting Syndrome
The Institute of Biophysics of the Chinese Academy of Sciences, the Institute of Zoology, the Institute of Stem Cell and Regeneration, and the Xuanwu Hospital of the Capital Medical University, the First Affiliated Hospital of Peking University, and the University of Sun Yat-sen University have found that the "long-lived protein" SIRT6 can regulate the brains of primates. Developmental speed. This study, for the first time, combines non-human primate models, human stem cell models, and gene editing techniques to reveal key molecular switches that regulate prenatal developmental programs in primates, providing an important model for studying human prenatal stunting syndrome. The system, for the first time, reveals the vast differences in aging regulatory pathways between primates and rodents, and lays an important foundation for human development and aging mechanisms and related disease interventions. The related papers were published online on August 23 in the international authoritative academic journal Nature.
Aging is a process in which the physiological functions of the body gradually degenerate over time, and is the greatest risk factor for chronic diseases such as neurodegenerative diseases, atherosclerosis, diabetes and malignant tumors. Researcher Liu Guanghui, one of the research directors and the Institute of Biophysics of the Chinese Academy of Sciences, said that as early as 1999, it was discovered that the Sir2 gene has the effect of prolonging the lifespan of Saccharomyces cerevisiae, so it is called the "longevity gene." Later, in rodents, SIRT6, a gene homologous to Sir2, was also involved in the regulation of aging and longevity: overexpression of SIRT6 prolonged the lifespan of male mice, while knockdown of SIRT6 caused mice to show subcutaneous fat reduction. The aging phenotype, spine curvature and deformation, decreased bone density, impaired intestinal epithelium, telomere shortening, etc., and the lifespan of mice is shortened to about 1 month. It is unclear whether SIRT6 can perform similar functions in primates.
The research team of the Institute of Biophysics and the Institute of Zoology of the Chinese Academy of Sciences has been working together for 3 years to obtain the world's first cynomolgus monkey model with specific longevity gene knockout, and for the first time to achieve SIRT6 knockdown in non-human primates. except.
The team found that the accelerated aging phenotypes of SIRT6 knockout mice were significantly different, and SIRT6 knockout cynomolgus monkeys died within hours of birth. A number of analyses showed that SIRT6 knockout cynomolgus monkeys did not show an accelerated aging phenotype, but showed severe systemic developmental delay. The brain, muscle and various other organ tissues of the newborn SIRT6 knockout monkey showed obvious embryonic immature cell and molecular characteristics.
At the same time, the researchers used the human stem cell model to study the molecular mechanism and found that the lack of SIRT6 can also block the differentiation of human neural stem cells into neurons, leading to brain development retardation. (Reporter Wang Yuyu)
Source: Health News
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