The discovery may lead to treatments for atherosclerosis, osteoporosis, Alzheimer’s and other age-related disorders
The fountain of youth may reside in an embryonic stem cell gene named Nanog.
In a series of experiments at the University at Buffalo, the gene kicked into action dormant cellular processes that are key to preventing weak bones, clogged arteries and other telltale signs of growing old.
The findings, published June 29 in the journal Stem Cells, also show promise in counteracting premature aging disorders such as Hutchinson-Gilford progeria syndrome.
“Our research into Nanog is helping us to better understand the process of aging and ultimately how to reverse it,” says Stelios T. Andreadis, PhD, professor and chair of the Department of Chemical and Biological Engineering at the UB School of Engineering and Applied Sciences, and the study’s lead author.
Additional authors come from UB’s Department of Biomedical Engineering, a joint program between UB’s engineering school and the Jacobs School of Medicine and Biomedical Sciences at UB, and the Department of Biostatistics and Bioinformatics at Roswell Park Cancer Institute in Buffalo.
To battle aging, the human body holds a reservoir of nonspecialized cells that can regenerate organs. These cells are called adult stem cells, and they are located in every tissue of the body and respond rapidly when there is a need.
But as people age, fewer adult stem cells perform their job well, a scenario which leads to age-related disorders. Reversing the effects of aging on adult stem cells, essentially rebooting them, can help overcome this problem.
Andreadis previously showed that the capacity of adult stem cells to form muscle and generate force declines with aging. Specifically, he examined a subcategory of muscle cells called smooth muscle cells which reside in arteries, intestines and other tissues.
In the new study, Panagiotis Mistriotis, a graduate student in Andreadis’ lab and first author of the study, introduced Nanog into aged stem cells. He found that Nanog opens two key cellular pathways: Rho-associated protein kinase (ROCK) and Transforming growth factor beta (TGF-?).
In turn, this jumpstarts dormant proteins (actin) into building cytoskeletons that adult stem cells need to form muscle cells that contract. Force generated by these cells ultimately helps restore the regenerative properties that adult stem cells lose due to aging.
“Not only does Nanog have the capacity to delay aging, it has the potential in some cases to reverse it,” says Andreadis, noting that the embryonic stem cell gene worked in three different models of aging: cells isolated from aged donors, cells aged in culture (see below), and cells isolated from patients with Hutchinson-Gilford progeria syndrome.
Additionally, the researchers showed that Nanog activated the central regulator of muscle formation, serum response factor (SRF), suggesting that the same results may be applicable for skeletal, cardiac and other muscle types.
The researchers are now focusing on identifying drugs that can replace or mimic the effects of NANOG. This will allow them to study whether aspects of aging inside the body can also be reversed. This could have implications in an array of illnesses, everything from atherosclerosis and osteoporosis to Alzheimer’s disease.
The Latest on: Nanog
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The Latest on: Nanog
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Co-authored by Joao Damas, senior researcher at APNIC Labs and Geoff Huston, Chief Scientist at APNIC. At NANOG 79 earlier this month Craig Labowitz from Nokia Deepfield presented on the impact on the ...
- p53 destabilizing protein skews asymmetric division and enhances NOTCH activation to direct self-renewal of TICson June 17, 2020 at 2:09 am
TBC1D15–NOTCH1 interaction activated and stabilized NOTCH1 which upregulated transcription of NANOG essential for TIC expansion. TBC1D15 activated three novel oncogenic pathways to promote self ...
- NTT Communications Renews Long-Standing Support to NANOG Communityon June 16, 2020 at 1:24 am
Before it's here, it's on the Bloomberg Terminal.
- Enrichment of the Embryonic Stem Cell Reprogramming Factors Oct4, Nanog, Myc, and Sox2 in Benign and Malignant Vascular Tumorson June 15, 2020 at 5:00 pm
Thus, in this study we used immunohistochemical analysis to examine the expression of the stem cell reprogramming factors Oct4, Sox2, Nanog, Myc, and Klf4 in 71 diverse benign and malignant ...
- Enrichment of the Embryonic Stem Cell Reprogramming Factors Oct4, Nanog, Myc, and Sox2 in Benign and Malignant Vascular Tumorson June 12, 2020 at 5:00 pm
Background: The "stem cell theory of cancer" states that a subpopulation of cells with stem cell-like properties plays a central role in the formation, sustainment, spread, and drug resistant ...
- The IP Picture for iPS Cellson June 9, 2020 at 5:00 pm
or with Nanog and Lin28 in human somatic cells. Numerous reports since then have expanded upon these seminal findings, using normal and diseased somatic cells as a starting source. Not surprisingly, ...
- ZSCAN4 facilitates chromatin remodeling and promotes the cancer stem cell phenotypeon June 6, 2020 at 5:00 pm
Our data show that ZSCAN4 leads to a functional histone 3 hyperacetylation at the promoters of OCT3/4 and NANOG, leading to an upregulation of CSC factors. Consistently, ZSCAN4 depletion leads to ...
- A Genetic Weapon in the War on Agingon June 4, 2020 at 5:00 pm
Could the fountain of youth be tucked inside a gene? In a recent study, an embryonic gene called Nanog rebooted the activity of adult stem cells, which help to regenerate tissues and organs. Under ...
- IX53 Inverted Microscope from Olympus Life Science Solutionson August 4, 2017 at 5:16 am
iPS-cell expressing Nanog reporter (GFP) Image data courtesy of: Tomonobu Watanabe, Ph.D. Laboratory for Comprehensive Bioimaging, RIKEN Quantitative Biology Center iPS-cell expressing Nanog ...
- Institute for Cellular and Molecular Biologyon April 19, 2017 at 10:54 pm
(2014). The Bright/Arid3a transcription factor provides a singular barrier to somatic cell reprogramming though direct repression of Oct4, Sox2 and Nanog. Cell Stem Cell Reports. 2(1):26-35. Ippolito ...
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