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Archive - Feb 2, 2017


“In Vivo” Reprogramming Induces Signs of Telomere Rejuvenation

During the “in vivo” reprogramming process, cellular telomeres are extended due to an increase in endogenous telomerase. This is the main conclusion of a paper published online on February 2, 2017 in Stem Cell Reports by a team from the Spanish National Cancer Research Centre (CNIO). The open-access article is titled “Common Telomere Changes During In Vivo Reprogramming and Early Stages of Tumorigenesis.” The team’s observations show, for the first time, that the reprogramming of living tissue results in telomerase activation and telomere elongation; thus reversing one of the hallmarks of aging: i.e., the presence of short telomeres. "We have found that when you induce cell de-differentiation in an adult organism, the telomeres become longer, which is consistent with cellular rejuvenation,” explains Dr. María A. Blasco, head of the CNIO Telomeres and Telomerase Group and leader of this research. This lengthening of the telomeres is an unequivocal sign of cell rejuvenation, which has been quantified for the first time here in a living organism. Dr. Blasco and her colleagues have worked with the so-called "reprogrammable mice" - created by Dr. Manuel Serrano, also a CNIO researcher, whose group is also involved in this project. Broadly speaking, the cells of these transgenic animals carry the four Yamanaka factors (OSKM) whose expression is turned on when an antibiotic is administered. In doing so, the cells regress to an embryonic-like state, a condition known as known as pluripotency. In light of the importance of telomeres in tissue regeneration, aging, and cancer, the authors decided to analyze the changes that occur in these protective structures of the chromosomes during the “in vivo” reprogramming process, which leads to de-differentiation of the tissues.

University of Wisconsin Scientists Identify Two Proteins That May Aid Bone Growth to Restore Bone Tissue Lost to Disease or Injury

The prospect of regenerating bone lost to cancer or trauma is a step closer to the clinic as University of Wisconsin (UW)-Madison scientists have identified two proteins found in bone marrow as key regulators of the master cells responsible for making new bone. In a study published online on February 2, 2017 in the journal Stem Cell Reports, a team of UW-Madison scientists reports that the proteins govern the activity of mesenchymal stem cells -- precursor cells found in marrow that make bone and cartilage. The discovery opens the door to devising implants seeded with cells that can replace bone tissue lost to disease or injury. "These are pretty interesting molecules," explains Dr. Wan-Ju Li, a UW-Madison Professor of Orthopedics and Biomedical Engineering, of the bone marrow proteins lipocalin-2 and prolactin. "We found that they are critical in regulating the fate of mesenchymal stem cells." The open-access article is titled “Identification of Bone Marrow-Derived Soluble Factors Regulating Human Mesenchymal Stem Cells for Bone Regeneration.” Dr. Li and Dr. Tsung-Lin Tsai, a UW-Madison postdoctoral researcher, scoured donated human bone marrow using high-throughput protein arrays to identify proteins of interest and then determined the activity of mesenchymal stem cells exposed to the proteins in culture. A goal of the study, says Dr. Li, is to better understand the bone marrow niche where mesenchymal stem cells reside in the body so that researchers can improve culture conditions for growing the cells in the lab and for therapy. The Wisconsin researchers found that exposing mesenchymal stem cells to a combination of lipocalin-2 and prolactin in culture reduces and slows senescence, the natural process that robs cells of their power to divide and grow. Dr.

Landmark Genetic Study of Height in Humans

Variation in human height is partly due to diet and environment, but an estimated 80% of the variation is believed to be genetic. Combining genome-wide association methods and an unmatched dataset of more than 700,000 participants, a recent study narrowed down the set of candidate changes to 83 variants, some of which altering height by more than 2 cm (~0.8 inches). Over 300 scientists from across the globe, including researchers from the SIB Swiss Institute of Bioinformatics - among whom are group leaders Dr. Zoltán Kutalik, co-Principal Investigator of the paper, and Dr. Sven Bergmann - have combined their effort to study what makes us shorter or taller. In the context of precision medicine, the results also bring hope to understand the genetic basis of complex diseases such as diabetes or schizophrenia. The study was published online on February 1, 2017 in Nature. The article is titled “Rare and Low-Frequency Coding Variants Alter Human Adult Height.” Who will suffer from a heart attack before 55 years old despite a healthy lifestyle? Or which children will develop leukemia, and how will they respond to treatments? These and similar questions motivate precision medicine, that is an approach aiming to combine multiple types of data, including genetic information, to predict disease development and severity, and response to therapies. Adult height is mostly determined by the information encoded in our DNA: children from tall parents tend to be taller. “The idea is that if we can understand the genetics of a simple human trait like height, we could then apply this knowledge to develop tools to predict complex human diseases such as diabetes or schizophrenia,” explains Dr.