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Volume 36 Issue 1 | January 2018
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Highlighted Articles

Bone Marrow Stem Cells Do Not Contribute to Endometrial Cell Lineages in Chimeric Mouse Models

Yih Rue Ong et al., STEM CELLS

The endometrium (the lining of the uterus) is one of the most regenerative tissues in the body, is central to fertility, and is prone to disease. Bone marrow stem cells have been widely reported to transdifferentiate into endometrial cells. This phenomenon was investigated in mouse models, and no evidence of bone marrow cell transdifferentiation into endometrial-specific cell types was found. It was concluded that bone marrow cells are unlikely to transdifferentiate into endometrial cells and that previous reports of this occurring involve the misidentification of immune cells. This result has important implications for the development of therapies to treat diseases of the endometrium.

A Universal Approach to Correct Various HBB Gene Mutations in Human Stem Cells for Gene Therapy of Beta-Thalassemia and Sickle Cell Disease

Liuhong Cai et al., STEM CELLS Translational Medicine

This study devised and tested the universal strategy to achieve targeted insertion of the HBB complementary DNA in exon 1 of HBB gene using CRISPR-associated protein 9 (Cas9) and two validated guide ribonucleic acids. This method is expected to allow correction of most types of HBB mutations and to restore functional HBB gene expression for treating β-thalassemia and sickle cell disease. It will likely also be applicable to developing gene therapy strategies for treating other types of recessive monogenic diseases.

Subtle Deregulation of the Wnt-Signaling Pathway Through Loss of Apc2 Reduces the Fitness of Intestinal Stem Cells

Madeleine A. Young et al., STEM CELLS

To address the importance of subtle Wnt-signaling deregulation on intestinal stem cell (ISC) function, this population of cells was analyzed within an Apc2−/− mouse model. The study shows that systemic loss of Apc2 results in an increase in the number of cells displaying nuclear β-catenin at the base of the intestinal crypt. This subsequently impacts the expression levels of several ISC markers and the fitness of ISCs as assessed by organoid formation efficiency. This work provides the first evidence that the function and fitness of ISCs can be altered by even minor misregulation of the Wnt-signaling pathway. The data highlights the importance of correct maintenance of this crucial signaling pathway in the maintenance and function of the ISC population.

Neuroprotective Effects of Human Mesenchymal Stem Cells and Platelet-Derived Growth Factor on Human Retinal Ganglion Cells

Andrew Osborne et al., STEM CELLS

Stem cell therapies that work in rodent models are frequently proposed as potential treatments for human disease. Testing of such strategies in human tissue is an important interim between preclinical and clinical studies. We demonstrated that human mesenchymal stem cells and platelet-derived growth factor provide significant protection to cells of the human retina, supporting observations seen in rodent models of optic nerve injury. This work highlights that similar, although not identical, mechanisms are responsible for retinal protection and that future stem cell-based treatments may have the potential to reduce visual deterioration.

Press Releases

Study Shows How Growth Factor Aids Stem Cells’ Ability to Regenerate Damaged Teeth

New Study May Lead to Speedy Recovery From Hip Fractures

Stem Cells May Help Improve Corneal Wound Healing


Article Scans

Video Highlights

Video abstract from Drs. Banerjee, Surendran, Bharti, Morishita, Varshney, and Pal on their recently published STEM CELLS paper entitled, "Long non-coding RNA RP11-380D23.2 drives distal-proximal patterning of the lung by regulating PITX2 expression." Read the paper here.

Video abstract from Drs. Sayed, Ospino, Himmati, Lee, Chanda, Mocarski, and Cooke on their recently published STEM CELLS paper entitled, "Retinoic Acid Inducible Gene 1 Protein (RIG1)-like Receptor Pathway is Required for Efficient Nuclear Reprogramming." Read the paper here.

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