You are hereFebruary 28, 2019
What’s the Stem Cells Buzz this Week? - MSC Homing, iPSC-MSC Misidentification, Attenuating T1D Bone Loss, and Coordinated Tissue Repair!
The Stem Cells Portal brings you a roundup of some of the new and exciting stories in the ever-changing world of stem cells, regenerative medicine, and beyond!
CREKA Improves the Targeted Homing Ability of Mesenchymal Stem Cells
A team of researchers from Fudan University, Shanghai (China) recently sought to improve mesenchymal stem cell (MSC) homing to the injured myocardium to improve therapeutic outcomes. To this end, the authors modified MSCs with a homing peptide (cysteine-arginine-glutamic acid-lysine-alanine - CREKA) that targets fibrin, which is involved in the repair process of tissue injury. Overall, this STEM CELLS article establishes their CREKA-associated approach as an efficient means to enhance homing in vitro and in vivo, highlighting the utility of active fibrin targeting in cardiac cellular therapy.
Lineage Misidentification of iPSC-derived Mesenchymal Stem Cells
Previous comparisons between bone marrow‐derived mesenchymal stem cells (BM-MSCs) and induced pluripotent stem cell (iPSC)-derived MSCs have revealed variances in trilineage differentiation potential, even though marker expression profiles display broad similarities. In a recent STEM CELLS article, researchers from the lab of Frank Barry (National University of Ireland Galway, Ireland) set out to reveal the cellular basis underlying these differences. Interestingly, Xu et al. established that while iPSC-MSCs share phenotypic traits with BM‐MSCs in terms of standard cell surface marker expression profiles, they exhibit markedly different gene expression profiles, especially in genes associated with vascular progenitor cell function.
Bone Morphogenetic Protein‐6 Attenuates Type I Diabetes-Associated Bone Loss
Patients with type 1 diabetes (T1D) often suffer from bone loss and increased risk of bone fracture, although the connecting mechanism linking hyperglycemia and bone remains unknown. Now, researchers from the lab of Wan‐Ju Li (University of Wisconsin‐Madison, USA) report that bone marrow‐derived mesenchymal stem cells (BM-MSCs) from streptozotocin‐induced diabetic mice display lower levels of bone morphogenetic protein‐6 (BMP6) and reduced osteogenic potential. However, Wang et al. also established that intraperitoneal injection of BMP6 mitigated bone loss and increased bone mineral density in diabetic mice. For all the details, see STEM CELLS Translational Medicine now!
Coordinated Tissue Repair with TGF‐β activated kinase 1
Researchers from the labs of Benjamin Levi and Yuji Mishina (University of Michigan, Ann Arbor, Michigan, USA) recently employed a model of musculoskeletal injury to demonstrate that loss of TGF‐β activated kinase 1 (TAK1) signaling reduces inappropriate tissue formation (heterotopic ossification) through reduced cellular differentiation. Employing a mouse model, Hsieh et al. then inactivated and reactivated the Tak1 gene, revealing that this can improve bony healing through the coordination of increased proliferation followed by differentiation. This approach elucidates a new paradigm in regenerative medicine in which coordination between treatment and withdrawal of treatment can augment healing. For all the juicy details, make your way to STEM CELLS now!
That’s a wrap for now! Please feel free to leave a comment and discuss the papers covered here on the Stem Cells Buzz. Happy reading!