Finding MyoD and lessons learned along the way.

Semin Cell Dev Biol

Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 240 Longwood Ave., Boston, MA, 02115, United States. Electronic address:

Published: December 2017

In 1987, Robert Davis, Hal Weintraub and I reported the identification of MyoD, a transcription factor that could reprogram fibroblasts into skeletal muscle cells. In this recollection, I both summarize the prior work of Helen Blau, Woody Wright, Peter Jones and Charlie Emerson that inspired my entry into this field, and the subsequent events that led to finding MyoD. Lastly, I highlight some of the principles in developmental biology that have emerged during the past 30 years, which are particularly relevant to skeletal muscle biology.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5723223PMC
http://dx.doi.org/10.1016/j.semcdb.2017.10.021DOI Listing

Publication Analysis

Top Keywords

finding myod
8
skeletal muscle
8
myod lessons
4
lessons learned
4
learned 1987
4
1987 robert
4
robert davis
4
davis hal
4
hal weintraub
4
weintraub reported
4

Similar Publications

The aim of this study was to evaluate the effectiveness of an aquatic progressive resistance exercise (APRE) and PBM (associated or not) on morphology of skeletal muscle and biochemical markers using an experimental model of knee osteoarthritis (OA). Fifty male Wistar rats were randomly distributed into 5 groups: control group (CG); OA control (OAC); OA submitted to APRE (OAE); OA submitted to PBM (OAL); OA submitted to APRE and PBM (OAEL). Trained rats performed a water-jumping program carrying a load equivalent to 50-80% of their body mass strapped to their chest.

View Article and Find Full Text PDF

An actin-binding protein, known as Calponin 3 (CNN3), modulates the remodeling of the actin cytoskeleton, a fundamental process for the maintenance of skeletal muscle homeostasis. Although the roles of CNN3 in actin remodeling have been established, its biological significance in myoblast differentiation remains largely unknown. This study investigated the functional significance of CNN3 in myogenic differentiation, along with its effects on actin remodeling and mechanosensitive signaling in C2C12 myoblasts.

View Article and Find Full Text PDF

Background: Duchenne muscular dystrophy (DMD) is a prevalent, fatal degenerative muscle disease with no effective treatments. Mdx mouse model of DMD exhibits impaired muscle performance, oxidative stress, and dysfunctional autophagy. Although antioxidant treatments may improve the mdx phenotype, the precise molecular mechanisms remain unclear.

View Article and Find Full Text PDF

Noggin Combined With Human Dental Pulp Stem Cells to Promote Skeletal Muscle Regeneration.

Stem Cells Int

December 2024

Shanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Shanghai Stomatological Hospital and School of Stomatology, Fudan University, Shanghai, China.

Article Synopsis
  • Dental pulp stem cells (DPSCs) show promise for muscle injury repair, but their ability to differentiate into muscle cells is currently limited.
  • Treating DPSCs with Noggin, which inhibits bone morphogenetic protein (BMP) signals, enhances myogenic differentiation, increases myogenic markers, and generates satellite-like cells, improving muscle regeneration.
  • Implanting Noggin-treated DPSCs in a mouse model of muscle loss resulted in significant reductions in defect size and scar tissue, indicating that BMP/Smad signaling regulation by Noggin effectively promotes muscle repair.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!