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Spatial Transcriptomics Analysis: Maternal Obesity Impairs Myogenic Cell Migration and Differentiation during
Yao Gao1, Md Nazmul Hossain1, Liang Zhao2
1Nutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA.
International Journal of Molecular Sciences
|September 14, 2024
Summary
Maternal obesity (MO) hinders embryonic limb muscle development by impeding myogenic cell migration and differentiation. This study reveals MO
Area of Science:
- Developmental Biology
- Reproductive Biology
- Skeletal Muscle Physiology
Background:
- Myogenic cell migration is crucial for embryonic limb muscle formation.
- Maternal obesity (MO) is known to negatively impact prenatal skeletal muscle development.
- The specific effects of MO on embryonic myogenic cell migration remain largely unexamined.
Purpose of the Study:
- To investigate the impact of maternal obesity on myogenic cell migration during embryonic limb development.
- To identify molecular pathways and genes affected by maternal obesity in migrating myogenic cells.
Main Methods:
- Utilized C57BL/6 mouse embryos at embryonic day 13.5 (E13.5).
- Employed the GeoMx DSP platform to analyze gene expression in specific regions of the embryonic limb.
- Performed Gene Ontology (GO) enrichment analysis and analyzed signaling pathways.
Main Results:
- Maternal obesity led to the down-regulation of 2224 genes in E13.5 embryonic limbs.
- GO analysis indicated that MO inhibited crucial migration-related biological processes.
- Key signaling pathways (HGF, FGF, Wnt, GTPase) and myogenic migration genes (Pax3, Gab1, Pxn, Tln2, Arpc) were suppressed in the MO group, particularly in the limb.
- Myogenic differentiation genes were also down-regulated in MO limbs.
Conclusions:
- Maternal obesity significantly impedes myogenic cell migration and differentiation in the developing embryonic limb.
- This molecular disruption provides a mechanistic explanation for impaired fetal muscle development and potential long-term muscle function deficits in offspring of obese mothers.
