A5083805612- Hedgehog Signaling Pathway Studies
- Epigenetics and DNA Methylation
- Neurogenesis and neuroplasticity mechanisms
- Congenital Ear and Nasal Anomalies
- Congenital gastrointestinal and neural anomalies
- Genetics and Neurodevelopmental Disorders
Institut des Neurosciences Paris-Saclay
2016-2024
Université Paris-Saclay
2020-2022
CEA Paris-Saclay
2022
Commissariat à l'Énergie Atomique et aux Énergies Alternatives
2022
Centre National de la Recherche Scientifique
2016-2021
The regeneration of myelin is known to restore axonal conduction velocity after a demyelinating event. Remyelination failure in the central nervous system contributes severity and progression diseases such as multiple sclerosis. controlled by many signaling pathways, Sonic hedgehog (Shh) pathway, shown canonical activation its key effector Smoothened (Smo), which increases proliferation oligodendrocyte precursor cells via upregulation transcription factor Gli1. On other hand, inhibition Gli1...
Abstract In the adult mammalian brain, astrocytes are proposed to be major Sonic Hedgehog (Shh)-responsive cells. However, sources of Shh molecule mediating activation pathway still poorly characterized. The present work investigates distribution and phenotype cells expressing mRNA in mouse brain. Using single-molecule fluorescent situ hybridization (smfISH), we report much broader expression transcripts almost all brain regions than originally reported. We identify HuC/D + neuronal...
Astrocytes are glial cells proposed as the main Sonic hedgehog (Shh)-responsive in adult brain. Their roles mediating Shh functions still poorly understood. In hypothalamus, astrocytes support neuronal circuits implicated regulation of energy metabolism. this study, we investigated impact genetic activation signaling on hypothalamic and characterized its effects We analyzed distribution gene transcripts pathway (Ptc, Gli1, Gli2, Gli3) using single molecule fluorescence situ hybridization...
In the mature rodent brain, Sonic Hedgehog (Shh) signaling regulates stem and progenitor cell maintenance, neuronal glial circuitry brain repair. However, sources distribution of Shh mediating these effects are still poorly characterized. Here, we report in adult mouse a broad expression pattern recognized by specific monoclonal C9C5 antibody subset (11–12%) CC1+ oligodendrocytes that do not express carbonic anhydrase II. These cells also Olig2 Sox10, two oligodendrocyte lineage-specific...