Implication of basal lamina dependency in survival of Nrf2-null muscle stem cells via an antioxidative-independent mechanism
| Autor: | Lidan Zhang, Shoya Inaba, Akiyoshi Uezumi, Kazutake Tsujikawa, Yusei Takemoto, So-ichiro Fukada |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Satellite Cells Skeletal Muscle Physiology Cell Survival NF-E2-Related Factor 2 Clinical Biochemistry Cell Culture Techniques Apoptosis Biology Muscle Development digestive system environment and public health Basement Membrane 03 medical and health sciences Basal (phylogenetics) 0302 clinical medicine medicine Myocyte Animals Regeneration Muscle Skeletal Cells Cultured Cell Proliferation Mice Knockout Regeneration (biology) Skeletal muscle Cell Biology respiratory system Cell sorting Cell biology Drug Combinations Oxidative Stress 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Mice Inbred mdx Basal lamina Proteoglycans Collagen Laminin Stem cell Reactive Oxygen Species Signal Transduction |
| Zdroj: | Journal of cellular physiology. 234(2) |
| ISSN: | 1097-4652 |
| Popis: | Nuclear factor erythroid 2-related factor 2 (Nrf2) is a master regulator for the induction of antioxidative genes and plays roles in diverse cellular functions. The roles of Nrf2 in muscle regeneration have been investigated, and both important and unimportant roles of Nrf2 for muscle regeneration have been reported. Here, using aged Nrf2-null and Nrf2-dystrophic double-null mice, we showed nonsignificant phenotypes in the muscle regeneration ability of Nrf2-null mice. In contrast with these results, strikingly, almost all Nrf2-null muscle stem cells (MuSCs) isolated by fluorescence-activated cell sorting died in vitro of apoptosis and were not rescued by antioxidative reagents. Although their proliferation was still impaired, the Nrf2-null MuSCs attached to myofibers activated and divided normally, at least in the first round. To elucidate these discrepancies of MuSCs behaviors, we focused on the basal lamina, because both in vivo and single myofiber culture allow MuSCs within the basal lamina to become activated. In a basal lamina-disrupted model, Nrf2-null mice exhibited remarkable regeneration defects without increased levels of reactive oxidative species in MuSCs, suggesting that the existence of the basal lamina affects the survival of Nrf2-null MuSCs. Taken together, these results suggest that the basal lamina compensates for the loss of Nrf2, independent of the antioxidative roles of Nrf2. In addition, experimental conditions might explain the discrepant results of Nrf2-null regenerative ability. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text