Cyclin G1 Regulates the Alveolarization in Models of Bronchopulmonary Dysplasia by Inhibiting AT2 Cell Proliferation.
Ontology highlight
ABSTRACT: Disrupted neonatal lung alveologenesis often leads to bronchopulmonary dysplasia (BPD), the most common chronic lung disease in children. The inhibition of type 2 alveolar (AT2) cell proliferation plays an important role in the arrest of alveologenesis. However, the mechanism of AT2 cell proliferation retardation in BPD is still not fully elucidated. The purpose of the present study was to explore the effects of cyclin G1 (CCNG1) on AT2 cell proliferation in hyperoxia-induced lung injury in neonatal mice. Our findings revealed that hyperoxia significantly reduced the proportion of AT2 cells in the lungs of neonatal mice and coincided with an upregulation of CCNG1 expression. Notably, this upregulation of CCNG1 was accompanied by an increase in Wnt signaling. We observed colocalization of C
SUBMITTER: Xu P
PROVIDER: S-EPMC11764269 | biostudies-literature | 2025 Jan
REPOSITORIES: biostudies-literature
ACCESS DATA