ArticleInflammation2022
Calcitonin Gene-Related Peptide Attenuates Hyperoxia-Induced Oxidative Damage in Alveolar Epithelial Type II Cells Through Regulating Viability and Transdifferentiation.
Article in Inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Bronchopulmonary dysplasia and prematurity-associated lung disease: emerging therapies to improve lifelong respiratory outcomes.European journal of pediatrics · 2026Review
- αCGRP Activates PI3K/Akt to Exert Antioxidant Effects and Improve the Survival Rate and Functional Status of Cortical Neurons.Molecular neurobiology · 2026Article
- Mitochondrial programmed cell death in bronchopulmonary dysplasia: mechanisms and therapeutic targets.Frontiers in physiology · 2026Review
- MIF/CD74 axis regulates alveolar epithelial type II cell apoptosis, autophagy, and transdifferentiation in bronchopulmonary dysplasia via the TGFβ1/SMAD4 pathway.Respiratory research · 2025Article
- Activation of LXR signaling ameliorates apoptosis of alveolar epithelial cells in Bronchopulmonary dysplasia.Respiratory research · 2024Article
- AMPK/MTOR/TP53 Signaling Pathway Regulation by Calcitonin Gene-Related Peptide Reduces Oxygen-Induced Lung Damage in Neonatal Rats through Autophagy Promotion.Inflammation · 2024Article
- High throughput and targeted screens for prepilin peptidase inhibitors do not identify common inhibitors of eukaryotic gamma-secretase.Expert opinion on drug discovery · 2023Article
- Oxidative Stress and Inflammation in Acute and Chronic Lung Injuries.Antioxidants (Basel, Switzerland) · 2023Review
- Molecular mechanisms of cell death in bronchopulmonary dysplasia.Apoptosis : an international journal on programmed cell death · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a stem cell of alveolar epithelium, the physiological status of alveolar epithelium type II cells (AECII) after hyperoxia exposure is closely related to the occurrence of hyperoxia-induced lung injury and the restoration of normal morphological function of damaged alveolar epithelium. However, the relevant mechanisms involved are not very clear. Therefore, this study aimed to explore the effect of calcitonin gene-related peptide (CGRP) on AECII exposed to hyperoxia and its potential mechanisms. The AECII viability was detected using MTT assay. The malondialdehyde (MDA) level and superoxide dismutase (SOD) activity were detected by spectrophotometry. The transdifferentiation capacity of AECII was evaluated by flow cytometry. The expression levels of Notch1, Hes, HERP, and AECII markers were detected using immunohistochemistry and/or RT-qPCR or immunofluorescence. ELISA was used for the determination of inflammatory markers. The results showed that CGRP significantly promoted cell viability, and markedly suppressed hyperoxia-induced transdifferentiation of AECII; these biological alterations were coincided with decreased MDA level, increased SOD activity, and activated Notch signaling pathway (upregulated expression levels of Notch1, Hes, and HERP). Notably, the in vitro effects of CGRP on Notch signaling pathway were further investigated in animal model, and the HE staining results showed that CGRP reduced in vivo oxidative injury and inflammation in hyperoxia-treated AECII through the promotion of structural and functional regeneration, accompanied by elevated Notch1 expression and activated Notch signaling cascade as shown by immunohistochemistry and QPCR, respectively. Immunohistochemistry of APQ-5 and SPC indicated that CGRP reversed the transdifferentiation of AECIIs in vivo. Our current results were consistent across both in vitro and in vivo settings, and provide a new direction for the prevention and treatment of bronchopulmonary dysplasia (BPD).
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