ArticleAmerican journal of respiratory cell and molecular biology2014
Mitogen-activated protein kinase-activated protein kinase 2 mediates apoptosis during lung vascular permeability by regulating movement of cleaved caspase 3.
Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- Liposomal Amodiaquine for Localized Therapy of Non-Small Cell Lung Cancer (NSCLC).AAPS PharmSciTech · 2026Article
- Development of a preclinical model of ICU-associated sleep fragmentation and effects on pneumonia recovery in mice.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Studying the Pulmonary Endothelium in Health and Disease: An Official American Thoracic Society Workshop Report.American journal of respiratory cell and molecular biology · 2024Article
- Unlocking the protective potential of the angiotensin type 2 receptor (ATBiochemical pharmacology · 2024Article
- MK2 nonenzymatically promotes nuclear translocation of caspase-3 and resultant apoptosis.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Tumor MK2 transcript levels are associated with improved response to chemotherapy and patient survival in non-small cell lung cancer.Physiological genomics · 2023Article
- Mitogen-activated protein kinase-activated protein kinase-2 (MK2) and its role in cell survival, inflammatory signaling, and migration in promoting cancer.Molecular carcinogenesis · 2022Article
- Comparison of polynomial fitting versus single time point analysis of ECIS data for barrier assessment.Physiological reports · 2021Article
- Dexmedetomidine Protects Human Renal Tubular Epithelial HK-2 Cells against Hypoxia/Reoxygenation Injury by Inactivating Endoplasmic Reticulum Stress Pathway.Cell journal · 2021Article
- Role of Oxidative Stress in Reperfusion following Myocardial Ischemia and Its Treatments.Oxidative medicine and cellular longevity · 2021Review
- Genistein-3'-sodium sulphonate protects against lipopolysaccharide-induced lung vascular endothelial cell apoptosis and acute lung injury via BCL-2 signalling.Journal of cellular and molecular medicine · 2020Article
- A nonapoptotic endothelial barrier-protective role for caspase-3.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Recombinant Human Superoxide Dismutase andMolecules (Basel, Switzerland) · 2019Article
- The influence of isoflavone for denervation-induced muscle atrophy.European journal of nutrition · 2019Article
- Apoptosis regulation by subcellular relocation of caspases.Scientific reports · 2018Article
- Altered expression of TIAM1 in endotoxin-challenged airway epithelial cells and rodent septic models.Journal of thoracic disease · 2018Article
- XOR inhibition with febuxostat accelerates pulmonary endothelial barrier recovery and improves survival in lipopolysaccharide-induced murine sepsis.Physiological reports · 2017Article
- Flow-cytometric method for simultaneous analysis of mouse lung epithelial, endothelial, and hematopoietic lineage cells.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Glycyrrhizic Acid Prevents Sepsis-Induced Acute Lung Injury and Mortality in Rats.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2016Article
- Pivotal Role of Mitogen-Activated Protein Kinase-Activated Protein Kinase 2 in Inflammatory Pulmonary Diseases.Current protein & peptide science · 2016Review
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
Abstract
Apoptosis is a key pathologic feature in acute lung injury. Animal studies have demonstrated that pathways regulating apoptosis are necessary in the development of acute lung injury, and that activation of p38 mitogen-activated protein kinase (MAPK) is linked to the initiation of the apoptotic cascade. In this study, we assessed the role of the MAPK-activated protein kinase (MK) 2, one of p38 MAPK's immediate downstream effectors, in the development of apoptosis in an animal model of LPS-induced pulmonary vascular permeability. Our results indicate that wild-type (WT) mice exposed to LPS demonstrate increased apoptosis, as evidenced by cleavage of caspase 3 and poly (ADP-ribose) polymerase 1 and increased deoxynucleotidyl transferase-mediated dUDP nick-end labeling staining, which is accompanied by increases in markers of vascular permeability. In contrast, MK2(-/-) mice are protected from pulmonary vascular permeability and apoptosis in response to LPS. Although there was no difference in activation of caspase 3 in MK2(-/-) compared with WT mice, interestingly, cleaved caspase 3 translocated to the nucleus in WT mice while it remained in the cytosol of MK2(-/-) mice in response to LPS. In separate experiments, LPS-induced apoptosis in human lung microvascular endothelial cells was also associated with nuclear translocation of cleaved caspase 3 and apoptosis, which were both prevented by MK2 silencing. In conclusion, our data suggest that MK2 plays a critical role in the development of apoptosis and pulmonary vascular permeability, and its effects on apoptosis are in part related to its ability to regulate nuclear translocation of cleaved caspase 3.
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