ArticleImmunology2018
Low-molecular-mass hyaluronan induces pulmonary inflammation by up-regulation of Mcl-1 to inhibit neutrophil apoptosis via PI3K/Akt1 pathway.
Article in Immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Effects of Emodin on Lung Inflammation and Intestinal Microbes in Chronic Obstructive Pulmonary Disease.Journal of inflammation research · 2025Article
- Hyaluronic acid impacts hematological endpoints and spleen histological features in African catfish (Clarias gariepinus).BMC veterinary research · 2024Article
- Discovery of potential quality markers of Fritillariae thunbergii bulbus in pneumonia by combining UPLC-QTOF-MS, network pharmacology, and molecular docking.Molecular diversity · 2024Article
- Network Pharmacology Followed by Experimental Validation to Explore the Mechanism of Stigmasterol in Sangbaipi Decoction Regulating PI3K/Akt Signaling to Alleviate Acute Exacerbation of Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2024Article
- Hyaluronan promotes intracellular ROS production and apoptosis in TNFα-stimulated neutrophils.Frontiers in immunology · 2023Article
- Lung Hyaluronasome: Involvement of Low Molecular Weight Ha (Lmw-Ha) in Innate Immunity.Biomolecules · 2022Review
- Network Pharmacology and Experimental Validation to Explore the Mechanism of Qing-Jin-Hua-Tan-Decoction Against Acute Lung Injury.Frontiers in pharmacology · 2022Article
- Mechanism of protective effect of xuan-bai-cheng-qi decoction on LPS-induced acute lung injury based on an integrated network pharmacology and RNA-sequencing approach.Respiratory research · 2021Article
- Sialic acid-binding immunoglobulin-like lectin 9 as a potential therapeutic target for chronic obstructive pulmonary disease.Chinese medical journal · 2021Article
- Gender Differences in Low-Molecular-Mass-Induced Acute Lung Inflammation in Mice.International journal of molecular sciences · 2021Article
- Comprehensive Analysis of Common Different Gene Expression Signatures in the Neutrophils of Sepsis.BioMed research international · 2021Article
- Effects of Endotoxin Tolerance Induced by Porphyromonas gingivalis Lipopolysaccharide on Inflammatory Responses in Neutrophils.Inflammation · 2020Article
- Identification of the key differentially expressed genes and pathways involved in neutrophilia.Innate immunity · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although low-molecular-mass hyaluronan (LMMHA) has been implicated in pulmonary inflammatory diseases, the signalling pathway of LMMHA (200 000 molecular weight) that initiates the inflammatory response in lung is still unknown. In this study, we evaluate the role of phosphoinositide 3-kinase (PI3K) and its downstream signalling pathway in LMMHA-induced lung inflammatory responses. Our results indicate that pharmacological inhibition of PI3K or genetic deletion of Akt1 enhances neutrophil apoptosis, attenuates neutrophil influx into the lungs of mice and diminishes the expression of pro-inflammatory factors such as interleukin-6, keratinocyte cell-derived chemokine and pro-matrix metalloproteinase-9 in bronchoalveolar lavage fluid after intratracheal administration of LMMHA. More importantly, we found that PI3K/Akt1 participates in LMMHA-induced inflammatory responses, which are mainly mediated by the myeloid leukaemia cell differentiation protein (Mcl-1). Our study suggests that LMMHA induced significantly increased levels of inflammatory factors in bronchoalveolar lavage fluid and activation of the PI3K/Akt1 pathway, which up-regulates the expression of the anti-apoptotic protein Mcl-1 and inhibits the activation of caspase-3, thereby suppressing neutrophil apoptosis to trigger lung inflammation. These findings reveal a novel molecular mechanism underlying sterile inflammation and provides a new potential target for the treatment of pulmonary disease.
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