DAPK1 may be a potential biomarker for arterial aneurysm in clinical treatment and activated inflammation levels in arterial aneurysm through NLRP3 inflammasome by Beclin1
Autor: | Bu-Ping Jiang, Wei Lu, Guobing Cheng, Qiang Hu, Senyan Wu, Sheng Liao, Xiaoyang Li, Jiawen Wu |
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Rok vydání: | 2021 |
Předmět: |
Adult
Male Cell signaling Pathology medicine.medical_specialty Inflammasomes Health Toxicology and Mutagenesis Cell Inflammation Toxicology Mice NLR Family Pyrin Domain-Containing 3 Protein medicine Animals Humans Protein kinase A Mice Knockout business.industry Inflammasome General Medicine Middle Aged Angiotensin II Aneurysm Mice Inbred C57BL Death-Associated Protein Kinases medicine.anatomical_structure Apoptosis Beclin-1 Female medicine.symptom business Biomarkers medicine.drug Artery |
Zdroj: | Humanexperimental toxicology. 40(12_suppl) |
ISSN: | 1477-0903 |
Popis: | Background Death-associated protein kinase (DAPK1) is one of the positive regulators of apoptosis, and it is widely involved in apoptosis induced by multiple pathways. We examined that the function of DAPK1 in Clinical treatment of arterial aneurysm and its underlying mechanisms. Arterial aneurysm is a common cerebrovascular disease with high disability and fatality rate. Objectives Male C57BL/6 mice or DAPK1−/− mice were injected with 50 mg/kg pentobarbital sodium and then were injected with angiotensin II (AngII) infusion for vivo model. hASMCs (Human artery smooth muscle cell) were treated with murine recombinant IL-6 (20 ng ml−1; Cell Signaling) for vitro model. Results DAPK1 gene, mRNA expression, and protein expression were induced in mice of arterial aneurysm. DAPK1 mRNA expression was increased and Area Under Curve was 0.9075 in patients with arterial aneurysm. Knockout of DAPK1 decreased inflammation and vascular injury in mice model of arterial aneurysm. Beclin1/NLRP3 (NACHT, LRR, and PYD domains-containing protein 3) signal pathway is a critical downstream effector of DAPK1 by TAP production. The regulation of Beclin1 participated in the effects of DAPK1 on inflammation of arterial aneurysm by ATP-dependent NLRP3 inflammasome. The regulation of NLRP3 participated in the effects of DAPK1 on inflammation of arterial aneurysm. Conclusion Collectively, our data indicated that DAPK1 may be a potential biomarker for arterial aneurysm in clinical treatment and activated inflammation levels in arterial aneurysm through NLRP3 inflammasome by Beclin1. DAPK1 might be a key pathogenic event underlying excess inflammation of arterial aneurysm. |
Databáze: | OpenAIRE |
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