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A7191 - Secreted Galectin-7 Induced Bronchial Epithelial Cell MtDNA Damage and Apoptosis
Author Block: J. Tian1, Y. S. Zhao1, M. Song2; 1Beijing Children’s Hospital, affiliated with Capital Medical University, Beijing, China, 2Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences and Comparative Medicine Center, Peking Union Medical College, Beijing, China.
Jingtian1, MingjingSong2*, Shunying Zhao1*
1Department of Respiratory Disease, Beijing Children’s Hospital affiliated to the Capital Medical University
2Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences and Comparative Medicine Center, Peking Union Medical College
Corresponding author: MingjingSong2*, Shunying Zhao1*
Address: 1*Beijing Children’s Hospital, affiliated with Capital Medical University, 56 Nan Li Shi Road, Xi Cheng District, Beijing 100045, China
2*Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences and Comparative Medicine Center, Peking Union Medical College, 5 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China
E-mail: 1*zhaoshunying2001@163.com
2*songmj@cnilas.org
Tel: +86-13-661328133; +86-10-59616314
Fax: +86-10-59610836
Abstract
Rationale
The underlying mechanisms of asthma pathogenesis remains unknown. We have found that the apoptosis of airway epithelial cells is increased in patients suffering from asthma. Transmission electron microscopy showed that swollen mitochondria, and an absence of crests in the mitochondria in the bronchial epithelial cells of galectin-7 transgenic mice compared with wide-type control. Hence, we purposed that overexpressed galectin-7 induced bronchial epithelial cell mtDNA damage, which leads to the apoptosis of airway epithelial cells.We proposed that there were genetic differences in the genome DNA in the promoter regions of galectin-7 gene between the asthmatic patients and healthy people. So, we amplified the galectin-7 promoter region (639bp) of the DNA from them respectively and found the mutations in the promoter of asthmatic patients. Taken together, these results proved that the overexpress of galectin-7 maybe due to the DNA mutations and deletion in the promoter region of galectin-7, and the overexpressed galectin-7 induced bronchial epithelial cell mtDNA damage, which leads to the apoptosis of airway epithelial cells.
Methods
Plasmid constructions
Cell culture, transient transfection and luciferase assay
Results
The promoter regions of galectin-7 gene were 639bp long. There were 20 SNP mutations from 39bp to 249bp and two deletion of the nucleotide sequence from 95bp to 129 bp and 184bp to 229bp in the sequence of asthmatic children compared with healthy participants.
The pGL3 luciferase reporter vectors was successfully constructed with the DNA sequence from asthmatic children and healthy participants respectively.
Conclusions
We proved that overexpressed galectin-7 induced bronchial epithelial cell mtDNA damage and apoptosis .