Objective: To explore the mechanism by which KIAA1456 acts on alveolar epithelial cells through lentiviral transfection.
Materials And Methods: After constructing a KIAA1456 gene vector, 293T cells were co-transfected with lentiviral vectors and after incubation cells were examined by fluorescence microscopy. CCL-149 cells were transfected with LV-KIAA1456 and were examined by fluorescence microscopy. The proliferation capacity of transfected CCL-149 cells was evaluated using flow cytometry. The effect of KIAA1456 overexpression on CCL-149 cells proliferation was studied using the CCK-8 method.
Results: The expression level of KIAA1456 in the LV- KIAA1456 group was significantly higher compared with the LV-Con group and the blank group. Compared with the LV-Con and the blank groups, the proportion of responding cells in G2/M phase showed statistically significant differences. Viable cells had adarker color and higher OD value measured by ELISA. Compared with the control and the blank groups, the growth and proliferation in the CCL-149 transfection group were significantly slower.
Conclusions: KIAA1456 gene inhibited the proliferation of CCL-149 cells by negative regulation of the G2/M cell cycle. We suggest that it can be used as a specific target for the treatment of alveolar epithelium.
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Protein Expr Purif
March 2021
School of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing, 400054, PR China. Electronic address:
While the discovery of antibiotics has made a huge contribution to medicine, bacteria that are resistant to many antibiotics pose new challenges to medicine. Antimicrobial peptides (AMPs), a new kind of antibiotics, have attracted people's attention because they are not prone to drug resistance. In this study, glutathione transferase (GST) was used as a fusion partner to recombinantly expressed rat lung surfactant protein B precursor (proSP-B) in E.
View Article and Find Full Text PDFSci Rep
November 2017
Emergency Center, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuchang, Wuhan, Hubei, 430071, P. R. China.
Recent evidence indicates that the epithelial to mesenchymal transition (EMT) in primary alveolar cells (AECs) plays an important role in idiopathic pulmonary fibrosis (IPF). In vivo models have suggested that thalidomide (THL) has anti-fibrotic effects against pulmonary fibrosis, but the underlying mechanism of this effect is not clear. This study investigated whether THL regulates alveolar EMT and the possible mechanisms underlying this process.
View Article and Find Full Text PDFEur Rev Med Pharmacol Sci
February 2017
Department of Respiratory Medicine, the First Affiliated Hospital of Soochow University Suzhou, Jiangsu, P.R. China.
Objective: To explore the mechanism by which KIAA1456 acts on alveolar epithelial cells through lentiviral transfection.
Materials And Methods: After constructing a KIAA1456 gene vector, 293T cells were co-transfected with lentiviral vectors and after incubation cells were examined by fluorescence microscopy. CCL-149 cells were transfected with LV-KIAA1456 and were examined by fluorescence microscopy.
Eur Rev Med Pharmacol Sci
June 2016
State Key Laboratory of Trauma, Burns and Combined Injury, Department 4, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing, China.
Objective: Surfactant protein B (SP-B) is the only essential protein component of lung surfactant, the relationship between localization and function is very close. The localization of rat SP-B and influences of lipopolysaccharide (LPS) on it were investigated.
Materials And Methods: The localization of SP-B protein in lung tissue was detected by immunofluorescence after challenged with intratracheal instillation of LPS.
Chin Med J (Engl)
April 2015
Department of Respiratory Medicine, First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510632, China. Email:
Background: Found in inflammatory zone 1 (FIZZ1) protein increased in pulmonary epithelial cells and in limited amounts of other lung cells. FIZZ1 increased in murine model of smoke induced chronic obstructive pulmonary disease. However, the direct role of FIZZ1 produced by pulmonary epithelium stimulated with cigarette smoke extraction has not been determined.
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