This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
LncRNA MALAT1 Forms a Negative Feedback Loop With lncRNA CRNDE in Sepsis to Regulate Lung Cell Apoptosis
Caifang Yue
Department of Critical Care Medicine, No.1 Hospital Attached to Jiamusi University, No.348 Dexiang Street, Jiamusi City, Heilongjiang Province, 154002, PR. China
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: It has been reported that lncRNAs MALAT1 and CRNDE plays opposite roles in sepsis. Therefore, they may have crosstalk. We therefore explored the potential interaction between them in sepsis.
Methods: Plasma samples were collected from both sepsis patients (n=60) and healthy controls (n=60). Expression of MALAT1 and CRNDE in plasma samples before than after treatment was determined by RT-qPCR.
Results: Overexpression of MALAT1 and CRNDE in Human Bronchial Epithelial Cells (HBEpCs) was achieved to explore the relationship between them. The roles of MALAT1 and CRNDE in regulating the apoptosis of HBEpCs were analyzed by cell apoptosis assay. MALAT1 was upregulated in sepsis, while CRNDE was downregulated in sepsis. In lung cells, overexpression of MALAT1 and CRNDE mediated the downregulation of each other. With proper treatment, MALAT1 was downregulated in sepsis and CRNDE was upregulated in sepsis. In lung cells, LPS mediated the upregulation of MALAT1 and the downregulation of CRNDE. Cell apoptosis analysis showed that MALAT1 overexpression promoted the apoptosis of lung cells induced by LPS, and the overexpression of CRNDE played an opposite role. Moreover, CRNDE overexpression attenuated the effects of MALAT1 overexpression. Conclusion: MALAT1 may form a negative feedback loop with CRNDE in sepsis to regulate lung cell apoptosis.
Keywords
MALAT1, CRNDE, Human Bronchial Epithelial Cells, apoptosis
Figure 1
Figure 2
Figure 3
Figure 4
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 25 Sep, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Neurobiology of Disease
Learn more about our company.
This is a preprint. It has not completed peer review.
Research
LncRNA MALAT1 Forms a Negative Feedback Loop With lncRNA CRNDE in Sepsis to Regulate Lung Cell Apoptosis
Caifang Yue
Department of Critical Care Medicine, No.1 Hospital Attached to Jiamusi University, No.348 Dexiang Street, Jiamusi City, Heilongjiang Province, 154002, PR. China
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 25 Sep, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Neurobiology of Disease
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: It has been reported that lncRNAs MALAT1 and CRNDE plays opposite roles in sepsis. Therefore, they may have crosstalk. We therefore explored the potential interaction between them in sepsis.
Methods: Plasma samples were collected from both sepsis patients (n=60) and healthy controls (n=60). Expression of MALAT1 and CRNDE in plasma samples before than after treatment was determined by RT-qPCR.
Results: Overexpression of MALAT1 and CRNDE in Human Bronchial Epithelial Cells (HBEpCs) was achieved to explore the relationship between them. The roles of MALAT1 and CRNDE in regulating the apoptosis of HBEpCs were analyzed by cell apoptosis assay. MALAT1 was upregulated in sepsis, while CRNDE was downregulated in sepsis. In lung cells, overexpression of MALAT1 and CRNDE mediated the downregulation of each other. With proper treatment, MALAT1 was downregulated in sepsis and CRNDE was upregulated in sepsis. In lung cells, LPS mediated the upregulation of MALAT1 and the downregulation of CRNDE. Cell apoptosis analysis showed that MALAT1 overexpression promoted the apoptosis of lung cells induced by LPS, and the overexpression of CRNDE played an opposite role. Moreover, CRNDE overexpression attenuated the effects of MALAT1 overexpression. Conclusion: MALAT1 may form a negative feedback loop with CRNDE in sepsis to regulate lung cell apoptosis.
Figure 1
Figure 2
Figure 3
Figure 4