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Editor’s note iNature is China’s largest academic official account.
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
In the process of iNature virus infection, the expression of chemokines in epithelial cells is critical to the tissue inflammatory response mediated by neutrophils
.
Long-noncoding RNA (lncRNA) and RNA-binding protein (RNA-binding protein, RBP) can regulate gene expression, but whether lncRNA and RBP are involved in the regulation of epithelial chemokine expression is still lacking
.
On October 5, 2021, the team of Academician Cao Xuetao (Zhejiang University is the first unit) published a research paper entitled "Cis-acting lnc-Cxcl2 restrains neutrophil-mediated lung inflammation by inhibiting epithelial cell CXCL2 expression in virus infection" in PNAS online The non-coding RNA-lnc-Cxcl2 found in this study inhibits the expression of Cxcl2 in lung epithelial cells during the viral infection process, inhibits neutrophil-mediated lung tissue inflammation, in order to control lung tissue inflammatory damage and increase viral infections, etc.
The therapeutic effect of inflammatory diseases provides a new theoretical basis and drug development direction
.
Chemokines produced by epithelial cells are important for the recruitment of neutrophils during viral infection, and their proper regulation is essential for suppressing inflammation and reducing subsequent tissue damage
.
The epithelial cell expression of long non-coding RNA (lncRNA), RNA binding protein, and their functional interaction during viral infection and inflammation remains to be fully understood
.
The expression of lnc-Cxcl2 increases significantly during the virus infection process, which can selectively inhibit the expression of Cxcl2 in lung epithelial cells, thereby reducing the infiltration of neutrophils in the lung tissue of influenza virus-infected mice and the degree of inflammatory damage in the lung tissue
.
The study found that lnc-Cxcl2 mainly binds to the promoter region of the Cxcl2 gene and ribonucleoprotein La to inhibit the openness of the promoter region of the Cxcl2 gene and play a role in inhibiting the transcription of the Cxcl2 gene
.
The results of this study clarified the important role of epithelial cells and chemokines in pulmonary infectious diseases
.
The production of chemokines and the inflammatory response caused by the infiltration of neutrophils are the main causes of body damage and even fatalities caused by virus infection
.
In the global epidemic of new coronavirus pneumonia (COVID-19) that occurred in the past two years, it has been found that the increased levels of multiple cytokines, including chemokines, are closely related to the prognosis and mortality of the disease.
.
In addition, the ratio of neutrophils to lymphocytes in critically ill patients is significantly increased, and tissue damage caused by excessive reactive oxygen species produced by neutrophils is also an important factor in determining the severity of the disease, indicating that the expression and expression of chemokines are precisely regulated.
The migration of neutrophils plays an important role in the control of viral infectious diseases
.
As the body's first barrier and line of defense against pathogen invasion, epithelial cells express a variety of pathogen-specific receptors and are the main site of infection and inflammation
.
Especially in the respiratory tract, the dysregulation of the function of epithelial cells to produce chemokines is an important cause of pulmonary inflammation and a variety of lung diseases.
Therefore, in-depth study of the expression of chemokines in epithelial cells and their regulatory mechanisms are important for preventing tissues.
The inflammation damage is very necessary
.
In recent years, there have been reports in the literature that the lncRNA transcribed in the vicinity of the gene can cis-regulate the expression of the gene.
In the process of virus infection of lung epithelial cells, lnc-Cxcl2 is transcribed and expressed in the Cxcl2 gene region, and the expression of lnc-Cxcl2 can be cis- The formula combines the promoter region of Cxcl2 gene and regulates the degree of chromatin opening, and feedback inhibits the transcription of Cxcl2 in lung epithelial cells.
This provides a new theoretical basis for studying the relationship between lncRNA and neighboring coding mRNA
.
lnc-Cxcl2 can bind to a variety of protein molecules in the nucleus, including ribonucleoproteins involved in RNA splicing, such as hnRNP family proteins and DDX family proteins
.
However, through functional screening, only ribonucleoprotein La can participate in the regulation of Cxcl2 expression
.
Previous studies have found that La protein mainly binds to the transcription products of RNA polymerase III such as tRNA and participates in the post-transcriptional processing of these RNAs
.
In the process of virus infection of lung epithelial cells, La can bind to lnc-Cxcl2 through its RRM2 domain, and participate in lnc-Cxcl2 mediated transcriptional regulation of Cxcl2 gene
.
Consistent with this result, after specifically knocking out the expression of La in the mouse cerebral cortex neurons, the expression of some mRNAs in the cerebral cortex, including immune-related genes Ccl6, Ccl9, etc.
, also increased significantly, indicating that La is indeed also It can participate in the regulation of gene transcription mediated by RNA polymerase II
.
In addition, lnc-CXCL2-4-1 is also expressed downstream of the human CXCL2 gene.
During the virus infection of human lung epithelial cells, the expression of lnc-CXCL2-4-1 increases significantly, but it is different from the findings in mouse lung epithelial cells Human lnc-CXCL2-4-1 can regulate the expression of multiple immune genes including chemokines by binding to La, suggesting that lncRNA may have different expression and mode of action in different species
.
The results of this study provide in-depth understanding of the important functions of epithelial cells and chemokines in the inflammatory response, clarify the interaction mechanism between non-coding RNA and RNA-binding protein, and provide more theories for the prevention, diagnosis and treatment of viral infectious diseases Foundation
.
Reference message: https://
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
In the process of iNature virus infection, the expression of chemokines in epithelial cells is critical to the tissue inflammatory response mediated by neutrophils
.
Long-noncoding RNA (lncRNA) and RNA-binding protein (RNA-binding protein, RBP) can regulate gene expression, but whether lncRNA and RBP are involved in the regulation of epithelial chemokine expression is still lacking
.
On October 5, 2021, the team of Academician Cao Xuetao (Zhejiang University is the first unit) published a research paper entitled "Cis-acting lnc-Cxcl2 restrains neutrophil-mediated lung inflammation by inhibiting epithelial cell CXCL2 expression in virus infection" in PNAS online The non-coding RNA-lnc-Cxcl2 found in this study inhibits the expression of Cxcl2 in lung epithelial cells during the viral infection process, inhibits neutrophil-mediated lung tissue inflammation, in order to control lung tissue inflammatory damage and increase viral infections, etc.
The therapeutic effect of inflammatory diseases provides a new theoretical basis and drug development direction
.
Chemokines produced by epithelial cells are important for the recruitment of neutrophils during viral infection, and their proper regulation is essential for suppressing inflammation and reducing subsequent tissue damage
.
The epithelial cell expression of long non-coding RNA (lncRNA), RNA binding protein, and their functional interaction during viral infection and inflammation remains to be fully understood
.
The expression of lnc-Cxcl2 increases significantly during the virus infection process, which can selectively inhibit the expression of Cxcl2 in lung epithelial cells, thereby reducing the infiltration of neutrophils in the lung tissue of influenza virus-infected mice and the degree of inflammatory damage in the lung tissue
.
The study found that lnc-Cxcl2 mainly binds to the promoter region of the Cxcl2 gene and ribonucleoprotein La to inhibit the openness of the promoter region of the Cxcl2 gene and play a role in inhibiting the transcription of the Cxcl2 gene
.
The results of this study clarified the important role of epithelial cells and chemokines in pulmonary infectious diseases
.
The production of chemokines and the inflammatory response caused by the infiltration of neutrophils are the main causes of body damage and even fatalities caused by virus infection
.
In the global epidemic of new coronavirus pneumonia (COVID-19) that occurred in the past two years, it has been found that the increased levels of multiple cytokines, including chemokines, are closely related to the prognosis and mortality of the disease.
.
In addition, the ratio of neutrophils to lymphocytes in critically ill patients is significantly increased, and tissue damage caused by excessive reactive oxygen species produced by neutrophils is also an important factor in determining the severity of the disease, indicating that the expression and expression of chemokines are precisely regulated.
The migration of neutrophils plays an important role in the control of viral infectious diseases
.
As the body's first barrier and line of defense against pathogen invasion, epithelial cells express a variety of pathogen-specific receptors and are the main site of infection and inflammation
.
Especially in the respiratory tract, the dysregulation of the function of epithelial cells to produce chemokines is an important cause of pulmonary inflammation and a variety of lung diseases.
Therefore, in-depth study of the expression of chemokines in epithelial cells and their regulatory mechanisms are important for preventing tissues.
The inflammation damage is very necessary
.
In recent years, there have been reports in the literature that the lncRNA transcribed in the vicinity of the gene can cis-regulate the expression of the gene.
In the process of virus infection of lung epithelial cells, lnc-Cxcl2 is transcribed and expressed in the Cxcl2 gene region, and the expression of lnc-Cxcl2 can be cis- The formula combines the promoter region of Cxcl2 gene and regulates the degree of chromatin opening, and feedback inhibits the transcription of Cxcl2 in lung epithelial cells.
This provides a new theoretical basis for studying the relationship between lncRNA and neighboring coding mRNA
.
lnc-Cxcl2 can bind to a variety of protein molecules in the nucleus, including ribonucleoproteins involved in RNA splicing, such as hnRNP family proteins and DDX family proteins
.
However, through functional screening, only ribonucleoprotein La can participate in the regulation of Cxcl2 expression
.
Previous studies have found that La protein mainly binds to the transcription products of RNA polymerase III such as tRNA and participates in the post-transcriptional processing of these RNAs
.
In the process of virus infection of lung epithelial cells, La can bind to lnc-Cxcl2 through its RRM2 domain, and participate in lnc-Cxcl2 mediated transcriptional regulation of Cxcl2 gene
.
Consistent with this result, after specifically knocking out the expression of La in the mouse cerebral cortex neurons, the expression of some mRNAs in the cerebral cortex, including immune-related genes Ccl6, Ccl9, etc.
, also increased significantly, indicating that La is indeed also It can participate in the regulation of gene transcription mediated by RNA polymerase II
.
In addition, lnc-CXCL2-4-1 is also expressed downstream of the human CXCL2 gene.
During the virus infection of human lung epithelial cells, the expression of lnc-CXCL2-4-1 increases significantly, but it is different from the findings in mouse lung epithelial cells Human lnc-CXCL2-4-1 can regulate the expression of multiple immune genes including chemokines by binding to La, suggesting that lncRNA may have different expression and mode of action in different species
.
The results of this study provide in-depth understanding of the important functions of epithelial cells and chemokines in the inflammatory response, clarify the interaction mechanism between non-coding RNA and RNA-binding protein, and provide more theories for the prevention, diagnosis and treatment of viral infectious diseases Foundation
.
Reference message: https://
