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STAT1 regulates interferon-γ-induced angiotensinogen and MCP-1 expression in a bidirectional manner in primary cultured mesangial cells

STAT1 regulates interferon-γ-induced angiotensinogen and MCP-1 expression in a bidirectional manner in primary cultured mesangial cells

Objective: Intrarenal interferon-γ contributed significantly to the development of glomerular injury in which angiotensinogen and monocyte chemoattractant protein 1 levels were high. However, the exact nature of the role played by interferon-γ in regulating angiotensinogen and monocyte chemoattractant protein 1 expression has not been fully described. Therefore, the aim of this study was to investigate the role played by interferon-γ in angiotensinogen and monocyte chemoattractant protein 1 expression.


Methods: Primary cultured rat mesangial cells treated with 0-20 ng / mL interferon-γ for 2, 8 or 24 hours. angiotensinogen expression levels, monocyte chemoattractant protein 1, suppressor of cytokine signaling 1, suppressing the intracellular Janus kinase-signal transducer and activator of transcription signaling and activity of Janus kinase-signal transducer and activator of transcription pathway was evaluated by reverse transcriptase polymerase chain reaction and Western blot analysis.


Results: Interferon-γ increase the expression of angiotensinogen in mesangial cells was observed following the augmentation maximum 5 ng / mL interferon-γ at 8 hours of treatment (1.87 ± 0.05, mRNA, relative ratio). further increases reduced or no use of higher concentrations of interferon-γ. Following treatment, monocyte chemoattractant protein 1 expression is induced by a linear dose-dependent manner (6.85 ± 0.62-fold at 20 ng / mL interferon-γ at 24 hours). In addition, interferon-γ induced STAT1 phosphorylation and suppressor of cytokine signaling 1 expression with a linear dose-dependent manner.

Oppression STAT1 and suppressor of cytokine signaling 1 expression by small interference RNA angiotensinogen facilitated increased expression of interferon-γ-induced, suggesting that these two factors negatively regulate the expression of angiotensinogen. Conversely, an increase in interferon-γ-induced monocyte chemoattractant protein 1 expression was attenuated in STAT1-deficient mesangial cells, suggesting that STAT1 positively regulates monocyte chemoattractant protein 1 expression in mesangial cells.


Conclusion: These results indicate that while interferon-γ improve both angiotensinogen and monocyte chemoattractant protein 1 expression, STAT1 opponent played a role in the regulation of each of the factors in mesangial cells.

STAT1 regulates interferon-γ-induced angiotensinogen and MCP-1 expression in a bidirectional manner in primary cultured mesangial cells
STAT1 regulates interferon-γ-induced angiotensinogen and MCP-1 expression in a bidirectional manner in primary cultured mesangial cells

Interferon and virus induces novel primate-specific isoform dACE2 and not SARS-CoV-2 receptor ACE2

acute respiratory syndrome-2 coronavirus (SARS-CoV-2), which causes COVID-19, take advantage of the angiotensin-converting enzyme 2 (ACE2) to enter the target cells. ACE2 has been proposed as interferon-stimulated genes (ISG). Thus, the interferon-induced variability in the level of ACE2 expression may be important for susceptibility to COVID-19 or its results. Here, we report the discovery of a new isoform, primate-specific ACE2, which we refer to as deltaACE2 (dACE2).

We show that dACE2, but not ACE2, the ISG. In vitro, dACE2, which has 356 amino acid N-terminal, is non-functional in binding of SARS-CoV spike protein-2 and as Karboksipeptidase A. Our results reconcile the current knowledge on the expression of ACE2 and suggested that the ISG-type induction dACE2 IFN-high in the conditions created by the treatment, the inflammatory tumor microenvironment, or virus co-infection is unlikely to affect the cellular influx of SARS-CoV-2 and promote infection.

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Development and research into new therapies that selectively and effectively destroy tumor cells that overexpress ERBB2 receptor is a pressing task. More recently, research into the use of type I interferon in the treatment of cancer has been intensified.

Ricardo

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