Abstract
Schistosomiasis japonica is a significant health problem that leads to morbidity and mortality of humans. It is characterized by hepatic granulomatous response and fibrosis caused by eggs deposition in the liver. β-actin, a traditional housekeeping gene, is widely used as an internal control to normalize gene and protein expression. However, β-actin expression can fluctuate upon the treatment with pharmacological agents or under some physiological and pathological conditions. In this study, we found that the expressions of both β-actin mRNA and protein increased significantly with hepatic fibrosis formation after 6 weeks infection with Schistosoma japonicum and kept high level during the progression of hepatic fibrosis, while the levels of β-Tubulin and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) remained stable. The dynamic change of β-actin was similar with the profibrogenic factors, including α-SMA, Collagen I, and Collagen III. We employed immunofluorescence staining and further showed that the expression level of β-actin was positively correlated with α-SMA. What is more, there was a positive correlation between the level of β-actin mRNA and the content of hydroxyproline in liver. This study provides evidences that β-actin is variable and unsatisfied for application as an internal control in hepatic fibrosis induced by S. japonicum infection.
Highlights
Schistosomiasis japonica, caused by Schistosoma japonicum infection, continues to be a significant health problem that leads to human morbidity and mortality, especially in lake and marshland regions of China, the Philippines, and Sri Lanka, as well as the area near Lindu Lake (Barsoum et al, 2013; Colley et al, 2014)
In this study, in the progress of hepatic fibrosis in S. japonicum infected mice, the protein level of β-actin was increased in the liver after 6 wpi (p < 0.05) and peaked at 10 wpi (p < 0.001), but decreased at 14 wpi (Figures 1A,B)
Hepatic β-actin expression was significantly changed in mice with S. japonicum infection, suggesting that β-Actin and Hepatic Fibrosis β-actin might be an unsuitable internal control in schistosomiasis japonica
Summary
Schistosomiasis japonica, caused by Schistosoma japonicum infection, continues to be a significant health problem that leads to human morbidity and mortality, especially in lake and marshland regions of China, the Philippines, and Sri Lanka, as well as the area near Lindu Lake (Barsoum et al, 2013; Colley et al, 2014). Granulomous formation accompanies with recruitment of inflammatory cells, including macrophages, eosinophils, and activated hepatic stellate cells (HSCs) around the eggs. These granulomas contribute to severe fibrosis and even give rise to portal hypertension and β-Actin and Hepatic Fibrosis portacaval shunting due to the disturbance of the hepatic blood supply (Chuah et al, 2014; Colley et al, 2014; Carson et al, 2018). Developed cases can be reported in endemic regions (Song et al, 2017) It is still a major parasitic disease that needs sensitive diagnose and efficient therapy that prevents and targets fibrosis and portal hypertension. A lot of researches have been conducted for clarifying the pathogenesis and prevention of schistosomiasis japonica
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