CEACAM-1 promotes myocardial injury following coxsackievirus infection by regulating the coxsackievirus-adenovirus receptor.
Authors of this article are:
Zhang Z,, Long C, Li X, Xie Q, Song M, Zhang Y.
A summary of the article is shown below:
OBJECTIVE: To determine the effects and mechanism of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM-1, CC1)-mediated regulation of the Coxsackie and Adenovirus Receptor (CAR) after Coxsackievirus B3 (CVB3) infection.METHODS: A mouse CC1 overexpression recombinant virus was constructed, followed by insertion of a pLVX-CEACAM 1-zsgreen-puro (rLV-CEACAM 1) plasmid into the recombinant retrovirus. Cardiac myocytes were assigned into different groups according to various treatments. The apoptosis rate and cell activity in each group were observed. Further, CAR expression and SYK, IL-1β, and p-SYK levels were measured.RESULTS: The recombinant retrovirus titer was measured as 1.5 × 10 TUs/ml. The apoptosis rate of cardiac myocytes in the CC1 overexpression plus CVB3 group was significantly elevated, and the relative expression of the CAR gene was the highest in the CC1 overexpression plus CVB3 group. TNF-α and IL-1β levels increased due to CC1 overexpression and further increased after CVB3 infection. CAR protein expression also changed along with the levels of CC1, SYK, and TNF-α after infection.CONCLUSION: CC1 may promote CAR expression after CVB3 infection and regulate CAR protein expression by activating the CC1-SYK-TNF-α signaling axis during the infection process.
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This article is a good source of information and a good way to become familiar with topics such as: Animals; Apoptosis; Carcinoembryonic Antigen; Coxsackie and Adenovirus Receptor-Like Membrane Protein; Coxsackievirus Infections; Disease Models, Animal; Gene Expression Regulation; Heart Diseases; Interleukin-1beta; Intracellular Signaling Peptides and Proteins; Mice; Muscle Cells; Specific Pathogen-Free Organisms; Syk Kinase; Tumor Necrosis Factor-alpha.