Key result
Silencing fgl2 in rat myocardial endothelial cells decreases CCL3 and PLAGL1 while increasing CTSC.
Why the study?
Cardiac microvascular endothelial cells play a key role in diabetic cardiomyopathy, and the role of FGL2 and related genes in this pathology is not fully understood.
Does silencing the fgl2 gene alter gene expression profiles in rat myocardial microvascular endothelial cells?
Does silencing the fgl2 gene alter gene expression profiles in rat myocardial microvascular endothelial cells?
Silencing the fgl2 gene in rat myocardial microvascular endothelial cells alters the expression of genes related to metabolism and inflammation, providing potential insights into the mechanism of diabetic cardiomyopathy.
BACKGROUND: Cardiac microvascular endothelial cells (MMECs) is one of the key factors in the process of diabetic cardiomyopathy, a common chronic complication of diabetes. Fibrinogen-like protein 2 (FGL2) is linked to apoptosis, angiogenesis, and inflammatory response, all of which also occur in diabetes. Thus, we investigate the role of FGL 2 and other genes in the pathology of diabetic cardiomyopathy. METHODS: In the present study, we used high-throughput microarray to profile gene expression in rat myocardial MMECs with or without silencing the fgl2 gene and in different glucose environments. We use volcanic maps to isolate genes with significantly different expression levels between conditions, using the standard statistical criteria of fold changes ≥1.5 and P-values ≤0.05. From this list, we identified genes with the most signicant changes in RNA levels and confirmed their protein-level changes with Western blot. Furthermore, bioinformatic analysis predicts possible pathophysiology and clinical relevance of these proteins in diabetic cardiomyopathy. RESULTS: We identified 17 upregulated and 15 downregulated genes caused by silencing fgl2 gene. Most of them are involved in metabolism, ion transport, cell membrane surface recognition signal modification, inflammatory response, and immune response. Using Western blot, we were able to confirm protein-level expression changes of three genes. Specifically, in both normal and high glucose conditions, silencing fgl2 significantly decreased the expression levels of CCL3 and PLAGL1 while increasing the expression level of CTSC. Significantly, bioinformatic analyses show that CCL3 is related to type 1 diabetes, PLAGL1 to cardiomyocytes, and CTSC to albuminuria in type 2 diabetes. CONCLUSIONS: Our study provides clues for further studies on the mechanism of diabetic cardiomyopathy as well as function of FGL2 in this process, potentially offering new therapeutic strategies for treating diabetic cardiomyopathy.
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Zheng et al. (2018) studied Diabetic cardiomyopathy. fgl2 gene silencing vs. Without fgl2 gene silencing was evaluated on Gene expression profiles. Silencing the fgl2 gene in rat myocardial microvascular endothelial cells resulted in 17 upregulated and 15 downregulated genes, significantly decreasing CCL3 and PLAGL1 while increasing CTSC.
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