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Altered mRNA expression due to acute mesenteric ischaemia in a porcine model
T Block1, H S Isaksson, S Acosta
1Department of Vascular Surgery, Institution of Surgical Sciences, Uppsala University, Uppsala, Sweden. tomas.block@surgsci.uu.se
Introduction:
Messenger RNA (mRNA) changes in the small intestine in response to acute mesenteric ischaemia (AMI) could offer novel diagnostic possibilities, but have not been described. The aim was to characterize the mRNA response to experimental AMI.
Materials And Methods:
Twelve pigs underwent catheterisation of the superior mesenteric artery with injection of polivinylalcohol embolisation particles or sodium chloride. Laparotomy and intestinal tissue sampling were performed. Microarray analysis was performed using the GeneChip(®) whole porcine genome array.
Results:
Seven down-regulated cellular pathways were associated with protein, lipid and carbohydrate metabolism. Seventeen up-regulated pathways were associated with inflammatory and immunological activity, regulation of extracellular matrix and decreased cellular proliferation. Thrombospondin (THS), monocyte chemoattractant protein 1(MCP-1) and gap junction alpha 1(GJA-1) were consistently up-regulated in all embolised pigs. Genes encoding earlier proposed biomarkers for AMI were up-regulated, such as lactate dehydrogenase and creatine kinase, or down-regulated, such as intestinal fatty acid binding protein and glutathione S-transferase.
Conclusion:
This study describes the intestinal tissue response on a gene expression level to AMI. THS, MCP-1 and GJA-1 were consistently up-regulated by ischaemia, whereas earlier proposed biomarkers for AMI were not. Gene expression may not be directly linked to the use of the corresponding proteins as potential clinical biomarkers.
Insights
Messenger RNA (mRNA) changes in the small intestine reveal new diagnostic markers for acute mesenteric ischemia (AMI). Thrombospondin (THS), monocyte chemoattractant protein 1 (MCP-1), and gap junction alpha 1 (GJA-1) were consistently upregulated, unlike previously proposed biomarkers.
Area of Science:
- Gastroenterology
- Molecular Biology
- Surgical Research
Background:
- Acute mesenteric ischemia (AMI) impacts small intestine function.
- Messenger RNA (mRNA) expression changes in response to AMI are not well-described.
- Understanding these changes could lead to novel diagnostic approaches.
Purpose of the Study:
- To characterize the mRNA expression profile in the small intestine following experimental AMI.
- To identify potential novel biomarkers for AMI based on gene expression.
Main Methods:
- Experimental AMI induced in pigs via superior mesenteric artery embolization.
- Intestinal tissue samples collected after laparotomy.
- Microarray analysis using a whole porcine genome array.
Main Results:
- Downregulated pathways involved in metabolism (protein, lipid, carbohydrate).
- Upregulated pathways associated with inflammation, immune response, extracellular matrix regulation, and reduced cell proliferation.
- Consistent upregulation of Thrombospondin (THS), monocyte chemoattractant protein 1 (MCP-1), and gap junction alpha 1 (GJA-1) mRNA.
- Variable expression of previously proposed AMI biomarkers (e.g., lactate dehydrogenase, intestinal fatty acid binding protein).
Conclusions:
- This study details the intestinal gene expression response to AMI.
- THS, MCP-1, and GJA-1 are consistently upregulated by ischemia.
- Current gene expression findings may not directly correlate with protein levels for clinical biomarker use.
