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CARD9 gene silencing with siRNA protects rats against severe acute pancreatitis: CARD9-dependent NF-κB and P38MAPKs
Zhi-Wen Yang1,2, Xiao-Xiao Meng3, Chun Zhang2
1Songjiang Hospital Affiliated Shanghai First People's Hospital, Shanghai Jiao Tong University, Shanghai, China.
Insights
Caspase recruitment domain 9 (CARD9) is elevated in severe acute pancreatitis (SAP). Reducing CARD9 with siRNA lessens pancreatic injury and inflammation by down-regulating NF-κB and P38MAPK pathways.
Area of Science:
- Gastroenterology
- Molecular Biology
- Immunology
Background:
- Caspase recruitment domain 9 (CARD9) expression is increased in severe acute pancreatitis (SAP).
- The regulatory mechanisms and therapeutic potential of CARD9 in SAP remain largely unexplored.
Purpose of the Study:
- To investigate the role of CARD9 in SAP pathogenesis.
- To evaluate CARD9 as a potential therapeutic target for SAP.
Main Methods:
- Small interfering RNA (siRNA) was employed to reduce CARD9 expression in sodium taurocholate-induced SAP rat models.
- Assessed pancreatic injury, neutrophil infiltration, myeloperoxidase activity, and pro-inflammatory cytokine levels.
Main Results:
- CARD9 overexpression correlated with pancreatitis severity.
- siRNA-mediated CARD9 reduction significantly decreased pancreatic injury, neutrophil infiltration, and pro-inflammatory markers.
- CARD9 knockdown led to down-regulation of NF-κBp65 and P38MAPK signaling pathways.
Conclusions:
- CARD9 is upregulated in SAP and contributes to the inflammatory response.
- Targeting CARD9, potentially via siRNA, offers a therapeutic strategy for SAP by inhibiting NF-κB and P38MAPK activation.
Abstract:
We previously reported the up-regulation of caspase recruitment domain 9 (CARD9) expressions in severe acute pancreatitis (SAP) patients, but little is known about its regulation. In this study, small interfering RNA (siRNA) was used to reduce the levels of CARD9 expression in sodium taurocholate-stimulated SAP rats. CARD9 was overexpressed in SAP rats, which correlated with the severity of pancreatitis. When compared to the untreated group, the cohort that received the siRNA treatment demonstrated a significant reduction in pancreatic injury, neutrophil infiltration, myeloperoxidase activity and pro-inflammatory cytokines. Furthermore, siRNAs showed that the reduction of CARD9 in SAP rats down-regulated the expression of NF-κBp65 and P38MAPK which are involved in the transcription and release of a wide variety of inflammatory cytokines. These findings provide evidence that CARD9 is up-regulated in SAP rats and acts as a potential therapeutic target for the treatment thereof. Blocking the activation of NF-κB and P38MAPK via siRNA-mediated gene knock-down of CARD9 appears to reduce the inflammatory response in pancreatic tissue.
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