Differential mRNA expression of inflammasome genes NLRP1 and NLRP3 in abdominal aneurysmal and occlusive aortic disease

• Published in: Therapeutic advances in cardiovascular disease Vol. 12; no. 4; pp. 123 - 129
• Main Authors: Gonzalez-Hidalgo, Carmen, De Haro, Joaquin, Bleda, Silvia, Cañibano, Cristina, Michel, Ignacio, Acin, Francisco
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01-04-2018; SAGE PUBLICATIONS, INC
• Subjects: Adaptor Proteins, Signal Transducing - genetics; Aged; Aneurysms; Aortic Aneurysm, Abdominal - etiology; Aortic Aneurysm, Abdominal - genetics; Aortic Aneurysm, Abdominal - surgery; Aortic aneurysms; Aortic Diseases - etiology; Aortic Diseases - genetics; Aortic Diseases - surgery; Apoptosis Regulatory Proteins - genetics; Arterial Occlusive Diseases - etiology; Arterial Occlusive Diseases - genetics; Arterial Occlusive Diseases - surgery; Cardiovascular disease; Case-Control Studies; Coronary vessels; DNA-Binding Proteins - genetics; Female; Gene expression; Humans; Inflammasomes - genetics; Inflammation; Male; Middle Aged; NLR Family, Pyrin Domain-Containing 3 Protein - genetics; Odds Ratio; Original Research; Real-Time Polymerase Chain Reaction; Reverse Transcriptase Polymerase Chain Reaction; Ribonucleic acid; Risk Factors; RNA; RNA, Messenger - genetics; Up-Regulation; NLRP3; NLRP1; inflammasomes; abdominal aortic aneurysm; aortic occlusive disease
• ISSN: 1753-9447; 1753-9455
• DOI: 10.1177/1753944717750338

NLRP1 and NLRP3 inflammasomes might differentially mediate the chronic inflammatory response in abdominal aortic aneurysm (AAA) and aortic occlusive disease (AOD). We measure differential relative gene expression of NLRP1 and NLRP3 inflammasomes in aortic tissues from 30 patients undergoing AAA open repair compared to aortic biopsies from 30 patients undergoing surgery to treat AOD. Aortic wall samples from autopsy without aortic disease were used as controls. NLRP3 was overexpressed in patients with AAA and AOD (RQ 1.185 ± 0.15, and 1.098 ± 0.05, respectively) compared to donors (RQ 1.001 ± 0.08) (OR 2.8, 95% CI 1.2–4.3, p < 0.05 for AAA and OR 2.1, 95% CI 1.1–3.8, p < 0.05 for AOD). NLRP1 gene expression was significantly upregulated in patients with AOD (RQ 1.197 ± 0.09). Meanwhile, NLRP1 was normal expressed in AAA (RQ 1.003 ± 0.07) as well as in autopsy aortic specimens (RQ 1.005 ± 0.11). Enhanced NLRP1 expression in AOD was even significant when compared to AAA (OR 2.3, 95% CI 1.2–3.3, p < 0.05) or controls (OR 2.2, 95% CI 1.1–3.1, p < 0.05). According to our findings, NLRP3 could be involved in the common etiology of AAA and AOD, whereas NLRP1 appears to have a specific role in AOD development.