Doppler Christian, Arnhard Kathrin, Dumfarth Julia, Heinz Katharina, Messner Barbara, Stern Christian, Koal Therese, Klavins Kristaps, Danzl Katarina, Pitterl Florian, Grimm Michael, Oberacher Herbert, Bernhard David
Cardiac Surgery Research Laboratory, University Clinic for Cardiac Surgery, Innsbruck Medical University, Innsbruck, Austria.
Cardiac, Vascular, and Thoracic Surgery, Medical Faculty, Johannes-Kepler University, Linz, Austria.
PLoS One. 2017 May 3;12(5):e0176727. doi: 10.1371/journal.pone.0176727. eCollection 2017.
Our basic understanding of ascending thoracic aortic aneurysm (ATAA) pathogenesis is still very limited, hampering early diagnosis, risk prediction, and development of treatment options. "Omics"-technologies, ideal to reveal tissue alterations from the normal physiological state due to disease have hardly been applied in the field. Using a metabolomic approach, with this study the authors seek to define tissue differences between controls and various forms of ATAAs.
Using a targeted FIA-MS/MS metabolomics approach, we analysed and compared the metabolic profiles of ascending thoracic aortic wall tissue of age-matched controls (n = 8), bicuspid aortic valve-associated aneurysms (BAV-A; n = 9), tricuspid aortic valve-associated aneurysms (TAV-A; n = 14), and tricuspid aortic valve-associated aortic dissections (TAV-Diss; n = 6).
With sphingomyelin (SM) (OH) C22:2, SM C18:1, SM C22:1, and SM C24:1 only 4 out of 92 detectable metabolites differed significantly between controls and BAV-A samples. Between controls and TAV-Diss samples only phosphatidylcholine (PC) ae C32:1 differed. Importantly, our analyses revealed a general increase in the amount of total sphingomyelin levels in BAV-A and TAV-Diss samples compared to controls.
Significantly increased levels of sphingomyelins in BAV-A and TAV-Diss samples compared to controls may argue for a repression of sphingomyelinase activity and the sphingomyelinase-ceramide pathway, which may result in an inhibition of tissue regeneration; a potential basis for disease initiation and progression.
我们对升主动脉瘤(ATAA)发病机制的基本认识仍然非常有限,这阻碍了早期诊断、风险预测和治疗方案的开发。“组学”技术非常适合揭示因疾病导致的组织从正常生理状态发生的改变,但在该领域几乎未得到应用。通过代谢组学方法,作者在本研究中试图明确对照组与各种形式的升主动脉瘤之间的组织差异。
我们采用靶向流动注射串联质谱代谢组学方法,分析并比较了年龄匹配的对照组(n = 8)、二叶式主动脉瓣相关动脉瘤(BAV - A;n = 9)、三叶式主动脉瓣相关动脉瘤(TAV - A;n = 14)以及三叶式主动脉瓣相关主动脉夹层(TAV - Diss;n = 6)的升主动脉壁组织的代谢谱。
在92种可检测代谢物中,只有鞘磷脂(SM)(OH)C22:2、SM C18:1、SM C22:1和SM C24:1在对照组和BAV - A样本之间存在显著差异。在对照组和TAV - Diss样本之间,只有磷脂酰胆碱(PC)ae C32:1存在差异。重要的是,我们的分析显示,与对照组相比,BAV - A和TAV - Diss样本中的总鞘磷脂水平普遍升高。
与对照组相比,BAV - A和TAV - Diss样本中鞘磷脂水平显著升高,这可能表明鞘磷脂酶活性和鞘磷脂酶 - 神经酰胺途径受到抑制,这可能导致组织再生受到抑制;这是疾病发生和进展的潜在基础。