Key Laboratory of Medical Biotechnology of Hebei Province, Department of Biochemistry and Molecular Biology, College of Basic Medicine, Cardiovascular Medical Science Center, Hebei Medical University, Shijiazhuang, China.
Department of Functional Region of Diagnosis, The Fourth Affiliated Hospital, Hebei Medical University, Shijiazhuang, China.
PLoS One. 2022 Mar 31;17(3):e0264942. doi: 10.1371/journal.pone.0264942. eCollection 2022.
Aortic aneurysm/dissection (AAD) is now encountered more often because of the increasing prevalence of atherosclerosis and hypertension in the population. Despite many therapeutic improvements, in particular timely and successful surgery, in-hospital mortality rates are still higher. Timely identification of patients at high risk will help improve the overall prognosis of AAD. Since early clinical and radiological signs are nonspecific, there is an urgent need for accurate biomarkers. Smooth muscle 22α (SM22α) is a potential marker for AAD because of its abundant expression in vascular smooth muscle, which is involved in development of AAD.
We prepared three different mouse models, including abdominal aortic aneurysm, neointimal hyperplasia and atherosclerosis. SM22α levels were assessed in serum and vascular tissue of the mice. Next, the relationships between serum SM22α level and vascular lesion were studied in mice. Finally, serum from 41 patients with AAD, 107 carotid artery stenosis (CAS) patients and 40 healthy volunteers were tested for SM22α. Serum levels of SM22α were measured using an enzyme-linked immunosorbent assay (ELISA).
Compared with the controls, serum SM22α levels were reduced in the models of aortic aneurysm, neointimal formation and atherosclerosis, and elevated in mice with ruptured aneurysm. Serum SM22α level was negatively correlated with apoptosis rate of vascular smooth muscle cells (VSMC), ratio of intima/ media (I/M) area and plaque size. Patients with AAD had significantly higher serum SM22α levels than patients with only CAS, or normal controls.
Serum SM22α could be a potential predictive marker for AAD, and regulation of VSMC is a possible mechanism for the effects of SM22α.
由于人口中动脉粥样硬化和高血压的患病率不断增加，现在更常遇到主动脉瘤/夹层（AAD）。尽管治疗有了许多改进，特别是及时且成功的手术，但住院死亡率仍然较高。及时识别高危患者将有助于改善 AAD 的总体预后。由于早期临床和影像学征象不具有特异性，因此迫切需要准确的生物标志物。平滑肌 22α（SM22α）是 AAD 的潜在标志物，因为其在血管平滑肌中大量表达，而平滑肌参与 AAD 的发展。
我们制备了三种不同的小鼠模型，包括腹主动脉瘤、新生内膜增生和动脉粥样硬化。在小鼠的血清和血管组织中评估 SM22α 水平。接下来，研究了血清 SM22α 水平与血管病变之间的关系。最后，检测了 41 例 AAD 患者、107 例颈动脉狭窄（CAS）患者和 40 名健康志愿者的血清 SM22α。使用酶联免疫吸附测定（ELISA）测量血清 SM22α 水平。
与对照组相比，主动脉瘤、新生内膜形成和动脉粥样硬化模型中的血清 SM22α 水平降低，而破裂性动脉瘤小鼠中的血清 SM22α 水平升高。血清 SM22α 水平与血管平滑肌细胞（VSMC）凋亡率、内膜/中膜（I/M）面积比和斑块大小呈负相关。AAD 患者的血清 SM22α 水平明显高于仅患有 CAS 或正常对照的患者。
血清 SM22α 可能是 AAD 的潜在预测标志物，VSMC 的调节可能是 SM22α 作用的一种机制。
