Xiaowei Liu1, Xiaofeng Chen2, Chen Xu2, Jiangjie Lou1, Yingzheng Weng1, Lijiang Tang3. 1. Department of Cardiology, Zhejiang Hospital, Hangzhou, Zhejiang 310013, PR China. 2. Department of Cardiology, Taizhou Hospital, Linhai, Zhejiang 317000, PR China. 3. Department of Cardiology, Zhejiang Hospital, Hangzhou, Zhejiang 310013, PR China. Electronic address: zjyytang@126.com.
Abstract
BACKGROUND: Inflammation is the primary cause of abdominal aortic aneurysm (AAA) formation and development. It has been reported that platelets protect against septic shock by inhibiting inflammation. However, it is unclear whether platelets protect AAA progress via suppressing inflammation. METHODS: A mouse model of AAA was established by a daily administration of angiotensin II (Ang II, 1000 ng/kg/min) for 28-day. The AAA mice received 1 × 109 platelets transfusion in normal saline every 3rd day for 1 month. Hematoxylin and eosin, Masson's trichrome, and elastic van Gieson staining techniques were used to analyze the morphology of the abdominal aorta. Immunohistochemistry was used to detect any infiltration of inflammatory cells, inflammatory factors, and matrix metalloproteins (MMPs) in the aortic tissue. Western blot and enzyme-linked immunosorbent assay (ELISA) were used to examine the inflammatory factor proteins levels in the aortic wall and peripheral blood, respectively. RESULTS: Platelets infusion significantly suppressed the Ang II-driven elevation of aortic diameter, AAA formation (52.38% decrease, P < 0.05), aortic expansion, elastic lamina destruction, and inflammatory response. In addition, MMP-2 and MMP-9 production were also reduced by platelets transfusion. CONCLUSIONS: For the first time, our study reported the beneficial effect of platelet transfusion in suppressing the Ang II-driven AAA progress in mice through the inhibition of inflammation.
BACKGROUND: Inflammation is the primary cause of abdominal aortic aneurysm (AAA) formation and development. It has been reported that platelets protect against septic shock by inhibiting inflammation. However, it is unclear whether platelets protect AAA progress via suppressing inflammation. METHODS: A mouse model of AAA was established by a daily administration of angiotensin II (Ang II, 1000 ng/kg/min) for 28-day. The AAA mice received 1 × 109 platelets transfusion in normal saline every 3rd day for 1 month. Hematoxylin and eosin, Masson's trichrome, and elastic van Gieson staining techniques were used to analyze the morphology of the abdominal aorta. Immunohistochemistry was used to detect any infiltration of inflammatory cells, inflammatory factors, and matrix metalloproteins (MMPs) in the aortic tissue. Western blot and enzyme-linked immunosorbent assay (ELISA) were used to examine the inflammatory factor proteins levels in the aortic wall and peripheral blood, respectively. RESULTS: Platelets infusion significantly suppressed the Ang II-driven elevation of aortic diameter, AAA formation (52.38% decrease, P < 0.05), aortic expansion, elastic lamina destruction, and inflammatory response. In addition, MMP-2 and MMP-9 production were also reduced by platelets transfusion. CONCLUSIONS: For the first time, our study reported the beneficial effect of platelet transfusion in suppressing the Ang II-driven AAA progress in mice through the inhibition of inflammation.
Authors: Anna Burban; Aleksandra Idzik; Agata Gelo; Krzysztof J Filipiak; Tomasz Jakimowicz; Katarzyna Jama; Marcin Grabowski; Aleksandra Gasecka; Aleksander Siniarski Journal: Front Cardiovasc Med Date: 2022-08-12
Authors: Ke Tao; Ming Li; Xuefeng Gu; Ming Wang; Tianwei Qian; Lijun Hu; Jiang Li Journal: Korean J Physiol Pharmacol Date: 2022-09-01 Impact factor: 1.718