TAK1 accelerates transplant arteriosclerosis in rat aortic allografts by inducing autophagy in vascular smooth muscle cells

Zheng, Xichuan; Yu, Qihong; Shang, Dan; Yin, Chuanzheng; Xie, Dawei; Huang, Tong; Du, Xiaoqiang; Wang, Wenjie; Yan, Xueke; Chen, Zhang; Wei, Li; Song, Zifang

doi:10.1016/j.atherosclerosis.2022.01.009

Cited by 6 publications

(5 citation statements)

References 47 publications

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“…Immunofluorescent staining was performed as previously described [ 23 ].Briefly, aorta roots were fixed with 4% PFA followed by permeabilization with 0.4% Triton X-100. Then, the tissue samples were blocked with 5% goat serum.…”

Section: Methodsmentioning

confidence: 99%

Genetic dissection of the impact of lncRNA AI662270 during the development of atherosclerosis

et al. 2023

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Background Atherosclerosis is driven by synergistic interactions between pathological biomechanical and lipid metabolic factors. Long noncoding RNAs (LncRNAs) have been implicated in atherogenesis. The purpose of this study was to investigate the potential mechanism of lncRNA AI662270 on macrophage cholesterol transport in atherosclerosis. Methods Apolipoprotein E deficiency (ApoE−/−) mice were fed a high fat diet for 16 weeks to construct atherosclerotic model, and the mice were injected with recombinant lentivirus carrying AI662270 gene to overexpress AI662270. Macrophages were cleared by liposomal clondronate in vivo. Fundamental experiments and functional assays, hematoxylin and eosin staining, oil red O staining and others, were performed to evaluate the function of AI662270 on atherogenesis. Peritoneal macrophages were treated with oxidized low density lipoprotein (ox-LDL) to simulate in vitro model. Mechanism assays, RNA-interacting protein immunoprecipitation, RNA–protein pulldown and others, were performed to study the regulatory mechanism of AI662270 in macrophages. Results The novel AI662270 was mainly enriched in macrophages, but not in endothelial cells, smooth muscle cells and fibroblasts of mouse atherosclerotic lesions and was upregulated by ox-LDL. Overexpression of AI662270 resulted in lipid accumulation, larger atherosclerotic plaques and cardiac dysfunction in vivo. After macrophages were removed, the pro-atherogenic effect of AI662270 disappeared. Downregulation of AI662270 in macrophages protected against foam cell formation by potentiating cholesterol efflux and reducing intracellular total cholesterol. The opposite effect was observed in macrophage-specific AI662270-overexpressed cells in vitro. AI662270 bound to adenosine triphosphate-binding cassette transporter A1 (Abca1) responsible for regulating cholesterol efflux in macrophages. Forced expression of AI662270 in macrophages decreased Abca1 expression. The reverse occurred when expression of AI662270 was repressed. Conclusion These findings reveal an essential role for AI662270 in atherosclerosis progression by regulating cholesterol efflux from macrophages.

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Section: Methodsmentioning

confidence: 99%

Genetic dissection of the impact of lncRNA AI662270 during the development of atherosclerosis

et al. 2023

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“…Rat model of abdominal aortic transplantation was established using a modified technique as our previous study [19,20]. Briefly, male Lewis rats were used as donors, syngeneic recipients and allogeneic recipients.…”

Section: Aortic Transplantation Model and Tissue Preparationmentioning

confidence: 99%

“…Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) assay and EdU incorporation assay as previously reported [20].…”

Section: Cell Proliferation Assaymentioning

confidence: 99%

Bves maintains vascular smooth muscle cell contractile phenotype and protects against transplant vasculopathy via Dusp1-dependent p38MAPK and ERK1/2 signaling

et al. 2022

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“…This event facilitates regulation of autophagy activation and thus constitutes an attractive molecular mechanism and prospective therapeutic target for restraining transplant vasculopathy. 28 Table 1 summarized relevant studies of TAK1 in different blood vessel cells.…”

Section: Introductionmentioning

confidence: 99%

TAK1 in Vascular Signaling: “Friend or Foe”?

Fan,

Lu,

Zha

et al. 2024

JIR

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The maintenance of normal vascular function and homeostasis is largely dependent on the signaling mechanisms that occur within and between cells of the vasculature. TGF-β-activated kinase 1 (TAK1), a multifaceted signaling molecule, has been shown to play critical roles in various tissue types. Although the precise function of TAK1 in the vasculature remains largely unknown, emerging evidence suggests its potential involvement in both physiological and pathological processes. A comprehensive search strategy was employed to identify relevant studies, PubMed, Web of Science, and other relevant databases were systematically searched using keywords related to TAK1, TABs and MAP3K7.In this review, we discussed the role of TAK1 in vascular signaling, with a focus on its function, activation, and related signaling pathways. Specifically, we highlight the TA1-TABs complex is a key factor, regulating vascular smooth muscle cells (VSMCs) and endothelial cells (ECs) involved in the processes of inflammation, vascular proliferation and angiogenesis. This mini review aims to elucidate the evidence supporting TAK1 signaling in the vasculature, in order to better comprehend its beneficial and potential harmful effects upon TAK1 activation in vascular tissue.

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TAK1 accelerates transplant arteriosclerosis in rat aortic allografts by inducing autophagy in vascular smooth muscle cells

Cited by 6 publications

References 47 publications

Genetic dissection of the impact of lncRNA AI662270 during the development of atherosclerosis

Genetic dissection of the impact of lncRNA AI662270 during the development of atherosclerosis

Bves maintains vascular smooth muscle cell contractile phenotype and protects against transplant vasculopathy via Dusp1-dependent p38MAPK and ERK1/2 signaling

TAK1 in Vascular Signaling: “Friend or Foe”?

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