Publications by authors named "Yuchen Jing"

7 Publications

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The protective effect of HOXA5 on carotid atherosclerosis occurs by modulating the vascular smooth muscle cell phenotype.

Mol Cell Endocrinol 2021 Aug 11;534:111366. Epub 2021 Jun 11.

Department of Vascular Surgery, The First Hospital of China Medical University, Shenyang, China. Electronic address:

The phenotypic change of vascular smooth muscle cells (VSMCs) from a contractile to a synthetic form is a key player in atherogenic processes. Homeobox A5 (HOXA5), a transcription factor of the homeobox gene family, has been shown to regulate cell differentiation and morphogenesis. The present study was designed to clarify the involvement of HOXA5 in VSMC phenotypic transition in carotid atherosclerosis (CAS). Activated VSMCs in vitro and ApoE mice in vivo were employed to determine HOXA5's function. Results showed that both the mRNA and protein expression levels of HOXA5 were decreased in platelet-derived growth factor-BB (PDGF-BB)-induced VSMCs. Overexpression of HOXA5 suppressed VSMC conversion from a contractile to a synthetic type in the presence of PDGF-BB, as evidenced by increased contractile markers (calponin, α-SMA and SM22α) along with decreased synthetic markers (vimentin, PCNA and thrombospondin). PDGF-BB-induced proliferation and migration of VSMCs were recovered by HOXA5. Knockdown of HOXA5 had the opposite effect on VSMCs. In vivo, a CAS model was established using ApoE mice fed with a Western-type diet and placing a perivascular carotid collar. We observed a significant reduction in HOXA5 in the carotid arteries of CAS mice. Similar to the in vitro results, HOXA5 overexpression reduced neointimal hyperplasia and plaque formation and inhibited VSMC dedifferentiation and migration. Furthermore, PPARγ was also downregulated in vitro and in vivo, and its antagonist GW9662 reversed HOXA5-mediated inhibition of VSMC dedifferentiation and migration. In summary, we suggest that HOXA5 protects against CAS progression by inhibiting VSMC dedifferentiation through activation of PPARγ.
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http://dx.doi.org/10.1016/j.mce.2021.111366DOI Listing
August 2021

HOXA5 induces M2 macrophage polarization to attenuate carotid atherosclerosis by activating MED1.

IUBMB Life 2021 Jun 11. Epub 2021 Jun 11.

Department of Vascular Surgery, The First Hospital of China Medical University, Shenyang, China.

Macrophage polarization is of great importance in the formation of atherosclerotic plaque. Homeobox A5 (HOXA5), one of the homeobox transcription factors, has been revealed to be closely associated with macrophage phenotype switching. This study aims to investigate the role of HOXA5 in carotid atherosclerosis (CAS). Herein, the role of HOXA5 was explored in polarized RAW264.7 macrophages in vitro and ApoE mice in vivo. Interestingly, compared with that in M0 macrophages, both the mRNA and protein expression levels of HOXA5 were decreased in lipopolysaccharide (LPS)/interferon (IFN)-γ-induced M1 macrophages, while increased in IL-4-induced M2 macrophages. In addition, in the presence of IL-4, HOXA5-overexpressing RAW264.7 cells preferred to polarizing toward M2 phenotypes. Furthermore, we found that HOXA5 bound to the promoter region and activated the expression of mediator subunit 1 (MED1), a gene known to regulate macrophage differentiation. Knocking MED1 down inhibited HOXA5-enhanced M2 macrophage polarization. In vivo, the CAS model was induced in ApoE mouse fed with a Western-type diet and placed a perivascular carotid collar. Decreased mRNA and protein expressions of HOXA5 were observed in carotid arteries of CAS mice. Forced overexpression of HOXA5 reduced intimal hyperplasia and lipid accumulation in carotid vessels, and it also promoted the polarization of macrophages to M2 subtypes. The expression of MED1 was decreased in atherosclerotic carotid vessels, while HOXA5 overexpression restored its change. Collectively, HOXA5 in carotid arteries is involved in the macrophage M1/M2 switching in atherosclerotic plaque, which may be associated with its transcriptional regulation of MED1.
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http://dx.doi.org/10.1002/iub.2515DOI Listing
June 2021

Melatonin Plays a Critical Protective Role in Nicotine-Related Abdominal Aortic Aneurysm.

Front Physiol 2020 17;11:866. Epub 2020 Jul 17.

Department of Vascular Surgery, The First Hospital of China Medical University, Key Laboratory of Pathogenesis, Prevention and Therapeutics of Aortic Aneurysm, Shenyang, China.

: Smoking is a major risk factor for abdominal aortic aneurysm (AAA). Among the components of smoke, nicotine is known to exert pro-atherosclerotic, prothrombotic, and proangiogenic effects on vascular smooth muscle cells (VSMCs). The current study was designed to investigate the mechanisms through which nicotine induces vascular wall dysfunction and to examine whether melatonin protects against nicotine-related AAA. : In this study, an enzyme-linked immunosorbent assay (ELISA) was used to measure melatonin and TNF-α levels, as well as total antioxidant status (TAS), in patients with AAA. We established a nicotine-related AAA model and explored the mechanisms underlying the therapeutic effects of melatonin. Tissue histopathology was used to assess vascular function, while western blotting (WB) and immunofluorescence staining were performed to detect protein expression. : We observed melatonin insufficiency in the serum from patients with AAA, particularly smokers. Moreover, melatonin level was positively correlated with antioxidant capacity. In the model, nicotine accelerated AAA expansion and destroyed vascular structure. Furthermore, OPN, LC3II, p62, matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), NF-κB p65, TNF-α, phosphorylated AKT, and phosphorylated mTOR levels were increased, , following nicotine treatment, while SM22α and α-SMA levels were reduced. Additionally, melatonin attenuated the effects of nicotine on AAA and reversed changes in protein expression. Moreover, melatonin lost its protective effects following bafilomycin A1-mediated inhibition of autophagy. : Based on our data, melatonin exerts a beneficial effect on rats with nicotine-related AAA by downregulating the AKT-mTOR signaling pathway, improving autophagy dysfunction, and restoring the VSMC phenotype.
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http://dx.doi.org/10.3389/fphys.2020.00866DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7379742PMC
July 2020

Upregulated level of lncRNA HOXA-AS2 in peripheral blood of systemic lupus erythematosus patients aggravates disease progression via ERK pathway.

Minerva Med 2021 Aug 3;112(4):536-537. Epub 2020 Feb 3.

Department of Pain, The First Hospital of China Medical University, Shenyang, China -

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http://dx.doi.org/10.23736/S0026-4806.19.06361-4DOI Listing
August 2021

MiR-9 promotes proliferation and inhibits apoptosis of bladder cancer cells via notch signaling pathway.

Panminerva Med 2020 Jan 24. Epub 2020 Jan 24.

Department of Pain Treatment, The First Hospital of China Medical University, Shenyang, China -

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http://dx.doi.org/10.23736/S0031-0808.19.03818-7DOI Listing
January 2020

A case report of therapy-related acute myeloid leukemia secondary to histiocytic sarcoma and literature review.

Minerva Med 2020 Jan 20. Epub 2020 Jan 20.

Interventional Operating Room, The First Hospital of China Medical University, Shenyang, China.

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http://dx.doi.org/10.23736/S0026-4806.19.06421-8DOI Listing
January 2020

Saphenous vein graft aneurysm formation in a patient with idiopathic multiple aneurysms.

J Vasc Surg Cases Innov Tech 2018 Sep 17;4(3):197-200. Epub 2018 Aug 17.

Department of Vascular Surgery, The First Hospital, China Medical University, Shenyang, China.

True aneurysmal vein graft dilation is rare, and its etiology remains speculative. However, systemic dilation diathesis is regarded as a risk factor. We herein report a case of a rapidly expanding aneurysm in a great saphenous vein graft, resulting in distal malperfusion in a patient who had previously undergone open repair of multiple popliteal artery aneurysms. After an unsuccessful endovascular intervention, the dilated section was eventually replaced by a reversed segment of the contralateral great saphenous vein. Subsequent whole-exome sequencing identified no relevant mutations. This case provides further evidence that aneurysmal disease may be associated with systemic dilation diathesis.
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http://dx.doi.org/10.1016/j.jvscit.2018.04.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6105753PMC
September 2018
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