Haijiang Jin

Second Hospital of Shanxi Medical University

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Jie Hu

Second Hospital of Shanxi Medical University

Genmao Cao

Fudan University

Xuezhen Xuan

Second Hospital of Shanxi Medical University

Ruijing Zhang

Second Hospital of Shanxi Medical University

Honglin Dong

Second Hospital of Shanxi Medical University

Yaling Li

Affiliated Hospital of Southwest Medical University

Sheng Yan

Shandong University

Mingqiang Zhou

Chongqing University

Honglin Dong

Second Hospital of Shanxi Medical University

Ruijing Zhang

Second Hospital of Shanxi Medical University

Cooperative Institutions

Shanxi Medical University

Second Hospital of Shanxi Medical University

Chongqing University

Air Force Medical University

North China University of Science and Technology

Peking University

South China University of Technology

Chinese Academy of Sciences

Zhengzhou University

Dalian Medical University

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Single-cell RNA sequencing reveals the vascular smooth muscle cell phenotypic landscape in aortic aneurysm

Cell Communication and Signaling (2023)

Genmao Cao Xuezhen Xuan Yaling Li Jie Hu Ruijing Zhang

Abstract Background and objectives Phenotypic switching in vascular smooth muscle cells (VSMCs) has been linked to aortic aneurysm, but the phenotypic landscape in aortic aneurysm is poorly understood. The present study aimed to analyse the phenotypic landscape, phenotypic differentiation trajectory, and potential functions of various VSMCs phenotypes in aortic aneurysm. Methods Single-cell sequencing data of 12 aortic aneurysm samples and 5 normal aorta samples (obtained from GSE166676 and GSE155468) were integrated by the R package Harmony. VSMCs were identified according to the expression levels of ACTA2 and MYH11. VSMCs clustering was determined by the R package ‘Seurat’. Cell annotation was determined by the R package ‘singleR’ and background knowledge of VSMCs phenotypic switching. The secretion of collagen, proteinases, and chemokines by each VSMCs phenotype was assessed. Cell‒cell junctions and cell–matrix junctions were also scored by examining the expression of adhesion genes. Trajectory analysis was performed by the R package ‘Monocle2’. qPCR was used to quantify VSMCs markers. RNA fluorescence in situ hybridization (RNA FISH) was performed to determine the spatial localization of vital VSMCs phenotypes in aortic aneurysms. Results A total of 7150 VSMCs were categorize into 6 phenotypes: contractile VSMCs, fibroblast-like VSMCs, T-cell-like VSMCs, adipocyte-like VSMCs, macrophage-like VSMCs, and mesenchymal-like VSMCs. The proportions of T-cell-like VSMCs, adipocyte-like VSMCs, macrophage-like VSMCs, and mesenchymal-like VSMCs were significantly increased in aortic aneurysm. Fibroblast-like VSMCs secreted abundant amounts of collagens. T-cell-like VSMCs and macrophage-like VSMCs were characterized by high chemokine levels and proinflammatory effects. Adipocyte-like VSMCs and mesenchymal-like VSMCs were associated with high proteinase levels. RNA FISH validated the presence of T-cell-like VSMCs and macrophage-like VSMCs in the tunica media and the presence of mesenchymal-like VSMCs in the tunica media and tunica adventitia. Conclusion A variety of VSMCs phenotypes are involved in the formation of aortic aneurysm. T-cell-like VSMCs, macrophage-like VSMCs, and mesenchymal-like VSMCs play pivotal roles in this process.

Phenotypic switching

10.1186/s12964-023-01120-5

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The Deep Fusion of Topological Structure and Attribute Information for Link Prediction

IEEE Access (2020)

Mingqiang Zhou Yihan Kong Shenshen Zhang Dan Liu Haijiang Jin

The link prediction can be used to seek missing or future links in the network, so it has become a hot research topic. The network generally contains two types of information: the topological structure of network formed by the connection between nodes, and the attribute information of nodes. However, the existing topology-based link prediction algorithms consider little attribute information. In this paper, a novel algorithm called Network Embedding with Attribute Deep Fusion for Link Prediction (NEADF-LP) is proposed. We get the embedded vectors with topological structure and attribute information by structure encoder and attribute encoder respectively, and fuse two vectors deeply. Compared with mainstream baselines on CiteSeer and Cora datasets, the results show that the deep fusion of topological structure and attribute information improve the accuracy of link prediction effectively.

Link (geometry)

Fuse (electrical)

10.1109/access.2020.2974016

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Inhibition of Abdominal Aortic Aneurysm Progression Through the CXCL12/CXCR4 Axis via MiR206‐3p Sponge

Journal of Cellular and Molecular Medicine (2025)

Xuezhen Xuan Yaling Li Genmao Cao Jie Hu Sheng Yan

ABSTRACT Notably, the C‐X‐C Motif Chemokine Ligand 12/C‐X‐C Chemokine Receptor Type 4 (CXCL12/CXCR4) signalling pathway's activation is markedly increased in a mouse model of abdominal aortic aneurysms (AAA). Nonetheless, the precise contribution of this pathway to AAA development remains to be elucidated. The AAA mouse model was induced by local incubation with elastase and oral administration of β‐aminopropionitrile. The activity level of the CXCL12/CXCR4 axis was evaluated in both human AAA patients and the mouse model. Smooth muscle cell lineage tracing determined the expression and localisation of CXCR4 in normal aorta and AAA tissue. By transfecting the MiR206‐3p sponge to reduce the level of MiR206‐3p in AAA, the effects of the CXCL12/CXCR4 pathway on AAA progression as well as the apoptosis and phenotypic transformation of vascular smooth muscle cells (VSMCs) were studied in vivo and in vitro. Single‐cell RNA sequencing analysis, serum ELISA, and in vivo experiments indicate a pronounced activation of the CXCL12/CXCR4 axis in both AAA patients and the mouse model. Specific blocking of the CXCL12/CXCR4 axis significantly inhibited further expansion and rupture of the abdominal aorta and reduced the infiltration of inflammatory cells in the aorta and inhibited the phenotypic transformation of contractile VSMCs into a macrophage‐like state. Our findings propose that MiR206‐3p sponge represents an innovative therapeutic strategy to attenuate AAA progression and rupture risk, primarily through the suppression of the CXCL12/CXCR4 signalling pathway.

10.1111/jcmm.70328

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How vascular smooth muscle cell phenotype switching contributes to vascular disease

Cell Communication and Signaling (2022)

Genmao Cao Xuezhen Xuan Jie Hu Ruijing Zhang Haijiang Jin

Abstract Vascular smooth muscle cells (VSMCs) are the most abundant cell in vessels. Earlier experiments have found that VSMCs possess high plasticity. Vascular injury stimulates VSMCs to switch into a dedifferentiated type, also known as synthetic VSMCs, with a high migration and proliferation capacity for repairing vascular injury. In recent years, largely owing to rapid technological advances in single-cell sequencing and cell-lineage tracing techniques, multiple VSMCs phenotypes have been uncovered in vascular aging, atherosclerosis (AS), aortic aneurysm (AA), etc. These VSMCs all down-regulate contractile proteins such as α-SMA and calponin1, and obtain specific markers and similar cellular functions of osteoblast, fibroblast, macrophage, and mesenchymal cells. This highly plastic phenotype transformation is regulated by a complex network consisting of circulating plasma substances, transcription factors, growth factors, inflammatory factors, non-coding RNAs, integrin family, and Notch pathway. This review focuses on phenotypic characteristics, molecular profile and the functional role of VSMCs phenotype landscape; the molecular mechanism regulating VSMCs phenotype switching; and the contribution of VSMCs phenotype switching to vascular aging, AS, and AA.

Phenotypic switching

10.1186/s12964-022-00993-2

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Citations (154)

Contribution of FOS in neutrophils to venous thromboembolism via miR‐144 based on bioinformatic prediction and validation

Journal of Cellular and Molecular Medicine (2024)

Ping Wang Lin Zheng Xiaotong Qi Heng Wang Ruijing Zhang

Abstract The Finkel‐Biskis‐Jinkins Osteosarcoma (c‐Fos; encoded by FOS ) plays an important role in several cardiovascular diseases, including atherosclerosis and stroke. However, the relationship between FOS and venous thromboembolism (VTE) remains unknown. We identified differentially expressed genes in Gene Expression Omnibus dataset, GSE48000, comprising VTE patients and healthy individuals, and analysed them using CIBERSORT and weighted co‐expression network analysis (WGCNA). FOS and CD46 expressions were significantly downregulated (FOS p = 2.26E‐05, CD64 p = 8.83E‐05) and strongly linked to neutrophil activity in VTE. We used GSE19151 and performed PCR to confirm that FOS and CD46 had diagnostic potential for VTE; however, only FOS showed differential expression by PCR and ELISA in whole blood samples. Moreover, we found that hsa‐miR‐144 which regulates FOS expression was significantly upregulated in VTE. Furthermore, FOS expression was significantly downregulated in neutrophils of VTE patients ( p = 0.03). RNA sequencing performed on whole blood samples of VTE patients showed that FOS exerted its effects in VTE via the leptin‐mediated adipokine signalling pathway. Our results suggest that FOS and related genes or proteins can outperform traditional clinical markers and may be used as diagnostic biomarkers for VTE.

10.1111/jcmm.18370

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Citations (1)

[Analysis and safeguard for misdiagnosis of nasopharyngeal carcinoma].

PubMed (2014)

Shuxia Dong Yuanxia Wei Haijiang Jin

Safeguard

Source

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Fluoroquinolones increase susceptibility to aortic aneurysm and aortic dissection: Molecular mechanism and clinical evidence

Vascular Medicine (2023)

Xuezhen Xuan Yaling Li Genmao Cao Ruijing Zhang Jie Hu

Aortic aneurysm (AA) and aortic dissection (AD) are prevalent severe cardiovascular diseases that result in catastrophic complications and unexpected deaths. Owing to the lack of clinically established and effective medications, the only treatment options are open surgical repair or endovascular therapy. Most researchers have focused on the development of innovative medications or therapeutic targets to slow the progression of AA/AD or lower the risk of malignant consequences. Recent studies have shown that the use of fluoroquinolones (FQs) may increase susceptibility to AA/AD to some extent, especially in patients with aortic dilatation and those at a high risk of AD. Therefore, it is crucial for doctors, particularly those in cardiovascular specialties, to recognize the dangers of FQs and adopt alternatives. In the present review, the main clinical observational studies on the correlation between FQs and AA/AD in recent years are summarized, with an emphasis on the relative physiopathological mechanism incorporating destruction of the extracellular matrix (ECM), phenotypic transformation of vascular smooth muscle cells, and local inflammation. Although additional data are required, it is anticipated that the rational use of FQs will become the standard of care for the treatment of aortic diseases.

10.1177/1358863x231198055

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Citations (2)

Genetic evidence for a causal link between gut microbiota and arterial embolism and thrombosis: a two-sample Mendelian randomization study

Frontiers in Microbiology (2024)

Yong-Bin Shi Honglin Dong Wenkai Chang Yan Zhao Haijiang Jin

Background Previous research has hinted at a crucial link between gut microbiota and arterial embolism and thrombosis, yet the causal relationship remains enigmatic. To gain a deeper understanding, we aimed to comprehensively explore the causal relationship and elucidate the impact of the gut microbiota on the risk through a two-sample Mendelian randomization (MR) study. Methods Genetic instrumental variables for gut microbiota were identified from a genome-wide association study (GWAS) of 18,340 participants. Summary statistics for IBS were drawn from a GWAS including 1,076 cases and 381,997 controls. We used the inverse-variance weighted (IVW) method as the primary analysis. To test the robustness of our results, we further performed the weighted median method, MR-Egger regression, and MR pleiotropy residual sum and outlier test. Results We identified three bacterial traits that were associated with the risk of arterial embolism and thrombosis: odds ratio (OR): 1.58, 95% confidence interval (CI): 1.08–2.31, p = 0.017 for genus Catenibacterium ; OR: 0.64, 95% CI: 0.42–0.96, p = 0.031 for genus Dialister ; and OR: 2.08, 95% CI: 1.25–3.47, p = 0.005 for genus Odoribacter . The results of sensitivity analyses for these bacterial traits were consistent ( P <0.05). Conclusion Our systematic analyses provided evidence to support a potential causal relationship between several gut microbiota taxa and the risk of arterial embolism and thrombosis. More studies are required to show how the gut microbiota affects the development of arterial embolism and thrombosis.

Mendelian Randomization

Genome-wide Association Study

10.3389/fmicb.2024.1396699

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Betweenness centrality-based community adaptive network representation for link prediction

Applied Intelligence (2021)

Mingqiang Zhou Haijiang Jin Quanwang Wu Hong Xie Qizhi Han

Representation

Link (geometry)

Dynamic network analysis

10.1007/s10489-021-02633-7

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Inhibition of Elastase induced Abdominal Aortic Aneurysm Progression through the CXCL12/CXCR4 Axis via MiR206 3p Sponge

Research Square (Research Square) (2024)

Xuezhen Xuan Yaling Li Genmao Cao Jie Hu Sheng Yan

Abstract Background Prior research has established a significant association between the progression of abdominal aortic aneurysms (AAA) and the apoptosis and phenotypic transformation of vascular smooth muscle cells (VSMCs). Notably, the CXCL12/CXCR4 signaling pathway's activation is markedly increased in a mouse model of AAA. Nonetheless, the precise contribution of this pathway to AAA development remains to be elucidated. Materials and Methods We utilized a single-cell sequencing dataset pertaining to AAA from the Gene Expression Omnibus database, employing the R package CellChat (v1.1.3) to analyze communication strength, signaling pathways, and modes of interaction among various VSMC phenotypes and immune cells. The activity level of the CXCL12/CXCR4 axis was evaluated in both human AAA patients and a mouse model. We examined the impact of CXCR4-specific inhibitors on AAA progression and the regulatory influence of MiR206-3p sponge on this axis. Results Single-cell RNA sequencing analysis revealed a significant upregulation of CXCL12/CXCR4 axis in AAA tissues. Further, Serum ELISA and in vivo experiments indicate a pronounced activation of the CXCL12/CXCR4 axis in both AAA patients and the elastase-induced AAA mouse model. CXCR4-specific inhibitors inhibited further expansion and rupture of the abdominal aorta and reduced the infiltration of macrophages in the aorta. Diminishing miR206-3p levels in VSMCs led to a decrease in CXCR4 expression within AAA tissues and a reduction in serum CXCL12 concentrations. Furthermore, transfecting VSMCs with miR206-3p sponge curtailed apoptosis and phenotypic transformation, markedly reducing AAA diameter and rupture frequency in mice. In vitro experiments corroborated that blocking the CXCL12/CXCR4 axis mitigated apoptosis and phenotypic transformation of VSMCs. Conclusion Our findings propose that MiR206-3p sponge represents an innovative therapeutic strategy to attenuate AAA progression and rupture risk, primarily through the suppression of the CXCL12/CXCR4 signaling pathway.

Sponge

Pancreatic elastase

10.21203/rs.3.rs-4119276/v1

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