Jae‐Hoon Choi
Hanyang University · Medicine
About the Lab
Professor Jae-Hoon Choi's research lab focuses on the immunological and molecular mechanisms underlying atherosclerosis and aortic valve disease, with a particular emphasis on monocyte/macrophage biology, dendritic cell function, and epigenetic regulation in vascular inflammation. The lab employs advanced single-cell omics technologies—such as scRNA-seq—to dissect cellular heterogeneity and phenotypic transitions in leukocytes, vascular cells, and immune populations within the aortic microenvironment under hyperlipidemic conditions. Key research directions include the role of lipid metabolism, histone acetylation, and transcriptional regulation (e.g., PPARγ pathway) in driving inflammatory cell activation and lesion progression. The lab also investigates the impact of metabolic hormones like growth hormone on atherosclerotic and hepatic metabolic phenotypes.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Rationale: Monocyte infiltration into the subintimal space and its intracellular lipid accumulation are the most prominent features of atherosclerosis. To understand the pathophysiology of atherosclerotic disease, we need to understand the characteristics of lipid-laden foamy macrophages in the subintimal space during atherosclerosis. Objective: We sought to examine the transcriptomic profiles of foamy and nonfoamy macrophages isolated from atherosclerotic intima. Methods and Results: Single-cel
Presumptive dendritic cells (DCs) bearing the CD11c integrin and other markers have previously been identified in normal mouse and human aorta. We used CD11c promoter-enhanced yellow fluorescent protein (EYFP) transgenic mice to visualize aortic DCs and study their antigen-presenting capacity. Stellate EYFP(+) cells were readily identified in the aorta and could be double labeled with antibodies to CD11c and antigen-presenting major histocompatability complex (MHC) II products. The DCs proved to
OBJECTIVE: Histone acetylation has been shown to be involved in expression of a restricted set of cellular genes including various proinflammatory molecules. We aimed to investigate the relationship between histone acetylation and atherosclerosis. METHODS AND RESULTS: In low-density lipoprotein (LDL) receptor-deficient (Ldlr(-/-)) mice fed an atherogenic diet for 4 or 8 weeks, trichostatin A (TSA), a specific histone deacetylase inhibitor, exacerbated atherosclerosis without alteration on plasma
Abstract Valvular inflammation triggered by hyperlipidemia has been considered as an important initial process of aortic valve disease; however, cellular and molecular evidence remains unclear. Here, we assess the relationship between plasma lipids and valvular inflammation, and identify association of low-density lipoprotein with increased valvular lipid and macrophage accumulation. Single-cell RNA sequencing analysis reveals the cellular heterogeneity of leukocytes, valvular interstitial cells
The recombinant human growth hormone (GH) has been used for the treatment of growth hormone deficiency (GHD) and diverse short stature state, and its physiological and therapeutic effects are well documented. However, since the effect of GH treatment on metabolic disorders has not been well characterized, we injected GH to Western diet-fed low-density lipoprotein receptor-deficient (Ldlr−/−) mice to understand the exact effect of GH on metabolic diseases including atherosclerosis, hepatic steato
Elevated local IgE is a common feature of AR in children and adults. Local measures in NAR showed naïve state of immune response which disagree with the hypothesis of local allergic rhinitis. Children showed intense local inflammation and close local-systemic interactions compared to adults supporting pediatric AR as a distinct feature.
Recently, it has been demonstrated that high cholesterol diet induced hypercholesterolemia and vascular lipid oxidation and accumulation in zebrafish larvae, suggesting that zebrafish is a new promising atherosclerosis model in addition to mouse models. However, up to date, there was no report regarding inflammatory cytokine expression during the lipid accumulation in zebrafish larva and adult fish. In this study, we first demonstrated the expression levels of IL-1β and TNF-α in high cholesterol
Hematein, a natural compound, is a known anti-inflammatory and antiatherogenic agent in the rabbit model. The authors investigated the effects of this compound on atherogenesis and possible mechanisms of the actions in the hyperlipidemic mice. Low-density lipoprotein receptor-deficient (Ldlr-/-) mice fed a high-cholesterol diet alone for 8 weeks developed the fatty streak lesion in the aortic sinus, whereas this lesion was significantly reduced by hematein treatment without a change in plasma li
Resistin-like molecule alpha (Retnla), also known as 'Found in inflammatory zone 1', is a secreted protein that has been found in bronchoalveolar lavage (BAL) fluid of ovalbumin (OVA)-induced asthmatic mice and plays a role as a regulator of T helper (Th)2-driven inflammation. However, the role of Retnla in the progress of Th2-driven airway inflammation is not yet clear. To better understand the function of Retnla in Th2-driven airway inflammation, we generated Retnla-overexpressing (Retnla-Tg)
Abstract A compact multiband multiple‐input multiple‐output (MIMO) antenna with an embedded chip inductor is proposed for next generation universal serial bus (USB) dongle applications. The proposed MIMO antenna consists of a longer strip with an embedded chip inductor and a shorter radiating strip. The longer radiating strip with a 15‐nH embedded chip inductor has a length of only about 34 mm (about 0.08 wavelength at 0.77 GHz), but it supports a wide resonant mode for long‐term evolution band
The PD-1/PD-L1 pathway may be responsible for the immune modulatory function of gastric DCs that protects the gastric mucosa from Helicobacter-induced inflammation, but allows persistent Helicobacter colonization.
Calcific aortic valve disease (CAVD) is the most common degenerative heart valve disease. Among the many risk factors for this disease are age, hypercholesterolemia, hypertension, smoking, type-2 diabetes, rheumatic fever, and chronic kidney disease. Since many of these overlap with risk factors for atherosclerosis, the molecular and cellular mechanisms of CAVD development have been presumed to be similar to those for atherogenesis. Thus, attempts have been made to evaluate the therapeutic effic
Research Areas
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