Leukocyte cell‐derived chemotaxin 2 (LECT2) is an obesity‐upregulated hepatokine inducing skeletal muscle insulin resistance. The study's aim was to explore whether LECT2 is expressed in human adipose tissue and whether the expression is dysregulated during obesity and associated with obesity‐related metabolic disorders.

Adipose tissue LECT2 expression is associated with obesity and insulin resistance in Korean women

Purpose Current treatments for diabetic retinopathy (DR) have considerable limitations, emphasizing the need for new therapeutic options. The effect of leukocyte cell-derived chemotaxin 2 (LECT2) on diabetes-induced blood–retinal barrier impairment and the possible underlying mechanism were investigated both in vivo and in vitro. Methods Twenty diabetic and 22 nondiabetic eyes were included in this study. Additionally, we established a streptozotocin-induced diabetic mouse model and observed vascular leakage in mice treated with or without recombinant LECT2 (rLECT2) intravitreal injection (40 µg/mL, 1 µL). The levels of LECT2 and interendothelial junction proteins (ZO1, VE-cadherin, and occludin) were analyzed by western blot and/or immunofluorescence. Endothelial junctions in mouse retinas were observed by transmission electron microscopy (TEM). Moreover, confluent human retinal microvascular endothelial cells (HRMECs) and human umbilical vein endothelial cells (HUVECs) were treated (0–72 hours) with glucose (0 or 30 mM) in the presence or absence of rLECT2 (40–360 ng/mL). After treatment, intact cell monolayers were monitored for permeability to 40-kD FITC-dextran. Interendothelial junction targets and Tie2/Akt/mTOR signaling pathway components were investigated by western blot. Results In diabetic human and mouse retinas and high-glucose (30 mM)–treated HRMECs and HUVECs, the levels of LECT2 and interendothelial junction proteins were decreased. rLECT2 treatment (80 ng/mL) significantly attenuated the hyperglycemia-induced reduction in endothelial cell barrier function and inhibited the migration and tube formation of HRMECs and HUVECs. In addition, rLECT2 increased the levels of interendothelial junction proteins via activation of the Tie2/Akt/mTOR signaling pathway. Furthermore, intravitreal rLECT2 injections increased the levels of interendothelial junction proteins and reversed diabetes-induced junction disruption. Conclusions rLECT2 can increase the levels of interendothelial tight junction proteins through activation of the Tie2/Akt/mTOR signaling pathway and can ameliorate inner blood–retinal barrier impairment secondary to diabetes. LECT2 might be a potential target to prevent the progression of DR.

LECT2 Ameliorates Blood–Retinal Barrier Impairment Secondary to Diabetes Via Activation of the Tie2/Akt/mTOR Signaling Pathway

Leukocyte cell-derived chemotaxin 2 (LECT2), a multifunctional hepatokine, is involved in many pathological conditions. However, its role in atherosclerosis remains undefined. In this study, we administered vehicle or LECT2 to male Apoe-/- mice fed a Western diet for 15 weeks. Atherosclerotic lesions were visualized and quantified with Oil-red O and hematoxylin staining. The mRNA expression levels of MCP-1, MMP-1, IL-8, IL-1β, and TNF-α were analyzed by quantitative real-time polymerase chain reaction. Serum TNF-α, IL-1β, IL-8, MCP-1, and MMP-1 concentrations were measured by enzyme-linked immunosorbent assay. CD68, CD31, and α-SMA, markers of macrophages, endothelial cells, and smooth muscle cells, respectively, were detected by immunostaining. Results showed that LECT2 reduced total cholesterol and low-density lipoprotein concentrations in serum and inhibited the development of atherosclerotic lesions, accompanied by reductions in inflammatory cytokines and lower MCP-1, MMP-1, TNF-α, IL-8, and IL-1β mRNA abundance. Furthermore, LECT2 decreased CD68, but increased α-SMA in atherosclerotic lesions, suggesting an increase in smooth muscle cells and reduction in macrophages. In summary, LECT2 inhibited the development of atherosclerosis in mice, accompanied by reduced serum total cholesterol concentration and lower inflammatory responses.

Leukocyte cell-derived chemotaxin 2 inhibits development of atherosclerosis in mice

Many studies have shown that leukocyte cell-derived chemotaxin 2 (LECT2) is associated with metabolic disorders, which is a risk factor of arteriosclerosis. We assessed the level of LECT-2 in patients with coronary artery disease (CAD) and its severity and prognosis. We selected 666 participants who underwent coronary angiography in our hospital and included patients with non-CAD, patients with stable angina pectoris (SAP), patients with unstable angina (UA), patients with non-ST-segment elevation myocardial infarction (NSTEMI) and patients with ST-segment elevation myocardial infarction (STEMI). The serum level of LECT-2 was higher in patients with CAD than in patients with non-CAD and was an independent predictor for CAD. Subgroup analysis showed that compared with the SAP group, the UA, NSTEMI, and STEMI groups had higher serum levels of LECT-2. In addition, the level of LECT-2 was related to the SYNTAX score and SYNTAX II score. Finally, patients with acute myocardial infarction (AMI) with elevated levels of LECT-2 had a higher risk of major adverse cardiovascular events (MACEs) within 12 months than those with lower levels of LECT-2. Plasma LECT-2 levels may be useful for the diagnosis of CAD and as predictors of MACE in patients with AMI.

Plasma Leukocyte Cell-Derived Chemotaxin 2 (LECT2) as a Risk Factor of Coronary Artery Disease: A Cross-Sectional Study.

Endoplasmic reticulum stress increases LECT2 expression via ATF4.

Circulating LECT2 levels in newly diagnosed type 2 diabetes mellitus and their association with metabolic parameters: An observational study.

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Circulating LECT2 levels in newly diagnosed type 2 diabetes mellitus and their association with metabolic parameters: An observational study.