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Protein arginine methyltransferase 2 (PRMT2) is closely related to the occurrence and development of atherosclerosis. However, its underlying mechanisms remain to be elucidated. The purpose of this study is to observe the effect of overexpression of PRMT2 on the formation of foam cells and to explore its possible mechanism in RAW 264.7 macrophage. Lentivirus vector of overexpression PRMT2 (LV-PRMT2) was constructed. LV-PRMT2 and lentivirus vector GV492 were transfected into RAW 264.7 macrophages, positive clone cells were screened by treatment with 4.0 μg/mL puromycin for 4 weeks. The macrophages were treated with ox-LDL (50 μg/mL) for 48 h to induce foaming. The lipid accumulation of macrophages was observed by oil red O staining. The levels of cellular total cholesterol (TC), free cholesterol (FC) and cholesteryl ester (CE) were measured by high performance liquid chromatography (HPLC) assays. The cholesterol efflux of macrophages was tested by the [3H] labeled cholesterol. The expressions of ATP binding cassette transporter A1 (ABCA1), ATP binding cassette transporter G1 (ABCG1), CD36 and scavenger receptor A1 (SR-A1) in macrophages were measured by Western Blot. The results showed that LV-PRMT2 and lentivirus vector has been successfully transfected into RAW 264.7 macrophage. Compared with the Vector group, the mRNA and protein expressions of PRMT2 were significantly up-regulated (P < 0.05). Compared with Control group, the expression of PRMT2 was significantly down-regulated in ox-LDL group (P < 0.05). A large number of red lipid droplets appeared in the cells in Vector group. Compared with Vector group, lipid droplets, the levels of TC, FC and CE and CE/TC, cholesterol efflux rate and expression of ABCA1 in RAW 264.7 macrophage was significantly decreased in LV-PRMT2 group (all P < 0.05). There was no significant difference about the expressions of ABCG1, CD36 and SR-A1 between LV-PRMT2 group and Vector group (all P > 0.05). Overexpression of PRMT2 inhibits the formation of foam cell induced by ox-LDL in RAW 264.7 macrophage, and the mechanism may be related to the increase of ABCA1 expression and ABCA1 mediated cholesterol efflux. • Ox-LDL down-regulated the expression of PRMT2 in RAW 264.7 macrophages. • Overexpression of PRMT2 inhibited formation of foam cell in macrophages involving ABCA1 mediated cholesterol efflux. • Overexpression of PRMT2 decreased the cholesterol level in RAW 264.7 macrophage induced by ox-LDL. • Effect of overexpression of PRMT2 on the expression of ABCA1, ABCG1, CD36 and SR-A1. [ABSTRACT FROM AUTHOR]

The species Citrus hongheensis is an endangered species and the most primitive Citrus species with the most developed winged leaves. It is endemic to south Yunnan Province, southwest China, and only distributed in a very narrow area along the south bank of the Honghe river (the Yuanjiang river). By combining ISSR and morphological data from 11 populations, it shows that the species has rich genetic diversity among and within populations although the population is declining gradually. According to field and market surveys, the local Hani people have traditionally used C. hongheensis for a long time, such as the dried young fruits of the species as Chinese traditional medicine, leaves as food spice, as well as other organs. By collecting all existing knowledge of traditional and present uses, as well as further potential uses, we demonstrate that the species has good development prospects. Based on rich diversity, ethnobotanical uses, and a positive cultural environment, it was decided to choose four populations (YJNNDM, LCDX, HHDYJ, and YJYJYJ) of C. hongheensis for in situ conservation and artificial sexual reproduction. This will allow to develop new uses of the species, while providing indications for the conservation of other endangered species. [ABSTRACT FROM AUTHOR]

[Display omitted] • (a) In both physiological and pathological conditions, nicotine stimulation induces cardiac fibrosis and injury. • (b) Nicotine induces cardiac fibrosis by directly binding to LDHA. • (c) Nicotine induces autophagy flux impairment in cardiac fibroblasts through LDHA-mediated AMPK/mTOR/TFEB signaling pathway and the decreased activity of CTSB. Cardiac fibrosis is a typical feature of cardiac pathological remodeling, which is associated with adverse clinical outcomes and has no effective therapy. Nicotine is an important risk factor for cardiac fibrosis, yet its underlying molecular mechanism remains poorly understood. This study aimed to identify its potential molecular mechanism in nicotine-induced cardiac fibrosis. Our results showed nicotine exposure led to the proliferation and transformation of cardiac fibroblasts (CFs) into myofibroblasts (MFs) by impairing autophagy flux. Through the use of drug affinity responsive target stability (DARTS) assay, cellular thermal shift assay (CETSA), and surface plasmon resonance (SPR) technology, it was discovered that nicotine directly increased the stability and protein levels of lactate dehydrogenase A (LDHA) by binding to it. Nicotine treatment impaired autophagy flux by regulating the AMPK/mTOR signaling pathway, impeding the nuclear translocation of transcription factor EB (TFEB), and reducing the activity of cathepsin B (CTSB). In vivo, nicotine treatment exacerbated cardiac fibrosis induced in spontaneously hypertensive rats (SHR) and worsened cardiac function. Interestingly, the absence of LDHA reversed these effects both in vitro and in vivo. Our study identified LDHA as a novel nicotine-binding protein that plays a crucial role in mediating cardiac fibrosis by blocking autophagy flux. The findings suggest that LDHA could potentially serve as a promising target for the treatment of cardiac fibrosis. [ABSTRACT FROM AUTHOR]