Publications by authors named "Hao-Jie Jin"

Article Synopsis
  • * It finds that silencing DRP1 and using the treatment isoliquiritigenin (ISL) can reduce the adverse effects of diabetes on VSMCs, such as heightened oxidative stress and cell proliferation.
  • * ISL works by directly binding to a specific site on DRP1, decreasing its activity related to mitochondrial fission, and ultimately mitigating intimal hyperplasia in diabetic models.
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Article Synopsis
  • Vascular calcification (VC) in diabetes is driven by the switching of vascular smooth muscle cells to an osteogenic phenotype, which can be mitigated by mitophagy, a process that cleans up damaged mitochondria.
  • This study evaluates how the GLP-1 receptor agonist exendin 4 (EX4) impacts mitophagy-related phenotype switching in VSMCs, using T2DM mice models and cultured human cells under high glucose conditions.
  • EX4 was found to enhance mitophagy, improve mitochondrial function, and activate the AMPK signaling pathway, which collectively reduced VC in diabetic mice and inhibited the problematic osteogenic differentiation of VSMCs.
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Excessive proliferation and migration of vascular smooth muscle cells (VSMCs) contribute to the intimal hyperplasia in type 2 diabetes mellitus (T2DM) patients after percutaneous coronary intervention. We aimed to investigate the role of lncRNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) in VSMC proliferation and migration, as well as the underlying mechanism. T2DM model mice with carotid balloon injury were used in vivo and mouse aortic vascular smooth muscle cells (MOVAS) stimulated by insulin were used in vitro to assess the role of CDKN2B-AS1 in VSMC proliferation and migration following vascular injury in T2DM state.

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Background: The expression of brain cytoplasmic RNA1 () is linked to the clinicopathology and prognosis of several types of cancers, among which hepatocellular carcinoma (HCC) is one of the most frequent types of cancer worldwide.

Aim: To explore the prognostic value and immunotherapeutic potential of in HCC by bioinformatics and meta-analysis.

Methods: Information was obtained from the Cancer Genome Atlas database.

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Article Synopsis
  • Insulin resistance leads to excessive growth of vascular smooth muscle cells (VSMCs), which contributes to intimal hyperplasia in type 2 diabetes mellitus (T2DM), and this process is regulated by N6-methyladenosine (mA) methylation modifications.
  • The study found that FTO, an mA demethylase, is increased in insulin-treated VSMCs and T2DM mice, and knocking down FTO raised mA methylation levels, thereby inhibiting VSMC proliferation and migration.
  • Additionally, the study revealed that FTO knockdown results in higher SM22α expression, which, aided by the IGF2BP2 protein, stabilizes SM22α mRNA and
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Understanding mechanisms of cancer metastasis is crucial for reduction of cancer mortality. Acyl-CoA medium-chain synthetase 3 (ACSM3) is an acyl-CoA synthetase which takes part in the first step of fatty acid metabolism. However, the expression, clinical significance and biological function of ACSM3 remain unknown in hepatocellular carcinoma (HCC).

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Purpose: To explore the role of 4-1BBL in nicotine-treated immature dendritic cells (imDCs) mediated anti-tumor effects.

Methods: Bone marrow-derived imDCs were stimulated with nicotine and 4-1BBL expression was determinated by flow cytometry, Western blot and RT-PCR respectively. Then, the roles of 4-1BBL in nicotine-augmented DCs-dependent T cell proliferation, CTL priming and anti-tumor effects were investigated by BrdU cell proliferation assay, enzyme-linked immunospot assay and in vivo preventive effect on tumor development, respectively.

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Our previous studies have revealed that nicotine-treated immature dendritic cells (imDCs) have anti-tumor effects in murine lymphoma models. The present study is to explore HBV-specific CTL priming and its cytolytic activities of nicotine-treated murine DCs, the mechanism of α7 nicotinic acetylcholine receptor (nAChR) up-regulation by nicotine and the efficiency of nicotine with other cytokines. To address these hypotheses, bone marrow-derived imDCs were stimulated by nicotine and expression of α7 nAChR was firstly determined by flow cytometry and Western blot.

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The reported effects of nicotine on dendritic cells (DCs) are controversial. To investigate the factors which determine the effects of nicotine on DCs, immature dendritic cells (imDCs) induced from murine bone marrow were treated with different doses of nicotine with or without lipopolysaccharides (LPS). The morphology and expression of the co-stimulatory molecules CD80, CD86, CD40 and CD54 were observed and determined by microscopy and flow cytometry, respectively.

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A nitrogen-fixing bacterium, designated strain Be17(T), was isolated from rhizosphere soil of Begonia semperflorens planted in Beijing Botanical Garden, PR China. Phylogenetic analyses based on a segment of the nifH gene sequence and a full-length 16S rRNA gene sequence revealed that strain Be17(T) was a member of the genus Paenibacillus. High levels of 16S rRNA gene sequence similarity were found between strain Be17(T) and Paenibacillus graminis RSA19(T) (97.

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A nitrogen-fixing bacterium, designated strain S27(T), was isolated from rhizosphere soil of Sophora japonica. Phylogenetic analysis based on a fragment of the nifH gene and the full-length 16S rRNA gene sequence revealed that strain S27(T) is a member of the genus Paenibacillus. High levels of 16S rRNA gene sequence similarity were found between strain S27(T) and Paenibacillus durus DSM 1735(T) (97.

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The ethylene-forming enzyme gene (efe) from Pseudomonas syringae pv. glycinea was transferred into Pseudomonas putida KT2440 by recombination at five of the seven 16S rDNA sites. PCR analysis demonstrated that strains DC1, DC2 and DC3 contained three, four and five copies of efe, respectively.

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