Publications by authors named "Yuming Kang"

5 Publications

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MiR-506-3p Promotes the Proliferation and Migration of Vascular Smooth Muscle Cells via Targeting KLF4.

Pathobiology 2021 Apr 21:1-12. Epub 2021 Apr 21.

Department of Physiology & Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Xi'an, China.

Background: The dysregulation of proliferation and migration of vascular smooth muscle cells (VSMCs) is one of the major causes of atherosclerosis (AS). Accumulating studies confirm that Kruppel-like factor 4 (KLF4) can regulate the proliferation and differentiation of VSMCs through multiple signaling pathways. However, the mechanism of KLF4 dysregulation remains unknown.

Methods: Apolipoprotein E-knockout (ApoE-/-) mice and human VSMCs were used to establish AS animal model and cell model, respectively. qRT-PCR was employed to determine the expressions of miR-506-3p and KLF4. Cell Counting Kit -8, Transwell, TUNEL assays, and flow cytometry were performed to measure the proliferation, migration, and apoptosis of VSMCs. The upstream miRNAs of KLF4 were predicted by microT, miRanda, miRmap, and TargetScan databases. The interaction between KLF4 and miR-506-3p was confirmed using qRT-PCR, Western blot, and luciferase reporter gene assay.

Results: KLF4 expression was significantly decreased in the VSMCs of ApoE-/- mice fed with high-fat diet and in human VSMCs treated with oxidized low-density lipoprotein in time-dependent and dose-dependent manners. The transfection of miR-506-3p mimics or KLF4 shRNA promoted the proliferation and migration of VSMCs but inhibited the apoptosis while miR-506-3p inhibitors and pcDNA3.1-KLF4 exerted opposite effects. Additionally, KLF4 was confirmed as a target gene of miR-506-3p and could be negatively regulated by miR-506-3p.

Conclusion: MiR-506-3p can promote the proliferation and migration of VSMCs via targeting KLF4, which can probably contribute to the pathogenesis of AS.
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http://dx.doi.org/10.1159/000513506DOI Listing
April 2021

Activation of the TLR4/MyD88 signaling pathway contributes to the development of human hepatocellular carcinoma via upregulation of IL-23 and IL-17A.

Oncol Lett 2018 Jun 26;15(6):9647-9654. Epub 2018 Apr 26.

Department of Pathogen Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.

Toll-like receptor 4 (TLR4) and the interleukin (IL)-23/IL-17A axis serve an important role in tumor immunology. In the present study, the activation of the TLR4/myeloid differentiation primary response 88 (MyD88)-mediated signal transduction pathway in human hepatocellular carcinoma (HCC) cells was examined using immunohistochemistry, and the association between TLR4 expression and the IL-23/IL-17A axis was detected by ELISA, reverse transcription-quantitative polymerase chain reaction and western blot analysis in order to determine whether TLR4 and IL-23/IL-17A serve a role in HCC. It was observed that TLR4 expression was upregulated in HCC tissues compared with that in adjacent normal tissues. In addition, the TLR4 expression level was correlated with the degree of tumor differentiation and TNM stage. The expression levels of IL-17A and IL-23, which are key mediators of inflammation that contribute to carcinogenesis, are correlated with TLR4 expression in HCC. Cell line studies further revealed that activation of TLR4/MyD88 upregulated the expression of IL-17A and IL-23 at the mRNA and protein levels. Furthermore, activation of TLR4/MyD88 enhanced the expression of TLR4. IL-17A and IL-23 expression levels in HCC also appeared to be correlated with the TNM stage and tumor metastasis. In conclusion, the current results suggested that the TLR4/MyD88 signaling pathway is involved in HCC cell proliferation and metastasis via regulation of the IL-23/IL-17A axis; thus, the TLR4/IL-23/IL-17A pathway may represent a novel therapeutic target in HCC.
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http://dx.doi.org/10.3892/ol.2018.8586DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6004652PMC
June 2018

Oleuropein improves mitochondrial function to attenuate oxidative stress by activating the Nrf2 pathway in the hypothalamic paraventricular nucleus of spontaneously hypertensive rats.

Neuropharmacology 2017 02 12;113(Pt A):556-566. Epub 2016 Nov 12.

Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Xi'an Jiaotong University Cardiovascular Research Center, Xi'an Jiaotong University, Xi'an 710061, China. Electronic address:

Hypertension is associated with increased reactive oxygen species (ROS) production in the paraventricular nucleus (PVN) of the hypothalamus. Oleuropein (OL) has a variety of biochemical roles, including antihypertensive and antioxidative functions. However, there have been few reports on the effects of OL on oxidative stress in the PVN on hypertension. In spontaneously hypertensive rats (SHR), eight-week administration of 60 mg/kg/day of OL significantly reduced blood pressure, pro-inflammatory cytokines and the expression of components of the renin-angiotensin system (RAS) compared with SHR rats treated with saline. Concomitantly, OL inhibited superoxide, and increased the antioxidant defense system in the PVN of SHR. We also found that OL increased mitochondrial biogenesis through mtDNA, PGC-1α, Complex II and Complex IV expression and regulated mitochondrial dynamics through the fusion-related protein Mfn2 and fision-related protein DRP1 to attenuate mitochondrial impairment. Furthermore, the phase II enzyme levels of Nrf2 and its downstream proteins NQO-1 and HO-1 were all markedly increased in the PVN of the OL-treated SHR group compared with the saline-treated SHR rats. Our findings demonstrate that OL administration can protect the PVN of the hypothalamus from oxidative stress by improving mitochondrial function through the activation of the Nrf2-mediated signaling pathway.
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http://dx.doi.org/10.1016/j.neuropharm.2016.11.010DOI Listing
February 2017

Pomegranate extract decreases oxidative stress and alleviates mitochondrial impairment by activating AMPK-Nrf2 in hypothalamic paraventricular nucleus of spontaneously hypertensive rats.

Sci Rep 2016 10 7;6:34246. Epub 2016 Oct 7.

Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology and Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.

High blood pressure, or "hypertension," is associated with high levels of oxidative stress in the paraventricular nucleus of the hypothalamus. While pomegranate extract is a known antioxidant that is thought to have antihypertensive effects, the mechanism whereby pomegranate extract lowers blood pressure and the tissue that mediates its antihypertensive effects are currently unknown. We have used a spontaneously hypertensive rat model to investigate the antihypertensive properties of pomegranate extract. We found that chronic treatment of hypertensive rats with pomegranate extract significantly reduced blood pressure and cardiac hypertrophy. Furthermore, pomegranate extract reduced oxidative stress, increased the antioxidant defense system, and decreased inflammation in the paraventricular nucleus of hypertensive rats. We determined that pomegranate extract reduced mitochondrial superoxide anion levels and increased mitochondrial function in the paraventricular nucleus of hypertensive rats by promoting mitochondrial biogenesis and improving mitochondrial dynamics and clearance. We went on to identify the AMPK-nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) pathway as a mechanism whereby pomegranate extract reduces oxidative stress in the paraventricular nucleus to relieve hypertension. Our findings demonstrate that pomegranate extract alleviates hypertension by reducing oxidative stress and improving mitochondrial function in the paraventricular nucleus, and reveal multiple novel targets for therapeutic treatment of hypertension.
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http://dx.doi.org/10.1038/srep34246DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5054377PMC
October 2016

Oleanolic acid induces apoptosis in human leukemia cells through caspase activation and poly(ADP-ribose) polymerase cleavage.

Acta Biochim Biophys Sin (Shanghai) 2007 Oct;39(10):803-9

Department of Histology and Embryology, Guangdong Medical College, Zhanjiang 524023, China.

It has been shown that Fructus Ligustri Lucidi (FLL), a promising traditional Chinese medicine, can inhibit the growth of tumors. However, the effective component and molecular mechanism of FLL act to inhibit tumor proliferation are unclear. In this study, we demonstrated that oleanolic acid (OA), a principal chemical component of FLL, inhibited the proliferation of human leukemia HL60 cells in culture. MTT assay showed that treatment of HL60 cells with FLL crude extracts or OA dramatically blocked the growth of target tumor cell in a time- and dose-dependent manner. Morphological changes of the nuclei and DNA fragmentation showed that apoptotic cell death occurred in the HL60 cells after treating with FLL extracts (20 mg/ml) or OA (3.65 x 10(-2) mg/ml). Furthermore, flow cytometry assay showed that treatment of HL60 cells with FLL or OA caused an increased accumulation of G(1) and sub-G(1) subpopulations. Western blot analysis showed that caspase-9 and caspase-3 were activated, accompanied by the cleavage of poly(ADP-ribose) polymerase (PARP) in the target cells during FLL- or OA-induced apoptosis. These results suggest that OA acts as the effective component of FLL by exerting its cytotoxicity towards target tumor cells through activation of caspases and cleavage of PARP.
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http://dx.doi.org/10.1111/j.1745-7270.2007.00335.xDOI Listing
October 2007