Effect of palmitoleic acid on the differentiation of bovine skeletal muscle satellite cells

( Junfang Zhang ),( Qiang Li ),( Kim Margarette Corpuz Nogoy ),( Jianfu Sun ),( Bin Sun ),( Ying Wang ),( Lin Tang ),( Jia Yu ),( Xin Jin ),( Xiangzi Li ),( Seong-Ho Choi ) 한국축산학회 2021 한국축산학회지 Vol.63 No.4

We hypothesized that the unsaturated fatty acid palmitoleic acid (POA) could promote the expression of adipogenic/lipogenic genes in bovine skeletal muscle satellite cells (BSCs). The BSCs were cultured in a growth medium containing 10% fetal bovine serum. When the cells reached 80%-90% confluence, we used the differentiation medium with 5% horse serum for differentiation for 96 h. The differentiation medium contained 50 μM, 100 μM and 200 μM POA. Control BSC were cultured only in differentiation media. Compared with the control BSC, the POA BSC significantly up-regulated the expression of paired box 3 (Pax3) and paired box 7 (Pax7) and down-regulated myogenin gene expression (p < 0.01), which indicates a depression in muscle fiber development. However, all POA treatments up-regulated the expression of the adipocyte transcription factors peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding protein alpha and beta (C/EBP α and C/EBP β), and other genes (p < 0.01) and increased the expression of PAT-family proteins and the concentration of adiponectin in the media. These results indicate that POA can convert part of BSCs into adipocytes.

Interface contact pressure-based virtual gradient material model for the dynamic analysis of the bolted joint in machine tools

Jingping Liao,Jianfu Zhang,Pingfa Feng,Dingwen Yu,Zhijun Wu 대한기계학회 2016 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.30 No.10

Bolted joints have significant influence on the dynamic characteristic of the machine tool assembly. This study proposes a new modeling method using virtual gradient material. On the basis of Hertz contact theory and fractal geometry theory, the relationship between contact stiffness and normal contact load is deduced. The contact pressure distribution at the interface is obtained through finite element contact analysis. An orthogonal material model is introduced to describe the properties of virtual material. The virtual material is divided into several layers, and the elastic modulus and shear modulus in each sub-layer are derived based on Hooke’s Law. Both experimental and theoretical results for a bolted lap structure are obtained. The experimental results are compared with theoretical ones in terms of qualitative comparison of similar mode shapes and quantitative comparison of corresponding natural frequencies. The comparison shows that the theoretical first three-order vibration mode shapes are in good line with the experimental ones. The relative errors of corresponding natural frequencies between the virtual gradient material model and the experiment are less than 9%, which are smaller than those between the traditional virtual uniform material model and the experiment. The proposed virtual gradient material method would be useful to accurately model the bolted joint in CNC machine tools.

NEDD8-activating enzyme inhibitor, MLN4924 (Pevonedistat) induces NOXA-dependent apoptosis through up-regulation of ATF-4

Liu, Xiaojun,Jiang, Yanan,Wu, Jianfu,Zhang, Wenjuan,Liang, Yupei,Jia, Lijun,Yu, Jinha,Jeong, L.S.,Li, Lihui Elsevier 2017 Biochemical and biophysical research communication Vol. No.

<P><B>Abstract</B></P> <P>It has been reported that MLN4924 can inhibit cell growth and metastasis in various kinds of cancer. We have reported that MLN4924 is able to inhibit angiogenesis through the induction of cell apoptosis both in vitro and in vivo models. Moreover, Neddylation inhibition using MLN4924 triggered the accumulation of pro-apoptotic protein NOXA in Human umbilical vein endothelial cells (HUVECs). However, the mechanism of MLN4924-induced NOXA up-regulation has not been addressed in HUVECs yet. In this study, we investigated how MLN4924 induced NOXA expression and cellular apoptosis in HUVECs treated with MLN4924 at indicated concentrations. MLN4924-induced apoptosis was evaluated by Annexin V-FITC/PI analysis and expression of genes associated with apoptosis was assessed by Quantitative RT-PCR and western blotting. As a result, MLN4924 triggered NOXA-dependent apoptosis in a dose-dependent manner in HUVECs. Mechanistically, inactivation of Neddylation pathway caused up-regulation of activating transcription factor 4 (ATF-4), a substrate of Cullin-Ring E3 ubiquitin ligases (CRL). NOXA was subsequently transactivated by ATF-4 and further induced apoptosis. More importantly, knockdown of ATF-4 by siRNA significantly decreased NOXA expression and apoptotic induction in HUVECs. In summary, our study reveals a new mechanism underlying MLN4924-induced NOXA accumulation in HUVECs, which may help extend further study of MLN4924 for angiogenesis inhibition treatment.</P> <P><B>Highlights</B></P> <P> <UL> <LI> MLN4924 triggered NOXA-dependent apoptosis in a dose-dependent manner in HUVECs. </LI> <LI> Inactivation of neddylation caused up-regulation of ATF4, a substrate of CRL. </LI> <LI> NOXA was transactivated by ATF4 and further induced apoptosis. </LI> <LI> Knockdown of ATF-4 significantly decreased NOXA expression and apoptotic induction. </LI> <LI> We revealed a new mechanism underlying MLN4924-induced NOXA accumulation in HUVECs. </LI> </UL> </P>

Genome-wide single-nucleotide polymorphism data and mitochondrial hypervariable region 1 nucleotide sequence reveal the origin of the Akhal-Teke horse

Zhoucairang Kang,Jinping Shi,Ting Liu,Yong Zhang,Quanwei Zhang,Zhe Liu,Jianfu Wang,Shuru Cheng Asian Australasian Association of Animal Productio 2023 Animal Bioscience Vol.36 No.10

Objective: The study investigated the origin of the Akhal-Teke horse using genome-wide single-nucleotide polymorphism (SNP) data and mitochondrial hypervariable region 1 (HVR-1) nucleotide sequences Methods: Genome-wide SNP data from 22 breeds (481 horses) and mitochondrial HVR-1 sequences from 24 breeds (544 sequences) worldwide to examine the origin of the Akhal-Teke horse. The data were analyzed using principal component analysis, linkage disequilibrium analysis, neighbor-joining dendrograms, and ancestry inference to determine the population relationships, ancestral source, genetic structure, and relationships with other varieties. Results: A close genetic relationship between the Akhal-Teke horse and horses from the Middle East was found. Analysis of mitochondrial HVR-1 sequences showed that there were no shared haplotypes between the Akhal-Teke and Tarpan horses, and the mitochondrial data indicated that the Akhal-Teke horse has not historically expanded its group. Ancestral inference suggested that Arabian and Caspian horses were the likely ancestors of the Akhal-Teke horse. Conclusion: The Akhal-Teke horse originated in the Middle East.

Neuroprotective Effects of Luteolin Against Spinal Cord Ischemia–Reperfusion Injury by Attenuation of Oxidative Stress, Inflammation, and Apoptosis

Jian Fu,Haibin Sun,Yongzhe Zhang,Wei Xu,Chuan Wang,Yanwei Fang,Jianhui Zhao 한국식품영양과학회 2018 Journal of medicinal food Vol.21 No.1

Luteolin (LU) is a widely distributed flavonoid with multitarget effects. The objective of this study was to determine whether LU could reduce the ischemia–reperfusion injury of the spinal cord (SCII) in a rat model. Forty-eight rats were divided into four groups: sham, SCII, SCII+L-LU (50 mg/kg), and SCII+H-LU (100 mg/kg). Abdominal aortic occlusion was carried out for 40 min in all groups. Hindlimb motor functions were evaluated using the Tarlov scoring system. Nissl and terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end labeling (TUNEL) staining were used to detect cell survival and apoptosis in the spinal cord. Spinal cord samples were taken for determination of malondialdehyde, xanthine oxidase, superoxide dismutase, and glutathione peroxidase activities. The levels of tumor necrosis factor-α, interleukin (IL)-1β, and IL-18 were assessed using ELISA kits to examine the inflammatory responses in the spinal cord. Western blot analysis was used to examine the expression of nuclear factor erythroid 2-related factor (Nrf2) and nod-like receptor pyrin domain-containing 3 protein (NLRP3) levels. We found that LU pretreatment significantly improved the locomotor function of rats after SCII, increased neuron survival, and inhibited apoptosis in the spinal cord. Furthermore, the oxidative stress and inflammatory response were significantly suppressed upon treatment with LU. Finally, LU upregulated Nrf2 levels and downregulated NLRP3 protein expression in SCII tissues. Thus, LU exhibited a neuroprotective effect following SCII by alleviating oxidative stress and inhibiting inflammatory responses and cell apoptosis. The possible mechanism may be related to the activation of Nrf2 and inhibition of NLRP3 inflammasome pathway.

Luteolin Modulates the NF-E2-Related Factor 2/Glutamate–Cysteine Ligase Pathway in Rats with Spinal Cord Injury

Jian Fu,Wei Xu,Yongzhe Zhang,Haibin Sun,Jianhui Zhao 한국식품영양과학회 2021 Journal of medicinal food Vol.24 No.3

Spinal cord ischemia–reperfusion injury (SCII) easily causes unalterable neurological deficits. We previously demonstrated that the flavonoid luteolin (LU) has strong antioxidant, anti-inflammatory, and other neuroprotective efficacies against SCII. In our current study, we examined the contributions of the NF-E2-related factor 2 (Nrf2)/glutamate–cysteine ligase (GCL) pathway to LU-mediated neuroprotection in the transient abdominal aorta occlusion rat model of SCII. Rats were divided into four groups: Sham surgery, SCII alone, SCII plus LU pretreatment (SCII + LU), and SCII plus cotreatment with LU and the Nrf2 inhibitor ML385 (SCII + LU + ML385). The Basso–Beattie–Bresnahan (BBB) scale was used to assess neurological function, hematoxylin and eosin staining to evaluate pathological change to the spinal cord, and enzyme-linked immunosorbent assay to measure tissue markers of oxidative stress and inflammation induced by SCII. Mitochondrial injury and apoptosis were examined by flow cytometry and expression levels of Nrf2, GCL catalytic subunit (GCLc), and GCL modifier subunit (GCLm) by real-time quantitative polymerase chain reaction. LU pretreatment significantly enhanced recovery of motor function as evidenced by the BBB score and attenuated the pathological damage. Furthermore, LU effectively enhanced the antioxidative activity, alleviated mitochondrial swelling, decreased the expression levels of several proinflammatory cytokines after SCII, and significantly upregulated Nrf2, GCLc, and GCLm expression levels. Cotreatment with ML385 reversed all these protective effects of LU except the anti-inflammatory response. Collectively, these findings indicate that the neuroprotective efficacy of LU depends on suppression of oxidative stress and preservation of mitochondrial function through signaling pathways involving Nrf2 activation and downstream gene expression.