China
Africa
Explore chapters and articles related to this topic
Inflammatory Responses Acquired Following Environmental Exposures Are Involved in Pathogenesis of Musculoskeletal Pain
Published in Kohlstadt Ingrid, Cintron Kenneth, Metabolic Therapies in Orthopedics, Second Edition, 2018
Ritchie C. Shoemaker, James C. Ryan
In 2017, Zhang [50] extends this research, but as opposed to Yamasaki, this paper showed that mice without miR-146a had far less cartilage degeneration. This paper also showed that miR 146a “aggravated pro-inflammatory cytokines induced suppressing the expression of cartilage matrix-associated genes,” especially targeting two specific genes, Camk2d and Ppp3r2. More importantly, miR-146a has a crucial role in cartilage homeostasis: inhibitors ameliorated OA.
LncRNA ANRIL protects against oxygen and glucose deprivation (OGD)-induced injury in PC-12 cells: potential role in ischaemic stroke
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Long non-coding RNAs (lncRNAs) are reported to play important roles in regulation of gene transcription in diverse biological processes, such as apoptosis, invasion, histone modification, regulation of mRNA splicing and as a sink for some miRNAs [6–9]. Importantly, lncRNAs, which are also abundant in the central nervous system, have been implicated in brain development [10]. Although the expression and functions of lncRNAs in stroke and neuroprotection remain not to be clarified [11], increasing evidence have prove that lncRNAs are closely involved in IS, such as maternally expressed gene 3 (MEG3), H19, CaMK2D-associated transcript 1 (C2dat1), Fos downstream transcript (FosDT), small nucleolar RNA host gene 14 (SNHG14), and taurine-upregulated gene 1 (TUG1) which have been found to affect cell apoptosis, inflammation, cell death, and angiogenesis in IS [12]. For example, previous study reported that lncRNA antisense non-coding RNA in the INK4 locus (ANRIL) has been related with a higher risk of developing cardiovascular events and ANRIL was demonstrated to be associated with IS [13]. Meanwhile, ANRIL was reported to play a role in inflammatory responses and atherosclerosis [13,14]. Moreover, one former study demonstrated that lncRNA ANRIL altered the expressions of vascular endothelial growth factor (VEGF) and apromoted ngiogenesis in rats [15], which provided potential effects of ANRIL in IS. Based on these valuable findings reported by previous studies, we aimed to explore the potential roles of lncRNA ANRIL in IS cells.
Hirsutine ameliorates myocardial ischemia-reperfusion injury through improving mitochondrial function via CaMKII pathway
Published in Clinical and Experimental Hypertension, 2023
Wen Jiang, Yuxiang Zhang, Wei Zhang, Xiaomei Pan, Jieyu Liu, Qiang Chen, Junhui Chen
Hirsutine was purchased from Must Biotechnology Company, Chengdu, China. The TUNEL Cell Apoptosis Detection Kit-POD was obtained from Boster, Wuhan, China. Hematoxylin and eosin (H&E) staining kit, Western and IP cell lysates, ROS detection kit and ATP content assay kit were obtained from Beyotime, Jiangsu, China. Kits for detecting the activity of mitochondrial complex I ~ IV were purchased from Solarbio, Beijing, China. The MitoSOX red for measurement of mitochondrial ROS was from Invitrogen, Waltham, MA, USA. TTC dyeing and kits for measurement of LDH, SOD, and MDA were obtained from the Nanjing Jiancheng Bioengineering Institute, Nanjing, China. Evans blue, succinate dehydrogenase activity kit and succinate kit were purchased from Sigma Aldrich, St Louis, MO, USA. Recombinant anti-DRP1 antibody (ab184247), recombinant anti-DRP1 (phosphor S637) antibody (ab193216), recombinant anti-Mitofusin 2 antibody (ab124773), recombinant anti-AKT (phosphor T308) antibody (ab38449), recombinant anti-CaMKII alpha + CaMKII beta (phosphor T286) antibody (ab124880), recombinant anti-p38 antibody (ab170099), recombinant anti-p38 (phosphor T180 + Y182) antibody (ab4822), Goat Anti-Rabbit IgG H&L (HRP) (ab205718) and goat anti-mouse IgG H&L (HRP) (ab205719) were purchased from Abcam, Cambridge, United Kingdom. Rabbit Anti-CAMK2A + CAMK2B + CAMK2D antibody (bs-0541 R), Rabbit Anti-AKT1 + 2 + 3 antibody (bs-6951 R), Mouse Anti-Bax antibody (bs-0127 M), Rabbit Anti-Bcl-2 antibody (bs-0032 R), Rabbit Anti-ASK1 antibody (bs-1425 R), Rabbit Anti-phospho-ASK1 (Thr845) antibody (bs-3031 R) and Mouse Anti-Active Caspase-3 antibody (bsm -33 199 M) were obtained from Bioss, Beijing, China. Beta-actin antibody was purchased from Sino Biological, Beijing, China.
Neuroinflammation after ischemic stroke involves INPP5D expression mediated by the TMPO-AS1-PU.1 complex
Published in Neurological Research, 2023
Wenhui Luan, Zhongwen Sun, Chunmei Wu, Manli Tao, Xiaoqian Shen
Ischemic stroke is one of the main causes of adult morbidity and death. It is a huge health challenge worldwide. There is an urgent need to better understand the molecular pathogenesis of stroke and develop new treatments for neuronal ischemic injury strategy [18]. LncRNA plays a key role in different types of diseases. In recent years, new technologies such as RNA-seq, deep sequencing, and microarray have been used to screen a large number of abnormally expressed lncRNAs in patients with ischemic stroke or animals with ischemic injury. Specifically, the antisense non-coding RNA, CaMK2D-related transcript 1, maternally expressed gene 3, taurine up-regulated gene 1, Small nucleolar RNA host gene 14, nuclear enriched abundant transcript 1 and Fos downstream transcript were found to be up-regulated in cerebral ischemic animals or hypoxic glucose (OGD) cells, and affect cell apoptosis, inflammation, cell death and angiogenesis during ischemic stroke [19–21]. TMPO-AS1 has been identified as an oncogene that promotes the progression of a variety of cancers, including bladder cancer [22], liver cancer [23], retinoblastoma [24] and glioma [25], etc. and its role in ischemic stroke has not been clearly reported. In this study, we found that the expression of TMPO-AS1 was significantly increased in the plasma of patients with acute ischemic stroke, MCAO/R mouse models, and BV2 microglia cultured after OGD stimulation. After the interference of TMPO-AS1, microglia pro-inflammatory markers, including the secretion of inflammatory factors TNF-α, IL-6 and IL-1β, ROS production and iNOS mRNA level were significantly reduced, while the anti-inflammatory markers Arg1 and CD206 mRNA levels were significantly increased. It can be seen that sh-TMPO-AS1 treatment could inhibit OGD/R-induced microglia activation and promote the transformation of microglia phenotype from M1 to M2.