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As mechanoreceptors, cells can sense and transmit mechanical forces exerted on their surfaces, meanwhile adjust their own mechanical properties to maintain stability. The mechanical force is transferred from cell surface or cytoplasm to the nucleus depending on the complete cytoskeletal system. This cytoskeletal system consists of cytoplasmic skeleton and nuclear skeleton, and these two parts are connected mechanically by the LINC complex (linker of nucleoskeleton and cytoskeleton complex), which plays an important role in cellular mechanotransduction. This review discusses the basic structure of mechanical transmission part in LINC complex and the changes in the nuclear morphology, the location of transcription factor, and the spatial conformation of chromatin induced by mechanotransduction, so as to lay a foundation for further exploring the role of LINC complex in cell mechanotransduction and gene expression.
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Objective To explore the link between the expression of long non-coding RNA(lncRNA)metastasis associated lung adenocarcinoma transcript 1(MALAT1)and IL-6/signal trans ducers and activators of transcription 3(STAT3)signaling pathway in isoniazid induced rats liver injury. Methods Fifty-six specific pathogen-free(SPF)SD rats were randomly divided into experimen?tal group(48 rats)and control group(8 rats),each with half females and half males. The rats in experimental group were given isonia?zid of 63 mg/(kg·d)for 3,7,10,14,21 and 28 d,with 8 rats at the same time point of each day. The rats in control group were giv?en distilled water by intragastric administration. Serum levels of ALT and AST were measured by automatic biochemical analyzer;SYBR green real-time polymerase chain reaction was used to test the expression level of lncRNA MALAT1 and IL-6/STAT3 mRNA in the liver. Results Liver tissue injury occurred after 7 days and worsened with the extention of administration time. Compared with the rats in the control group,the expression level of lncRNA MALAT1 and IL-6/STAT3 mRNA as well as ALT and AST showed a trend of increase(P<0.01). The expression of ALT,AST and lncRNA MALAT1 declined at different degrees on 28(P<0.05). LncRNA MALAT1 and IL-6/STAT3 mRNA expression levels were positively correlated(P<0.01). LncRNA MALAT1 and IL-6/STAT3 mRNA expression levels had a positive correlation with the contents of ALT and AST(P<0.01). Conclusion The expression level of lncRNA MALAT1 in isoniazid induced liver injury rat models showed an abnormal rising trend,and the positive detection time preceded that of ALT and AST. The mechanism may be related to the activation of IL-6/STAT3 signaling pathway.
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<p><b>OBJECTIVE</b>To investigate the effects of nano-lead exposure on learning and memory and iron homeostasis in the brain of the offspring rats on postnatal day 21 (PND21) and postnatal day 42 (PND42).</p><p><b>METHODS</b>Twenty adult pregnant female Sprague-Dawley rats were randomly divided into control group and nano-lead group. Rats in the nano-lead group were orally administrated 10 mg/kg nano-lead, while rats in the control group were administrated an equal volume of normal saline until PND21. On PND21, the offspring rats were weaned and given the same treatment as the pregnant rats until 42 days after birth. The learning and memory ability of offspring rats on PND21 and PND42 was evaluated by Morris water maze test. The hippocampus and cortex s amples of offspring rats on PND21 and PND42 were collected to determine iron and lead levels in the hippocampus and cortex by inductively coupled plasma-mass spectrometry. The distributions of iron in the hippocampus and cortex were observed by Perl's iron staining. The expression levels of ferritin, ferroportin 1 (FPN1), hephaestin (HP), and ceruloplasmin (CP) were measured by enzyme-linked immunosorbent assay.</p><p><b>RESULTS</b>After nano-lead exposure, the iron content in the cortex of offspring rats on PND21 and PND42 in the nano-lead group was significantly higher than those in the control group (32.63 ± 6.03 µg/g vs 27.04 ± 5.82 µg/g, P<0.05; 46.20 ±10.60 µg/g vs 36.61 ± 10.2µg/g, P<0.05). The iron content in the hippocampus of offspring rats on PND42 in the nano-lead group was significantly higher than that in the control group (56.9 ± 4.37µg/g vs 37.71 ± 6.92µg/g, P<0.05). The Perl's staining showed massive iron deposition in the cortex and hippocampus in the nano-lead group. FPNl level in the cotfex of offspring rats on PND21 in the nano-lead group was significantly lower than that in the control group (3.64 ± 0.23 ng/g vs 4.99 ± 0.95 ng/g, P<0.05). FPN1 level in the hippocampus of offspring rats on PND42 in the nano-lead group was significantly lower than that in the control group (2.28 ± 0.51 ng/g vs 3.69 ± 0.69 ng/g, P<0.05). The escape latencies of offspring rats on PND21 and PND42 in the nano-lead group were longer than those in the control group (15.54 ± 2.89 s vs 9.01 ± 4.66 s; 6.16 ± 1.42 s vs 4.26 ± 1.51 s). The numbers of platform crossings of offspring rats on PND21 and PND42 in the nano- lead group were significantly lower than those in the control group (7.77 ± 2.16 times vs 11.2 ± 1.61 times, P<0.05; 8.12 ± 1.51 times vs 13.0 ± 2.21 times, P<0.05).</p><p><b>ONCLUSION</b>n Nano-lead exposure can result in iron homeostasis disorders in the hippocampus and cortex of offspring rats and affect their learning and memory ability.</p>
Subject(s)
Animals , Female , Pregnancy , Rats , Cerebral Cortex , Metabolism , Hippocampus , Metabolism , Homeostasis , Iron , Metabolism , Lead , Toxicity , Learning , Maternal Exposure , Memory , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>To establish a method for determining cyanamide in workplace air by high-performance liquid chromatography (HPLC).</p><p><b>METHODS</b>Air samples were collected from the workplace using the shock absorption tube containing water solution at a rate of 2.8∼3.0 ml/min for 60 min; dansyl chloride was used as a derivatization reagent to conduct pre-column derivatization, and the procedure was as follows: acetone solution (2.5 ml), mixed solution (1.0 ml) containing 0.016 mol/L Na2CO3 and 0.184 mol/L NaHCO3, and 10 mg/ml acetone solution of dansyl chloride (0.5 ml) were added into the samples, and reaction proceeded in a water bath (50 °C) for 1 h. HPLC was performed on an ODS C18 column (250 mm × 4.6 mm, 5 üm) with a mobile phase of acetonitrile-phosphate buffer (35:65) at a flow rate of 1.0 ml/min and a column temperature of 25°C; a fluorescence detector was used at an excitation wavelength of 360 nm and an emission wavelength of 495 nm.</p><p><b>RESULTS</b>The minimum detectable concentration of cyanamide was 0.05 üg/ml; a good linear relationship was noted when the concentration of cyanamide was 0.2∼100.0 üg/ml; the intraday relative standard deviation (RSD) was 0.28%∼1.18%, and the interday RSD was 0.22∼2.16%; the recovery rate was 95.7%∼103.0%, and the sampling efficiency was 95.8%∼96.9%. Water solution of cyanamide (pH<6.5) could be stable in the dark at room temperature for 7 d.</p><p><b>CONCLUSION</b>This method is stable, reliable, easy to operate, and highly sensitive and suitable for determination of cyanamide in workplace air.</p>