No abstract

There is a distinct increase in the risk of heart disease in people exposed to ionizing radiation (IR). Radiation-induced heart disease (RIHD) is one of the adverse side effects when people are exposed to ionizing radiation. IR may come from various forms, such as diagnostic imaging, radiotherapy for cancer treatment, nuclear disasters, and accidents. However, RIHD was mainly observed after radiotherapy for chest malignant tumors, especially left breast cancer. Radiation therapy (RT) has become one of the main ways to treat all kinds of cancer, which is used to reduce the recurrence of cancer and improve the survival rate of patients. The potential cause of radiation-induced cardiotoxicity is unclear, but it may be relevant to oxidative stress. Oxidative stress, an accumulation of reactive oxygen species (ROS), disrupts intracellular homeostasis through chemical modification and damages proteins, lipids, and DNA; therefore, it results in a series of related pathophysiological changes. The purpose of this review was to summarise the studies of oxidative stress in radiotherapy-induced cardiotoxicity and provide prevention and treatment methods to reduce cardiac damage.

Atherosclerosis is still the major cause of morbidity and mortality all over the world. Recently, it has been reported increased levels of tissue iron increase the risk of atherosclerosis. However, the detailed mechanism of iron‐induced atherosclerosis progression is barely known. Here, we used apoE‐deficient mice models to investigate the effects of low iron diet (<0 mg iron carbonyl/kg), high iron diet (25,000 mg iron carbonyl/kg) on atherosclerosis in vivo. As exhibited, we observed that CD68 was significant enriched by high iron diet in apoE‐deficient mice. In addition, transforming growth factor β, tumor necrosis factor α, interleukin 6 (IL‐6), IL‐23, IL‐10, and IL‐1β levels were also greatly induced by high iron diet. Then, we found that the iron load promoted the inflammation response in macrophages. Moreover, macrophage polarization is a process by which macrophage can express various functional programs in activating macrophages. Here, we observed that iron‐load macrophages were polarized toward a proinflammatory macrophage phenotype. The polarization of M1 macrophage was promoted by ferric ammonium citrate (FAC) in bone marrow derived macrophages (BMDMs). Furthermore, ECAR and cellular OCR in BMDM with or without FAC was examined. As shown, BMDM indicated with 50 μM FAC showed a significant increase in basic state and maximal ECAR in contrast to the control group. However, there was no significant difference in OCR. This indicated that the glycolysis was involved in the polarization of M1 macrophage triggered by iron‐load. In conclusion, we indicated that the iron load exacerbates the progression of atherosclerosis via inducing inflammation and enhancing glycolysis in macrophages.

Hypoxia/reoxygenation (H/R)‐induced myocardial cell injury is the main cause of acute myocardial infarction (AMI). Many proofs show that circular RNA plays an important role in the development of AMI. The purpose of this study was to investigate the role of circSAMD4A in H/R‐induced myocardial injury. The levels of circular SAMD4A (circSAMD4A) were detected in the heart tissues of AMI mice and H/R‐induced H9C2 cells, and the circSAMD4A was suppressed in AMI mice and H/R‐induced H9C2 cells to investigate its’ function in AMI. The levels of circSAMD4A and miR‐138‐5p were detected by real‐time quantitative PCR, and MTT assay was used to detect cell viability. TUNEL analysis and Annexin V‐FITC were used to determine apoptosis. The expression of Bcl‐2 and Bax proteins was detected by Western blot. IL‐1β, TNF‐α and IL‐6 were detected by ELISA kits. The study found that the levels of circSAMD4A were up‐regulated after H/R induction and inhibition of circSAMD4A expression would reduce the H/R‐induced apoptosis and inflammation. MiR‐138‐5p was down‐regulated in H/R‐induced H9C2 cells. circSAMD4A was a targeted regulator of miR‐138‐5p. CircSAMD4A inhibited the expression of miR‐138‐5p to promote H/R‐induced myocardial cell injury in vitro and vivo. In conclusion, CircSAMD4A can sponge miR‐138‐5p to promote H/R‐induced apoptosis and inflammatory response.

Long intergenic nonprotein coding RNA p53‐induced transcript (LINC‐PINT) has been reported to participate in various cancers. Here, we investigated the effects of LINC‐PINT on lung cancer progression. Firstly, in our study, we implied that LINC‐PINT was obviously decreased in NSCLC. Thereafter, in A549 and H1299 cells, LINC‐PINT was upregulated via transfecting LV‐LINC‐PINT. As exhibited, LINC‐PINT repressed cell proliferation and cell colony formation of A549 and H1299 cells. Subsequently, flow cytometry evidenced that A549 and H1299 cell apoptosis was obviously triggered and the cell cycle was arrested in G1 phase. Then, migration and transwell invasion experiments were carried out to detect the cell migration and invasion capacity. We found A549 and H1299 cell migration and invasion capacity were restrained by the upregulation of LINC‐PINT. Meanwhile, we predicted that miR‐543 could function as the target of LINC‐PINT and the association was verified. Moreover, we exhibited that miR‐543 was remarkably increased in lung cancer, which could be regulated by LINC‐PINT negatively. Furthermore, PTEN could act as the downstream target of miR‐543 and upregulation of miR‐543 repressed PTEN, which was reversed by LV‐PINT in A549 and H1299 cells. Finally, xenografts were utilized to confirm the function of LINC‐PINT on lung cancer. All these findings concluded that LINC‐PINT exerted crucial biological roles in NSCLC through sponging miR‐543 and inducing PTEN.

No abstract

No abstract

Atherosclerosis is the main cause of cardiovascular disease. Systemic inflammation is one important characteristic in atherosclerosis. Pro-inflammatory macrophages can secrete inflammatory factors and promote the inflammation of atherosclerosis. It has a great value for the treatment of atherosclerosis by inhibiting the release of inflammatory factors in macrophages. However, the detailed mechanism of this process is still unclear. In this study, we constructed an APOE -/- mice model of atherosclerosis to research the molecular mechanism of atherosclerosis. Protein tyrosine phosphatase non-receptor type 2 ( PTPN2 ), an anti-inflammatory gene, was dramatically decreased in inflammatory mice. Deletion of PTPN2 could significantly induce monocytes toward M1 phenotype of macrophages, enhance the secretion of IL-12 and IL-1, and promote cell proliferation, invasion and metastasis. Mechanism research showed that PTPN2 -mediated p65/p38/STAT3 de-phosphorylation could block the process of macrophage inflammation. In vivo experiments showed that PTPN2 may effectively inhibit the inflammatory response during atherosclerosis. In conclusion, we uncovered the negative role of PTPN2 in the occurrence of atherosclerosis, and this study provides a new potential target for atherosclerosis treatment.