The identification of the expression patterns of long non-coding RNAs (lncRNAs) and mRNAs in the spinal cord under normal and cardiac ischemia/reperfusion (I/R) conditions is essential for understanding the genetic mechanisms underlying the pathogenesis of cardiac I/R injury. The present study used high-throughput RNA sequencing to investigate differential gene and lncRNA expression patterns in the spinal cords of rats during I/R-induced cardiac injury. Male Sprague Dawley rats were assigned to the following groups: i) Control; ii) 2 h (2 h post-reperfusion); and iii) 0.5 h (0.5 h post-reperfusion). Further mRNA/lncRNA microarray analysis revealed that the expression profiles of lncRNA and mRNA in the spinal cords differed markedly between the control and 2 h groups, and in total 7,980 differentially expressed (>2-fold) lncRNAs (234 upregulated, 7,746 downregulated) and 3,428 mRNAs (767 upregulated, 2,661 downregulated) were identified. Reverse transcription-quantitative polymerase chain reaction analysis was performed to determine the expression patterns of several lncRNAs. The results indicated that the expression levels of lncRNA NONRATT025386 were significantly upregulated in the 2 and 0.5 h groups when compared with those in the control group, whereas the expression levels of NONRATT016113, NONRATT018298 and NONRATT018300 were elevated in the 2 h group compared with those in the control group; however, there was no statistically significant difference between the 0.5 h and control groups. Furthermore, the expression of lncRNA NONRATT002188 was significantly downregulated in the 0.5 and 2 h groups when compared with the control group. The present study determined the expression pattern of lncRNAs and mRNAs in rat spinal cords during cardiac I/R. It was suggested that lncRNAs and mRNAs from spinal cords may be novel therapeutic targets for the treatment of I/R-induced cardiac injury.
The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has caused several outbreaks of highly contagious respiratory diseases worldwide. The respiratory symptoms of Coronavirus Disease-19 (COVID-19) have been closely monitored and studied, while the central nervous system (CNS) and peripheral system (PNS) lesions induced by COVID-19 have not received much attention. Currently, patients with COVID-19-associated encephalopathy present with dizziness, headache, anxiety and depression, stroke, epileptic seizures, the Guillain-Barre syndrome (GBS), and demyelinating disease. The exact pathologic basis for these neurological symptoms is currently not known. Rapid mutation of the SARS-CoV-2 genome leads to the appearance of SARS-CoV-2 variants of concern (VOCs), which have higher infectivity and virulence. Therefore, this narrative review will focus on the imaging assessment of COVID-19 and its VOC. There has been an increase in technologies, such as [18F]fluorodeoxyglucose positron emission tomography (18F-FDG-PET) and functional magnetic resonance imaging (fMRI), that have been used to observe changes in brain microstructure over time in patients with COVID-19 recovery. Medical imaging and pathological approaches aimed at exploring the associations between COVID-19 and its VOC, with cranial nerve and abnormal nerve discharge will shed light on the rehabilitation process of brain microstructural changes related to SARS-CoV-2, and aid future research in our understanding of the treatment and prognosis of COVID-19 encephalopathy.
There is now substantial evidence that myocardial ischemia-reperfusion (IR) injury affects the spinal cord and brain, and that interactions may exist between these two systems. In the present study, the spinal cord proteomes were systematically analyzed after myocardial IR injury, in an attempt to identify the proteins involved in the processes. The myocardial IR injury rat model was first established by cross clamping the left anterior descending coronary artery for 30-min ischemia, followed by reperfusion for 2 h, which resulted in a significant histopathological and functional myocardial injury. Then using the stable isotope dimethyl labeling quantitative proteomics strategy, a total of 2,362 shared proteins with a good distribution and correlation were successfully quantified. Among these proteins, 33 were identified which were upregulated and 57 were downregulated in the spinal cord after myocardial IR injury, which were involved in various biological processes, molecular function and cellular components. Based on these proteins, the spinal cord protein interaction network regulated by IR injury, including apop-tosis, microtubule dynamics, stress-activated signaling and cellular metabolism was established. These heart-spinal cord interactions help explain the apparent randomness of cardiac events and provide new insights into future novel therapies to prevent myocardial I/R injury.
Contrast‐induced nephropathy (CIN) is a common complication with adverse outcome after iodinated‐contrast injection, yet still lacking effective medication. Heme oxygenase‐1 (HO‐1) has been reported to play an important role against renal injuries. Hemin, a HO‐1 inducer and anti‐porphyria medicine, may have a promising effect against CIN. In this study, we aim to investigate the effect of hemin on CIN model and the underlying molecular mechanisms in human proximal tubule epithelial cells (HK‐2). To mimic a common condition in percutaneous coronary intervention (PCI) patients, CIN was induced by intravenous iopromide in high‐fat fed diabetic rats. We found hemin, given right before iopromide, mitigated CIN with enhanced antioxidative capacity and reduced oxidative stress. HK‐2 cells insulted by iopromide demonstrated decreased cell vitality and rising reactive oxygen species (ROS), which could also be inhibited by hemin. The effects of hemin involved a key molecule in ferroptosis, glutathione peroxidase (GPX4), whose down‐expression by small interfering RNA (siRNA) reversed the effect of hemin on HK‐2 cells. Furthermore, hemin's induction of GPX4 involved HO‐1 and nuclear factor erythroid 2‐related factor 2 (Nrf2). Either HO‐1 or Nrf2 inhibitor prevented hemin's effect on GPX4 to a comparable extent, and over‐expression of Nrf2 increased GPX4 expression. Moreover, intervention of ferroptosis inhibitor liproxstatin‐1 also alleviated CIN in vivo. Therefore, we showed hemin mitigated CIN, inhibiting oxidative stress and ferroptosis, by upregulation of GPX4 via activation of HO‐1/Nrf2. Hemin, as a clinical medicine, has a translational significance in treating CIN, and anti‐ferroptosis is a potential therapeutic strategy for CIN.
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