Pituitary adenoma (PA) accounts for 10–15% of all intracranial neoplasms. Even though most pituitary adenomas are benign, it is known that almost 35% of them exhibit an aggressive clinical course, including rapid proliferative activity and invasion of neighboring tissues. MicroRNAs (miRNAs) are short single-stranded RNA molecules that can influence post-transcriptional regulation by controlling target genes. Based on research data on miRNAs over the past 20 years, more than 60% of genes encoding human proteins are regulated by miRNAs, which ultimately control basic cellular mechanisms, including cell proliferation, differentiation, and apoptosis. Dysregulation of miRNAs has been observed in a number of diseases, especially tumors like PA. A majority of miRNAs are expressed within the cells themselves. However, the circulating miRNAs can be detected in several biological fluids of the human body. The identification of circulating miRNAs as new molecular markers may increase the ability to detect a tumor, predict the course of a disease, plan to choose suitable treatment, and diagnose at the earliest signs of impending neoplastic transformation. Therapy of PAs with aggressive behavior is a complex task. When surgery and chemotherapy fail, radiotherapy becomes the treatment of choice against PAs. Therefore, the possibility of implementing circulating miRNAs as innovative diagnostic and therapeutic agents for PA is one of the main exciting ideas.
Brain arteriovenous malformations (AVMs) are abnormal vessels that are prone to rupture, causing life-threatening intracerebral hemorrhage (ICH). Understanding the molecular basis of pathogenesis, timely diagnosis, and treatment of brain AVMs are some of the urgent problems in neurosurgery. MicroRNAs (miRNAs) are small endogenous RNAs that regulate gene-expression posttranscriptionally. MiRNAs are involved in almost all biological processes, including cell proliferation, apoptosis, and cell differentiation. Recent studies have shown that miRNAs can be involved in brain AVMs formation and rupture. There are also extracellular forms of miRNAs. Circulating miRNAs have been detected in the blood circulation and other body fluids. Owing to their stability and resistance to endogenous RNase activity, circulating miRNAs have been proposed as diagnostic and prognostic biomarkers for various diseases, such as tumors, cardiovascular and autoimmune diseases. In this review, we summarized the role of some miRNAs in brain AVMs pathogenesis and discussed their potential clinical application as non-invasive biomarkers.
The new coronavirus infection (COVID-19) is already known to cause serious respiratory illnesses such as pneumonia and lung failure. COVID-19 has caused catastrophic damage to the public health, economic and social stability. As COVID-19 has resulted in enormous human toll and serious economic loss that poses a global threat, urgent understanding of the current situation and the development of strategies to mitigate the spread of the virus is required. Today, many studies are being carried out around the world to study the pathogenesis of COVID-19, where the development of a cytokine storm or pulmonary fibrosis is a serious complication that can lead to unfavorable outcomes. This leads to the fact that a deeper understanding of the nature of the virus will allow to develop new approaches in pathogenetic therapy. In this regard, the stromal vascular fraction has tremendous therapeutic potential in COVID-19. Stromal vascular fraction provides anti-inflammatory and immunomodulatory effects and promotes the restoration and regeneration of damaged tissues. The availability, the ability to obtain a significant volume of viable cells of the stromal vascular fraction population, such as adipose tissue stem / stromal cells, as well as their use by the intravenous route, has proven safe and effective in other forms of lung disease, including fibrotic diseases. In other words, the goal of this therapy for COVID-19 is to eliminate the inflammatory process, restore trophic and regenerate damaged tissues, and remodel fibrous and connective tissue. However, stromal vascular fraction is not currently approved for the prevention or treatment of COVID-19 cases. However, clinical trials are ongoing to ensure maximum understanding in terms of efficacy and safety. In this paper, we will discuss this new approach to the use of stromal vascular fraction therapy, which serves as a ray of hope in the fight against severe forms of COVID-19
Metastases are considered to be a key mechanism for the spread of malignant tumors, whereby tumor cells separate from the primary site and form new tumor nodes in various parts of the body. Bone tissue, including the spine, is often affected by metastases, which can significantly worsen the prognosis and quality of life of patients. Metastasis comprises a complex multistep process during which tumor cells undergo molecular and phenotypic changes enabling them to migrate and adapt to new conditions in the body. Bone metastases can be osteolytic, causing bone destruction, or osteoblastic, stimulating excessive bone formation. Tumor cells enter the bone and activate osteoclasts or osteoblasts, thereby leading to remodelling of bone tissue and formation of a closed cycle of bone destruction and tumor growth. The characteristics of tumor cells are determined by their genetic and epigenetic changes, as well as interaction with the environment. Understanding the molecular and pathophysiological aspects of spinal metastasis is essential to developing effective treatments and improving therapeutic approaches. The paper considers new therapeutic approaches aimed at overcoming spinal metastasis in order to improve the prognosis and quality of life of patients.
Cancer metastasis is a multistep process in which cancer cells leave the primary focus, survive in the bloodstream, and colonize in a distant organ. This is the main cause of cancer morbidity and mortality. It is mediated by a multistep process called the metastatic cascade. Initial steps include local invasion and migration, angiogenesis, epithelial-mesenchymal transition (EMF) and intravasation. Non-coding RNAs represent a large part of the transcriptome, with long non-coding RNAs (lncRNAs) constituting a large proportion. The perception of long non-coding RNAs as fragments of RNA and transcriptional noise has been constantly replaced by their role as confirmed targets for various physiological processes in the past few years. A large amount of evidence has revealed their role at all stages of carcinogenesis and in modulating metastasis through regulatory networks. In this review, we focus on the role of long non-coding RNAs as promoters or inhibitors in the main stages of the metastatic cascade, and in particular consider their role in the metastasis of malignant tumors to the brain.
OBJECTIVE It has been reported that microRNA-195 (miR-195) protects against chronic brain injury induced by chronic brain hypoperfusion. However, neither the expression profile of miR-195 nor its potential role during acute ischemic stroke has been investigated. In this study, the authors’ aim was to verify the mechanism of miR-195 in acute ischemic stroke. METHODS The plasma levels of miR-195 expression were assessed using real-time PCR in 96 patients with acute ischemic stroke, and the correlation with the National Institutes of Health Stroke Scale score was evaluated. In addition, cerebral infarct volume, neurological score, and levels of miR-195 and CX3CL1/CX3CR1 mRNA and protein expression were assessed in mice subjected to middle cerebral artery occlusion (MCAO) with or without intra-cerebroventricular infusion of lentiviral vector. The inflammatory cytokines tumor necrosis factor–α (TNFα), interleukin (IL)–1β, and IL-6 of mouse brains after MCAO and BV2 cells treated with oxygen-glucose deprivation were measured using enzyme-linked immunosorbent assay, and apoptotic proteins were examined by Western blotting. Direct targeting of CX3CL1/CX3CR1 by miR-195 was determined by immunoblotting and dual luciferase assay. RESULTS In ischemic stroke patients, miR-195 was significantly downregulated and expression levels of miR-195 in these patients negatively correlated with the National Institutes of Health Stroke Scale score. In mice after MCAO, miR-195 overexpression decreased infarct volume, alleviated neurological deficits, and most importantly, suppressed an inflammatory response. Meanwhile, miR-195 suppressed the expression of the inflammatory cytokines TNFα, IL-1β, and IL-6 in vitro and in vivo. The authors further discovered that both CX3CL1 and CX3CR1 are direct targets of miR-195, but miR-195 exerts neuroprotective roles mainly through inhibiting CX3CR1-mediated neuroinflammation and subsequent neuronal cell apoptosis. CONCLUSIONS Taken together, these findings suggest that miR-195 promotes neuronal cell survival against chronic cerebral ischemic damage by inhibiting CX3CR1-mediated neuroinflammation. This indicates that miR-195 may represent a novel target that regulates neuroinflammation and brain injury, thus offering a new treatment strategy for cerebral ischemic disorders.
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