Exploration for Blood Biomarkers of Human Long Non-coding RNAs Predicting Oxaliplatin-Induced Chronic Neuropathy Through iPS Cell-Derived Sensory Neuron Analysis. | LitMetric
Department of Pharmacology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-Ku, Tokyo, 113-8602, Japan.
Published: September 2024
AI Article Synopsis
Article Abstract
Oxaliplatin, a platinum-based chemotherapeutic agent, frequently causes acute and chronic peripheral sensory neuropathy, for which no effective treatment has been established. In particular, chronic neuropathy can persist for years even after treatment completion, thus worsening patients' quality of life. To avoid the development of intractable adverse effects, a predictive biomarker early in treatment is awaited. In this study, we explored extracellular long non-coding RNAs (lncRNAs) released from primary sensory neurons as biomarker candidates for oxaliplatin-induced peripheral neuropathy. Because many human-specific lncRNA genes exist, we induced peripheral sensory neurons from human induced pluripotent stem cells. Oxaliplatin treatment changed the levels of many lncRNAs in extracellular vesicles (EVs) released from cultured primary sensory neurons. Among them, the levels of release of lncRNAs that were considered to be selectively expressed in dorsal root ganglia were correlated with those of lncRNAs in plasma EV obtained from healthy individuals. Several lncRNAs in plasma EVs early after the initiation of treatment showed greater changes in patients who did not develop chronic neuropathy that persisted for more than 1 year than in those who did. Therefore, these extracellular lncRNAs in plasma EVs may represent predictive biomarkers for the development of chronic peripheral neuropathy induced by oxaliplatin.
Vasculitic neuropathy is caused by inflammatory destruction of nerve blood vessels resulting in nerve ischemia. Nerve vasculitis can be divided into two categories based on vessel size - large arteriole vasculitis (≥75 µm) and microvasculitis (<75 µm). Herein, we characterize the clinical features of nerve large-arteriole vasculitis compared to nerve microvasculitis.
The neural mechanisms of the affective-motivational symptoms of chronic pain are poorly understood. In chronic pain, our innate coping mechanisms fail to provide relief. Hence, these behaviors are manifested at higher frequencies.
Background: There are currently seven coronaviruses that can infect humans and the latest addition to these viruses is the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Infection by SARS-CoV-2 is known commonly as coronavirus disease 2019 (COVID-19). Aside from common manifestations of cough and fever, neurologic symptoms such as headache, disturbed consciousness, paresthesia, and seizures have also been seen.
Objective: Studies have demonstrated a link between chronic inflammatory responses and diabetic microangiopathy, which include diabetic nephropathy, diabetic retinopathy, and diabetic neuropathy. However, it remains unclear whether there is a causal association between circulating inflammatory cytokines and the development of diabetic microvascular complications. This study aimed to investigate whether altered genetically predicted concentrations of circulating inflammatory cytokines were associated with the development of diabetic microvascular complications using two-sample Mendelian randomization (MR) analysis and clinical validation.
Charcot-Marie-Tooth disease (CMT) is the most common hereditary peripheral neuropathy. It presents a wide range of genetic and phenotypic heterogeneity. CMT disease type 1A (CMT1A), caused by PMP22 gene duplication, represents the most common subtype of CMT in Western countries.
