mProX™ Human OPRM1 Stable Cell Line

van Dokkum NH, et al. "Neonatal stress exposure and DNA methylation of stress-related and ." Early human development, 2023.
In the study conducted, it was found that extremely preterm infants may experience long-lasting effects on neurodevelopmental outcomes as a result of stress exposure during their stay in the Neonatal Intensive Care Unit (NICU). This may be attributed to altered DNA methylation of stress-related and neurodevelopmentally relevant genes. The study aimed to explore the association between neonatal stress exposure and DNA methylation in these genes at two different time points: 7-14 days after birth and at discharge from the NICU. The study included 45 infants, with a gestational age range of 24-30 weeks, and utilized the Neonatal Infant Stressor Scale (NISS) to measure daily neonatal stress exposure. Fecal samples were collected at days 7-14 and discharge, and DNA methylation analysis was performed on a subset of samples due to low DNA concentrations. Results showed that methylation rates of most genes did not significantly differ between the two time points, except for one gene (OPRM1). However, a moderate and mostly negative correlation was found between cumulative NISS scores and average DNA methylation status upon discharge for several genes, including NR3C1, SLC6A4, SLC1A2, IGF2, BDNF, and OPRM1. The study highlights the potential for differential gene regulation in response to higher neonatal stress exposure and suggests the need for further research to confirm and study the effects on gene expression.
Pubmed: 37797474   DOI: 10.1016/j.earlhumdev.2023.105868

Zeng H, et al. "Unbiased multitissue transcriptomic analysis reveals complex neuroendocrine ." Journal of neuroinflammation, 2023.
Spinal cord injury (SCI) results in the loss of sensory and motor function below the level of injury and is a devastating disease of the central nervous system. It leads to severe secondary immunosuppression, known as SCI-induced immunodeficiency syndrome (SCI-IDS), which increases the susceptibility to infections and worsens neurological dysfunction. Multiple studies have indicated that SCI-IDS is an independent risk factor for poor neurological prognosis. SCI-IDS is primarily observed in injuries above the T5 level and is believed to cause systemic immune failure through the sympathetic-adrenal medullary axis and the hypothalamic-pituitary-adrenal (HPA) axis, although the exact mechanism is unclear. The concentrations of adrenocorticotropic hormone and cortisol in plasma, as well as changes in sympathetic activity, were evaluated in rats with high-level (T3) spinal cord injury (T3-SCI) and low-level (T10) spinal cord injury (T10-SCI). Furthermore, the underlying gene network regulation between the sympathetic-adrenal medullary axis and the HPA axis was investigated through histology and multitissue transcriptomics to better understand the neuroendocrine-immune network associated with SCI-IDS. The results showed significant atrophy in secondary immune organs, such as the spleen and thymus gland, in rats with T3-SCI, and a marked increase in cortisol levels mediated by the adrenal glands but a decrease in norepinephrine levels. Transcriptome analysis also revealed distinct gene expression patterns in the hypothalamus and adrenal glands of rats with T3-SCI, with notable changes in genes involved in inflammatory pathways and immune response pathways. Additionally, disruptions in the hypothalamic-adrenal gland connection led to autonomous adrenal gland regulation, disturbance in circadian rhythm, and ultimately elevated cortisol levels, causing overall immunosuppression in the periphery. This study sheds light on the possible mechanism of SCI-IDS and its impact on neurological prognosis through persistent neuroinflammation and systemic immunosuppression.
Pubmed: 37775760   DOI: 10.1186/s12974-023-02906-7