mProX™ Human SCTR Stable Cell Line

Aiko M, et al. "Effects of Sleep Deprivation on Sleep and Sleep Electroencephalogram in ." Neuroscience research, 2023.
Recent studies have consistently demonstrated a relationship between secretin and autism-like behavior in mice. Therefore, secretin-receptor knockout (SCTR-KO) mice are often utilized in research on autism. However, studies on the effects of secretin in humans have shown conflicting results, with some reporting improvement in autistic symptoms after secretin administration and others showing no significant effects. Additionally, it has been found that many individuals with autism spectrum disorders (ASD) also experience sleep disorders. In order to explore the relationship between secretin and sleep, researchers recorded the core body temperature and locomotor activity of SCTR-KO (-/-) and wild-type (WT) (+/+) mice before and after a 4-hour sleep deprivation period. No significant differences were observed between the SCTR-KO and control mice in the baseline condition. However, during the first dark period following sleep deprivation, an increase in non-rapid eye movement sleep was observed in the SCTR-KO group. This suggests that the absence of secretin may lead to fragmentation of sleep, making it difficult for SCTR-KO mice to maintain wakefulness. These findings are consistent with previous research showing that many individuals with ASD experience drowsiness and difficulty with focus during the day. Secretin, which functions as both an intestinal peptide and a neuropeptide in the brain, may play a role in regulating sleep as well as social cognitive behavior. Therefore, it is possible that secretin plays a role in the modulation of sleep patterns.
Pubmed: 37774845   DOI: 10.1016/j.neures.2023.09.008

Berg P, et al. "Loss of the Secretin Receptor Impairs Renal Bicarbonate Excretion and Aggravates ." Journal of the American Society of Nephrology : JASN, 2023.
Evidence suggests that during acute base excess, the renal collecting duct beta -intercalated cells ( beta -ICs) are activated to increase urine base excretion. This process depends heavily on the presence of pendrin and cystic fibrosis transmembrane regulator (CFTR) in the apical membrane of the beta -ICs. However, the specific signal that triggers this activation remained unknown. Recent studies have shown that plasma secretin levels rise during acute alkalosis, and that the secretin receptor (SCTR) is functionally expressed in the beta -ICs. In fact, in mice with global knockout for the SCTR, the ability to acutely increase renal base excretion is lost. This results in a compensatory decrease in ventilation to cope with the acid-base challenge. These findings suggest that secretin plays a crucial role as a systemic bicarbonate-regulating hormone, likely being released from the small intestine during alkalosis. Further investigation revealed that the SCTR system is essential for renal base excretion during acute metabolic alkalosis. These findings were established through various experiments, including bladder catheterization, metabolic cage studies, blood gas analysis, barometric respirometry, and perfusion of isolated cortical collecting ducts. The study also involved the use of SCTR wild-type and knockout (KO) mice, as well as isolated rat small intestines to study secretin release. Results showed that in wild-type mice, secretin was able to acutely increase urine pH and pendrin function in isolated perfused cortical collecting ducts, which were absent in KO mice. The KO mice also failed to sufficiently increase renal base excretion during acute base loading and developed prolonged metabolic alkalosis when exposed to acute oral or intraperitoneal base loading. Furthermore, the KO mice exhibited transient but significant hypoventilation after base loading. This suggests that the loss of SCTR impairs the appropriate increase of renal base excretion during acute base loading, and that SCTR is necessary for the acute correction of metabolic alkalosis. Additionally, results from perfused rats showed that increased blood alkalinity in the upper small intestine led to higher secretin release. In conclusion, the findings suggest that secretin plays a critical role in maintaining bicarbonate homeostasis and that its release from the small intestine is triggered by blood alkalinity.
Pubmed: 37344929   DOI: 10.1681/ASN.0000000000000173