Lymphocytes are reported to express nicotinic acetylcholine receptors (nAChR). However, no data are available on the expression of these nAChR on activated lymphocyte relatively to resting lymphocytes. In this study, we examined nAChR subunits expression in PHA-stimulated versus un-stimulated lymphocytes, and four leukemic cell lines. Cell stimulation with nicotine triggered calcium responses only in some experiments conducted with PHA-stimulated lymphocytes. Likewise, only the Jurkat and HL-60 cell lines displayed calcium waves upon nicotine stimulation, whereas the Raji and CCRF-CEM did not. All responding cells displayed an active form of the nicotinic a-7 nAChR. Indeed, use of 2 different sets of primers for the corresponding mRNA showed that expression of the full-length a-7 subunit mRNA was only present in PHA-stimulated lymphocytes for which calcium waves had been evidenced. Microscopy analysis of lymphocytes structure showed a direct relationship between their size, their a-7 nAChR expression, and calcium release upon nicotine stimulation. Then, this relationship suggested that lymphocytes need a prime activation to express the a-7 nAChR, and therefore to release calcium in response to nicotine.
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http://dx.doi.org/10.2741/e152 | DOI Listing |
FASEB J
January 2025
Department of Urology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Acute Kidney Injury (AKI) is a significant medical condition characterized by the abrupt decline in kidney function.Low-intensity pulsed ultrasound (LIPUS), a non-invasive therapeutic technique employing low-intensity acoustic wave pulses, has shown promise in promoting tissue repair and regeneration. A novel LIPUS system was developed and evaluated in rat AKI models, focusing on its effects on glomerular filtration rate (GFR), blood urea nitrogen (BUN), serum creatinine (SCr), and the Notch1-Akt-eNOS signaling pathway.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Texas Tech University Health Sciences Center, Lubbock, TX, USA.
Background: The present study delves into the intricate molecular connections between ischemic stroke (IS) and Alzheimer's disease (AD) through an analysis of mitochondrial microRNA (miRNA) patterns. By exploring their shared signatures in the context of IS and AD, our aim is to unravel potential common pathways, understand shared molecular mechanisms, explore diagnostic and therapeutic opportunities, gain a comprehensive understanding of neurodegeneration, and advance the field of biomarker research.
Method: To explore these intriguing questions, mitochondria were isolated from postmortem brains of individuals with IS, AD, and healthy controls (n=10 each).
Background: While the formation of β-amyloid plaques and neurofibrillary "tau" tangles are considered hallmarks of AD pathology, therapeutic targeting of these pathways has been unsuccessful, highlighting the necessity to define the underlying molecular mechanisms driving AD progression. Previous studies from our lab demonstrated that mitochondrial calcium (Ca) overload through neuronal ablation of the mitochondrial Na/Ca exchanger (NCLX) is sufficient to trigger 'AD-like' pathology, including mitochondrial dysfunction, amyloid deposition and tau pathology, and cognitive decline. In addition, we found significant proteomic remodeling of components of the mitochondrial calcium uniporter channel (mtCU), the primary mediator of Ca uptake, in frontal cortex samples isolated post-mortem from patients diagnosed with non-familial/sporadic AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Kentucky College of Medicine, Sanders-Brown Center on Aging, Lexington, KY, USA.
Background: Astrocytes are a glial cell type responsible for many protective functions in the brain. While they are primarily recognized for regulating synaptic activity, they're also essential for maintaining the neurovascular unit, and cerebral hyperperfusion during metabolic demand. Calcium signaling has been identified as a regulatory process for these functions.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Ahmadu Bello University Zaria, Zaria, Kaduna, Nigeria.
Background: Studies suggest a potential link between stroke and Alzheimer's disease wherein stroke may serve as a trigger for the onset or acceleration of Alzheimer's pathogenesis as damage to the brain's blood vessels may lead to the accumulation of amyloid beta protein which is a hallmark of Alzheimer's disease. Recent research has shown that stroke treatment may hold the key to treating Alzheimer's disease. The anti-inflammatory potentials of Cholinergic signaling are a novel therapeutic target in memory decline associated with Alzheimer's.
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