CNS white matter, the collection of axons and supporting glia of the mammalian CNS, makes up close to 50% of the human brain by volume. Interruption of vital interconnects within this tissue, even over a short segment, often leads to serious morbidity in a broad range of neurological disorders. Axons, glia and myelin express a complex array of conventional voltage gated ion channels, intracellular Ca(2+) release channels, neurotransmitter uptake and release mechanisms, together with matching transmitter receptors. Dysregulation of ion homeostasis induced by injury or energy failure leads to depolarization and intracellular Na(+) accumulation, which in turn triggers inappropriate ion translocation (i.e. Ca(2+) influx) and transmitter release; together these events further promote more Ca(2+) influx, while at the same time triggering even more toxic Ca(2+) release from intracellular Ca(2+) stores. Uncontrolled intracellular Ca(2+) increases overactivate a variety of Ca(2+)-sensitive enzyme systems culminating in permanent injury to axon, myelin and glia.
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http://dx.doi.org/10.1016/j.expneurol.2012.04.016 | DOI Listing |
PLoS One
January 2025
Institute of Medical Biochemistry, Center for Molecular Biology of Inflammation, University of Muenster, Muenster, Germany.
Weibel-Palade bodies (WPB) are secretory organelles exclusively found in endothelial cells and among other cargo proteins, contain the hemostatic von-Willebrand factor (VWF). Stimulation of endothelial cells results in exocytosis of WPB and release of their cargo into the vascular lumen, where VWF unfurls into long strings of up to 1000 µm and recruits platelets to sites of vascular injury, thereby mediating a crucial step in the hemostatic response. The function of VWF is strongly correlated to its structure; in order to fulfill its task in the vascular lumen, VWF has to undergo a complex packing/processing after translation into the ER.
View Article and Find Full Text PDFJ Gen Physiol
March 2025
Department of Animal, Veterinary, and Food Sciences, College of Agricultural and Life Sciences, University of Idaho, Moscow, ID, USA.
The mechanisms underlying cooperative activation and inactivation of myocardial force extend from local, near-neighbor interactions involving troponin-tropomyosin regulatory units (RU) and crossbridges (XB) to more global interactions across the sarcomere. To better understand these mechanisms in the hearts of small and large mammals, we undertook a simplified mathematical approach to assess the contribution of three types of near-neighbor cooperative interactions, i.e.
View Article and Find Full Text PDFInt J Nanomedicine
January 2025
Shanghai Eighth People's Hospital, Xuhui District, Shanghai, 200030, People's Republic of China.
Purpose: Gastrostomy is the commonly used enteral feeding technology. The clinical risks caused by tube dislodgement and peristomal site infection are the common complications before complete tract maturation after gastrostomy. However, there is currently no relevant research to promote gastrostomy wound treatment and tract maturation.
View Article and Find Full Text PDFOncol Res
January 2025
Department of Physiology, China Medical University, Taichung, 404328, Taiwan.
Objectives: Mitochondrial Ca uniporter (MCU) provides a Ca influx pathway from the cytosol into the mitochondrial matrix and a moderate mitochondrial Ca rise stimulates ATP production and cell growth. MCU is highly expressed in various cancer cells including breast cancer cells, thereby increasing the capacity of mitochondrial Ca uptake, ATP production, and cancer cell proliferation. The objective of this study was to examine MCU inhibition as an anti-cancer mechanism.
View Article and Find Full Text PDFCell Death Dis
January 2025
Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, and the Department of Physiology, School of Basic Medicine, Shanxi Medical University, Taiyuan, China.
Programmed necrosis/necroptosis greatly contributes to the pathogenesis of cardiac disorders including myocardial infarction, ischemia/reperfusion (I/R) injury and heart failure. However, the fundamental mechanism underlying myocardial necroptosis, especially the mitochondria-dependent death pathway, is poorly understood. Synaptotagmin-1 (Syt1), a Ca sensor, is originally identified in nervous system and mediates synchronous neurotransmitter release.
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