The authors have examined the effects of pentoxifylline, a drug used to improve peripheral blood flow in patients with vascular disorders, on shear-induced periodic Ca2+ entry and its consequences in the rat erythrocyte. To study the effects of periodic Ca2+ entry on Ca2+ dependent processes, erythrocytes, with and without pentoxifylline, were subjected to rotational shear produced by swirling-cell suspensions in an isosmotic medium for 5-second intervals. Pulses of increasing duration from 5-30 seconds promoted increased accumulation of 45Ca2+; intermittent 5 sec pulses, at 10-minute intervals, produced a stepwise accumulation of 45Ca2+. Ca2+ accumulation was accompanied by elevated Ca2+ dependent transglutaminase. Shear induced Ca2+ entry and the increase in transglutaminase activity was reduced in cells treated with pentoxifylline. These findings suggest that pentoxifylline can reduce shear induced periodic Ca2+ entry that leads to transient activation of Ca2+ dependent transglutaminase, accumulation of crosslinked proteins, and loss of erythrocyte deformability.
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http://dx.doi.org/10.1002/j.1552-4604.1991.tb03733.x | DOI Listing |
Cell Mol Biol Lett
January 2025
PhD Program in Medical Neuroscience, Taipei Medical University, Taipei, Taiwan (R.O.C.).
Background: Regulation of messenger RNA (mRNA) transport and translation in neurons is essential for dendritic plasticity and learning/memory development. The trafficking of mRNAs along the hippocampal neuron dendrites remains translationally silent until they are selectively transported into the spines upon glutamate-induced receptor activation. However, the molecular mechanism(s) behind the spine entry of dendritic mRNAs under metabotropic glutamate receptor (mGluR)-mediated neuroactivation and long-term depression (LTD) as well as the fate of these mRNAs inside the spines are still elusive.
View Article and Find Full Text PDFBMC Med
January 2025
Physiological Institute, University of Regensburg, University Street 31, 93053, Regensburg, Germany.
Background: Dystonia is a common neurological hyperkinetic movement disorder that can be caused by mutations in anoctamin 3 (ANO3, TMEM16C), a phospholipid scramblase and ion channel. We previously reported patients that were heterozygous for the ANO3 variants S651N, V561L, A599D and S651N, which cause dystonia by unknown mechanisms.
Methods: We applied electrophysiology, Ca measurements and cell biological methods to analyze the molecular mechanisms that lead to aberrant intracellular Ca signals and defective activation of K channels in patients heterozygous for the ANO3 variants.
Cells
December 2024
Department of Physiology, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Injured or atrophied adult skeletal muscles are regenerated through terminal differentiation of satellite cells to form multinucleated muscle fibers. Transplantation of satellite cells or cultured myoblasts has been used to improve skeletal muscle regeneration. Some of the limitations observed result from the limited number of available satellite cells that can be harvested and the efficiency of fusion of cultured myoblasts with mature muscle fibers (i.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
January 2025
Department of Physiology (Cellular Physiology Research Group),Institute of Molecular Pathology Biomarkers (IMPB), University of Extremadura, 10003-Caceres, Spain.
Filamin A (FLNA) is an actin-binding protein that has been reported to interact with STIM1 modulating the activation of Orai1 channels. Cleaving of FLNA by calpain leads to a C-terminal fragment that is involved in a variety of functional and pathological events, including pro-oncogenic activity in different types of cancer. Here we show that full-length FLNA is downregulated in samples from colon cancer patients as well as in the adenocarcinoma cell line HT-29.
View Article and Find Full Text PDFJ Biol Chem
December 2024
Department of Pharmacology, Addiction Science, and Toxicology, College of Medicine, The University of Tennessee Health Science Center; Memphis, 38163. Electronic address:
Familial Alzheimer's disease (FAD) is frequently associated with mutations in the amyloid precursor protein (APP), which are thought to lead to cognitive deficits by impairing NMDA receptor (NMDAR)-dependent forms of synaptic plasticity. Given the reliance of synaptic plasticity on NMDAR-mediated Ca entry, shaping of NMDAR activity by APP and/or its disease-causing variants could provide a basis for understanding synaptic plasticity impairments associated with FAD. A region of APP (residues 639-644 within APP695) processed by the γ-secretase complex, which generates amyloid β (Aβ) peptides, is a hotspot for FAD mutations.
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