Calpain I requires low Ca2+ for activation and calpain II requires high Ca2+. It was generally accepted that erythrocytes contain calpain I and calpastatin, but no calpain II. We have recently found, however, that nucleated chicken erythrocytes contain both calpains I and II in addition to calpastatin. The finding is significant in rectifying the previous view that the chicken has only one molecular species of calpain, whereas mammals have two. Another erroneous view which prevailed previously was that polymorphonuclear (PMN) cells contain only one calpain species. We could also recently demonstrate that pig PMN cells do contain both calpains I and II. The cloning of cDNAs for calpastatin enabled us to utilize them as the probes in studying the expression of calpastatin in various hematopoietic cell-line cells. We found that several T cells infected with human retrovirus HTLV-I markedly increased the production of calpastatin, which could be measured both by calpain-inhibition assay and by Western blot analysis, but the level of mRNA for calpastatin did not significantly change when compared with noninfected T cells. The increase in calpastatin protein always parallels with the expression of interleukin 2 receptor protein by the HTLV-I-infected T cells, although the biological implication of such phenomena is almost entirely unknown yet.
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http://dx.doi.org/10.1007/978-1-4684-5679-0_47 | DOI Listing |
J Innate Immun
March 2025
Department of Critical Care Medicine, The Six Affiliated Hospital of Wenzhou Medical University, Lishui, China.
Introduction: Autophagy-lysosome pathways play a crucial role in the intracellular killing of pathogenic microorganisms. This study aimed to explore the mechanism by which acute lung injury (ALI) of Pseudomonas aeruginosa affects the autophagy-lysosome pathway.
Methods: ALI mouse models were induced by lipopolysaccharide and P.
Epilepsia
March 2025
Departamento de Neurologia e Neurocirurgia, Escola Paulista de Medicina, Universidade Federal de São Paulo (Unifesp), São Paulo, Brazil.
The immune system is crucial for the correct brain development, and recent findings also point toward central control of immune response. As the immune system is not fully developed at birth, the early years become an important window for infections and for the development of epilepsy. Both central and even peripheral inflammation may impact brain function, promoting opening of the blood-brain/blood and cerebrospinal barriers and allowing entry of immune cells and cytokines, which in turn may affect neuron function and connections.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
March 2025
Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, S.A.S. Nagar, Mohali, Punjab, India.
Alpha-synuclein pathology is a characteristic feature of Parkinson's disease (PD) and related synucleinopathies. As a result, reducing alpha-synuclein pathology is one of the mechanisms being looked at for the development of newer agents which target these diseases. In the present study, we investigated the potential of HC070, a transient receptor potential canonical 5 (TRPC5) channel inhibitor in reducing alpha-synuclein pathology in PD.
View Article and Find Full Text PDFRecent studies show that tumor cells undergo apoptosis after mechanical stretching, which promotes normal cell growth. Since ultrasound can produce similar sub-cellular mechanical stresses on the nanoscale, here we test the effect of ultrasound-mediated mechanical forces on tumors and normal cell survival. Surprisingly, tumor cells undergo apoptosis through a calpain-dependent mitochondrial pathway that relies upon calcium entry through the mechanosensitive Piezo1 channels.
View Article and Find Full Text PDFCell Rep
March 2025
Department of Neuroscience, Genentech, Inc., South San Francisco, CA 94080, USA. Electronic address:
Neurofilament light chain (NfL) is a neuron-specific cytoskeletal protein that provides structural support for axons and is released into the extracellular space following neuronal injury. While NfL has been extensively studied as a disease biomarker, the underlying release mechanisms and role in neurodegeneration remain poorly understood. Here, we find that neurons secrete low baseline levels of NfL, while neuronal damage triggers calpain-driven proteolysis and release of fragmented NfL.
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