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Exosomes Derived from Apelin-Pretreated Mesenchymal Stem Cells Ameliorate Sepsis-Induced Myocardial Dysfunction by Alleviating Cardiomyocyte Pyroptosis via Delivery of miR-34a-5p.
Int J Nanomedicine
January 2025
School of Medicine, South China University of Technology, Guangzhou, Guangdong, People's Republic of China.
Background: Exosomes sourced from mesenchymal stem cells (MSC-EXOs) have become a promising therapeutic tool for sepsis-induced myocardial dysfunction (SMD). Our previous study demonstrated that Apelin pretreatment enhanced the therapeutic benefit of MSCs in myocardial infarction by improving their paracrine effects. This study aimed to determine whether EXOs sourced from Apelin-pretreated MSCs (Apelin-MSC-EXOs) would have potent cardioprotective effects against SMD and elucidate the underlying mechanisms.
View Article and Find Full Text PDFPhysiology of the volume-sensitive/regulatory anion channel VSOR/VRAC: part 2: its activation mechanisms and essential roles in organic signal release.
J Physiol Sci
January 2025
National Institute for Physiological Sciences (NIPS), 5-1 Higashiyama, Myodaiji, 444-8787, Okazaki, Aichi, Japan; Department of Integrative Physiology, Graduate School of Medicine, Akita University, Akita, Japan; Department of Physiology, School of Medicine, Aichi Medical University, Nagakute, Japan; Graduate University for Advanced Studies (SOKENDAI), Hayama, Kanagawa, Japan. Electronic address:
The volume-sensitive outwardly rectifying or volume-regulated anion channel, VSOR/VRAC, which was discovered in 1988, is expressed in most vertebrate cell types, and is essentially involved in cell volume regulation after swelling and in the induction of cell death. This series of review articles describes what is already known and what remains to be uncovered about the functional and molecular properties as well as the physiological and pathophysiological roles of VSOR/VRAC. This Part 2 review article describes, from the physiological and pathophysiological standpoints, first the pivotal roles of VSOR/VRAC in the release of autocrine/paracrine organic signal molecules, such as glutamate, ATP, glutathione, cGAMP, and itaconate, as well as second the swelling-independent and -dependent activation mechanisms of VSOR/VRAC.
View Article and Find Full Text PDFLive imaging of paracrine signaling: Advances in visualization and tracking techniques.
Cell Struct Funct
January 2025
Department of Pathology and Biology of Diseases, Graduate School of Medicine, Kyoto University.
Live imaging techniques have revolutionized our understanding of paracrine signaling, a crucial form of cell-to-cell communication in biological processes. This review examines recent advances in visualizing and tracking paracrine factors through four key stages: secretion from producing cells, diffusion through extracellular space, binding to target cells, and activation of intracellular signaling within target cells. Paracrine factor secretion can be directly visualized by fluorescent protein tagging to ligand, or indirectly by visualizing the cleavage of the transmembrane pro-ligands or plasma membrane fusion of endosomes comprising the paracrine factors.
View Article and Find Full Text PDFApigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38.
Front Immunol
January 2025
Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet and University of Oslo, Oslo, Norway.
Introduction: CD38, a regulator of intracellular calcium signalling, is highly expressed in immune cells. Mice lacking CD38 are very susceptible to acute bacterial infections, implicating CD38 in innate immune responses. The effects of CD38 inhibition on NLRP3 inflammasome activation in human primary monocytes and monocyte-derived macrophages have not been investigated.
View Article and Find Full Text PDFAnti-skin aging effects of Gosori liquor lees extract by regulating interactions between senescent fibroblasts and adipose-derived stem cells.
Int J Cosmet Sci
January 2025
BioSpectrum Life Science Institute, A1805, U-TOWER, 767, Yongin, Republic of Korea.
When cellular ageing is accelerated by various extrinsic/endogenous stimuli, regenerative function deteriorates, and enriched secretomes, such as the senescence-associated secretory phenotype (SASP), contribute to chronic inflammation and cause matrix degeneration. SASPs from senescent fibroblasts exacerbate cellular senescence via autocrine signalling and also accelerate skin ageing through the induction of neighbouring cell senescence via paracrine signalling. The interaction between dermis fibroblasts and their neighbours, adipose-derived stem cells (ADSCs) in the hypodermis, which lies deep in the dermis, is a potential target for skin ageing.
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