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Oxidative-Damaged Mitochondria Activate GABARAPL1-Induced NLRP3 Inflammasomes in an Autophagic-Exosome Manner after Acute Myocardial Ischemia.
Oxid Med Cell Longev
October 2022
Department of Anesthesiology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.
Objective: This study is aimed at identifying the potential diagnostic markers for circulating endothelial cells (CECs) for acute myocardial ischemia (AMI) and exploring the regulatory mechanisms of the selected biomarker in mitochondrial oxidative damage and vascular inflammation in AMI pathology.
Methods: Utilizing the Gene Expression Omnibus dataset GSE66360, we scanned for differentially expressed genes (DEGs) in 49 AMI patients and 50 healthy subjects. To discover possible biomarkers, LASSO regression and support vector machine recursive feature elimination examinations were conducted.
Interplay between invertebrate C3a with vertebrate macrophages: functional characterization of immune activities of amphioxus C3a.
Fish Shellfish Immunol
October 2013
Laboratory for Evolution & Development, Institute of Evolution & Marine Biodiversity and Department of Marine Biology, Ocean University of China, Qingdao 266003, China.
Our current knowledge of the structure and function of C3a comes from the study of vertebrate C3a anaphylatoxins, virtually nothing is known about the structure and function of C3a molecules in invertebrates. Here we demonstrated that C3a from the invertebrate chordate Branchiostoma japonicum, BjC3a, was similar to vertebrate C3a possessing potential antibacterial activity, as revealed by sequence analysis and computational modeling. The antibacterial activity of BjC3a was definitely confirmed by both antibacterial assay and TEM observation showing that recombinant BjC3a was directly bactericidal.
View Article and Find Full Text PDFDifferential effects of human erythroid burst stimulating activity (HuEBSA) on human cord blood burst forming units-erythroid (BFU-Es) as a function of their differentiation state.
Cytokine
July 1999
Centre de Génétique Moléculaire et Cellulaire, UMR 5534 CNRS, Université Claude Bernard, Lyon I, France.
An erythroid stimulating activity which promotes the growth of small bursts probably arising from mature burst forming units-erythroid (BFU-Es) of adult human bone marrow cells and called human erythroid burst stimulating activity (HuEBSA), was previously found in media conditioned by a fetal human kidney cell line. In the present work we report that adding HuEBSA to cultures did not increase the burst number but increased the size of bursts from cord blood (CB) cells. A similar observation was made using stem cell factor (SCF).
View Article and Find Full Text PDFA human cell line isolated from fetal kidney produces an apparently erythroid-specific stimulating activity.
Cytokine
August 1998
Centre de Génétique Moléculaire et Cellulaire, UMR 5534 CNRS, Université Claude Bernard Lyon I, Villeurbanne, France.
The burst formation from human and murine burst forming unit-erythroid (BFU-E) requires the presence of erythropoietin (Epo) in semi-solid cultures of bone marrow cells. A number of haematopoietic factors are described that increase the burst number: interleukin 3 (IL-3), stem cell factor (SCF), granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-9, IL-11, insulin-like growth factor I, and erythroid potentiating activity (EPA). The authors now show that another activity present in medium conditioned from adult or fetal human kidney cells specifically stimulates the proliferation of BFU-E.
View Article and Find Full Text PDF[Recent findings on the pathogenesis and therapy of anemia in chronic kidney failure].
Recenti Prog Med
October 1992
Dipartimento di Medicina interna, Università, Genova.
Recent studies showed that the blood BFU-E, when subtracted from the uremic milieu, normally responds to the stimulating factor produced by T lymphocytes. The serum of uremic patients inhibits the in vitro growth of normal BFU-E, however, the inhibition is almost completely reversed by hemodialysis. These data allow to understand why the therapy with erythropoietin relieves the anemia of CRF.
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