Relative protein expression of XIAP was detected by western blot.
SNHG1 and XIAP were down-regulated, and miR-181a-5p was up-regulated in LPS-induced H9c2 cells. Overexpression of SNHG1 or inhibition of miR-181a-5p facilitated cell viability and repressed inflammation and oxidative stress in LPS-treated H9c2 cells. MiR-181a-5p was a target of and negatively regulated by SNHG1. At the same time, XIAP was a target gene of and inversely modulated by miR-181a-5p. selleck screening library In addition, XIAP was positively regulated by SNHG1. Up-regulation of miR-181a-5p or silencing of XIAP reversed the inhibitory effects of SNHG1 on inflammation and oxidative stress, as well as the promoting effects on cell viability in LPS-induced H9c2 cells.
SNHG1 protected H9c2 cells against LPS-induced injury through modulating the miR-181a-5p/XIAP axis.
SNHG1 protected H9c2 cells against LPS-induced injury through modulating the miR-181a-5p/XIAP axis.
Progranulin (PGRN) has been confirmed to exhibit anti-inflammatory activity. Nevertheless, the mechanisms of PGRN in acute lung injury (ALI) remain uncertain. The aim of this study was to explore the role of PGRN in a lipopolysaccharide (LPS)-induced ALI model and in primary bone marrow-derived macrophages, as well as to investigate the underlying mechanism of PGRN.
Mice were treated with recombinant PGRN protein to detect the effect of PGRN on mouse ALI. Bronchial alveolar lavage fluid (BALF) was analyzed to quantify the inflammatory cytokines, and the lung wet-to-dry ratio was calculated to assess the degree of pulmonary edema. Histological staining was completed on the lung tissues. CCK-8 assay was used to measure cell viability. Western blotting and quantitative polymerase chain reaction were performed to study the transcriptomic profiles during the MAPK pathway.
Recombinant human PGRN significantly suppressed cellular inflammatory response, increased lung permeability, and reduced the expression of inflammatory proteins in the BALF and serum, which further improved survival time. Also, PGRN inhibited the LPS-induced M1 marker gene expression and enhanced the M2 marker gene expression
and
. Further analysis revealed that PGRN suppresses the activity of the MAPK pathway in LPS-treated macrophages in a dose-dependent manner.
PGRN exhibited anti-inflammatory activity and regulated macrophage polarization by suppressing the phosphorylation of the MAPK pathway.
PGRN exhibited anti-inflammatory activity and regulated macrophage polarization by suppressing the phosphorylation of the MAPK pathway.
Patients with warm autoimmune hemolytic anemia (WAIHA) present with anemia that is highly heterogeneous, and often have macrocytic anemia with inappropriately elevated mean corpuscular volume (MCV). The goal of this retrospectivecase study is to elucidate the characteristics of anemia in patients with idiopathic WAIHA.
The hematological parameters were analyzed by automated hematology analyzers in 19 consecutive patients with idiopathic WAIHA. Thecontent of hemoglobin (Hb) in the reticulocytes was assessed as reticulocyte Hb equivalent (RET-He). Relevant laboratory data and medical records were retrospectively studied.
The median MCV was 102.7 fL and ten patients had macrocytic anemia with MCV above 100 fL. There was a significant correlation between the percentage of reticulocytes and MCV. The median RET-He value was 35.9 pg, and the reticulocytes of patients with higher MCV had higher RET-He. There was a significant correlation between red cell volume distribution width (RDW) andMCV, while the association between RDW and RET-He was not significant. Red blood cell agglutination was not seen in any of the patients. Relative folate deficiency was implied to contribute to the increased Hb content in the reticulocytes of WAIHA patients.
Reticulocytes in WAIHA patients often contain more Hb than normal reticulocytes and become inappropriately large, possibly due to relative folate deficiency. Elevated MCV in WAIHA patients is due to the increase in both the number and the Hb content of reticulocytes.
Reticulocytes in WAIHA patients often contain more Hb than normal reticulocytes and become inappropriately large, possibly due to relative folate deficiency. Elevated MCV in WAIHA patients is due to the increase in both the number and the Hb content of reticulocytes.
Protein S(PS) activity, especially PS-specific activity calculated by total PS activity (tPSAct) divided by total PS antigen (tPSAg), is important in the diagnosis of hereditary PS deficiency (PSD). The cleavage of PS at a thrombin-sensitive region (TSR) by proteases reduces the anticoagulant activity of PS. Therefore, we investigated the effect of sample processing and storage on tPSAct and PS cleavage.
Blood samples were collected from ten healthy subjects, and tPSAg and tPSAct were measured in whole blood or plasma stored at room temperature (RT) or 4°C. The cleaved PS was detected by western blotting, and the relationship between decreases in PS-specific activity and increase rates of cleaved PS was evaluated. Furthermore, the stability of tPSAg and tPSAct on the long-term storage of plasma was also evaluated.
Both whole blood and plasma stored at RT and whole blood stored at 4°C showed decreased tPSAct (50-80%) after 24 hours (
<0.05). PS-specific activity levels negatively correlated with the increase rate of cleaved PS (r =-0.84,
<0.001). The tPSAct was decreased to 60% after three days in plasma stored at 4°C (
<0.05) but was stable for about one month when stored at -20°C or below.
Inappropriate processing and storage result in falsely low PS-specific activity due to the cleavage of PS in the blood collection tubes, which may lead to misdiagnosis of PSD. Samples should be centrifuged immediately after collection, and the plasma should be frozen.
Inappropriate processing and storage result in falsely low PS-specific activity due to the cleavage of PS in the blood collection tubes, which may lead to misdiagnosis of PSD. Samples should be centrifuged immediately after collection, and the plasma should be frozen.Alzheimer's disease (AD) is a neurodegenerative disease caused by both genetic and environmental factors. This study aimed to explore the underlying molecular mechanism of AD by bioinformatic gene analysis. The gene expression profiles of GSE16759 and GSE28146 were downloaded, and co-differentially expressed genes (co-DEGs) were identified by R software. Subsequently, the data were analyzed using a combined bioinformatics approach and predicted the microRNAs (miRNAs) targeting the key gene using miRNA databases. Based on the results of these analyses, ADAMTS1, CITED2, and GABRA2 were identified as co-DEGs. They were all associated with learning disorders (inference Score 103.22, 140.41, and 96.26, respectively) and memory disorders (inference Score 102.77, 132.68, and 81.80, respectively). The hub-genes of ADAMTS1, CITED2, and GABRA2 may be associated with AD. Additionally, miR-548c- 3p is probably a common target for ADAMTS1, CITED2, and GABRA2.selleck screening library
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