Journal: Military Medical Research

Article Title: The cellular response capacity (CRC) as a novel immunomonitoring approach in sepsis

doi: 10.1016/j.mmr.2026.100010

Figure Lengend Snippet: Concentration-dependent change in the humoral inflammatory response following incubation with Escherichia coli ( E. coli ) in the ex vivo whole blood model. a Absolute plasma concentrations of IL-6, IL-8, and MMP9 determined by enzyme-linked immunosorbent assay. b Normalized values and EC 50 curve fit by BuC=0% and 50 000 CFU/ml E. coli= 100%, respectively, for IL-6, IL-8, and MMP9 as indicated by EC 50 (%) on the respective Y-axis. BuC indicates buffer control after 60 min incubation; numbers on the X-axis indicate E. coli bacteria in concentrations of 2000 to 50 000 CFU/ml after 60 min incubation; LPS indicates lipopolysaccharide (LPS) 100 ng/ml after 60 min incubation. Values are shown as median and interquartile range. n =8. Statistical analysis was performed using the Kruskal-Wallis test with Dunn’s post-hoc test, comparing all shown concentrations of E. coli bacteria and 100 ng/ml LPS with BuC. P -values are indicated above the respective data points. ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001. CFU. Colony-forming units; IL. Interleukin; MMP9. Matrix metallopeptidase 9.

Article Snippet: For the samples of the ex vivo whole blood model, the plasma concentrations of matrix metallopeptidase 9 (MMP9, #DY911, R&D Systems, Minneapolis, USA), IL-6 (#555220, BD Biosciences, San Jose, USA), and IL-8 (#DY208, R&D Systems) were measured in citrate-anticoagulated plasma using enzyme-linked immunosorbent assay according to the respective manufacturer’s instructions.

Techniques: Concentration Assay, Incubation, Ex Vivo, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Control, Bacteria

Journal: Military Medical Research

Article Title: The cellular response capacity (CRC) as a novel immunomonitoring approach in sepsis

doi: 10.1016/j.mmr.2026.100010

Figure Lengend Snippet: Diagnostic performance for the detection of bacteremia, analyzing the neutrophil phenotype by determining the median fluorescence intensity (MFI) and the cellular response capacity (CRC) in comparison with traditional markers of humoral inflammation (IL-6, IL-8, MMP9). a Comparison of receiver operating characteristic (ROC) at 10,000 CFU/ml Escherichia coli ( E. coli ) with the respective 95% confidence interval (CI) and P -value, and half-maximal effective concentration (EC 50 ) as a function of the E. coli concentration. b Detailed comparison of the EC 50 as a function of the E. coli concentration. c Exemplary comparison of EC 50 curve fit after normalization as indicated by EC 50 (%) on the respective Y-axis to BuC=100% and 50 000 CFU/ml E. coli =0% for the humoral marker IL-6 (the IL-6 values were multiplied by −1 before EC 50 calculation to facilitate comparability with the CRC) and the change in neutrophil phenotype represented by CD11b CRC. BuC indicates buffer control after 60 min incubation; numbers on the X-axis of c indicate E. coli bacteria in concentrations of 2000 to 50 000 CFU/ml after 60 min incubation. Values are shown as median and interquartile range. n =8. Statistical analysis was performed using the Kruskal-Wallis test with Dunn’s post-hoc test, evaluating the EC 50 of IL-8, MMP9, the MFI, and CRC of CD10, CD11b, and CD62L in comparison to the EC 50 of IL-6. P -values are indicated above the respective data points. ⁎ P <0.05. CFU. Colony-forming units; IL. Interleukin; MMP9. Matrix metallopeptidase 9.

Article Snippet: For the samples of the ex vivo whole blood model, the plasma concentrations of matrix metallopeptidase 9 (MMP9, #DY911, R&D Systems, Minneapolis, USA), IL-6 (#555220, BD Biosciences, San Jose, USA), and IL-8 (#DY208, R&D Systems) were measured in citrate-anticoagulated plasma using enzyme-linked immunosorbent assay according to the respective manufacturer’s instructions.

Techniques: Diagnostic Assay, Fluorescence, Comparison, Concentration Assay, Marker, Control, Incubation, Bacteria

Journal: Military Medical Research

Article Title: The cellular response capacity (CRC) as a novel immunomonitoring approach in sepsis

doi: 10.1016/j.mmr.2026.100010

Figure Lengend Snippet: Clinical specifications and parameters over all time points of the sepsis cohort. a Suspected infection cause of sepsis. b Distribution of the individual score points of the Sequential Organ Failure Assessment (SOFA) score. c Total SOFA score. d-h Traditional and humoral markers of inflammation: leukocytes and neutrophil-lymphocyte ratio ( d ), C-reactive protein (CRP) and procalcitonin (PCT) ( e ), interleukin-6 (IL-6) and interleukin-8 (IL-8) ( f ), serum amyloid A (SAA) and calprotectin ( g ), matrix metallopeptidase 9 (MMP9) and myeloperoxidase (MPO) ( h ). Values are shown as median and interquartile range. n =14. CNS. Central nervous system; HV. Healthy volunteers.

Article Snippet: For the samples of the ex vivo whole blood model, the plasma concentrations of matrix metallopeptidase 9 (MMP9, #DY911, R&D Systems, Minneapolis, USA), IL-6 (#555220, BD Biosciences, San Jose, USA), and IL-8 (#DY208, R&D Systems) were measured in citrate-anticoagulated plasma using enzyme-linked immunosorbent assay according to the respective manufacturer’s instructions.

Techniques: Infection

Journal: Materials Today Bio

Article Title: Human iPSC-EV-loaded nanofiber stent coatings accelerate vascular repair by enhancing EGFR/HIF-1α signaling and suppressing ROCK1-mediated remodeling

doi: 10.1016/j.mtbio.2026.103564

Figure Lengend Snippet: In vivo evaluation of re-endothelialization and inhibition of intimal hyperplasia following stent implantation. (A–E) SEM images of the luminal surface treated with EV-loaded (A, B) or DPBS-loaded (D, E) nanofibrous membranes. The EV-treated group exhibited a continuous, smooth, and intact endothelial layer (A, B), whereas the DPBS group displayed incomplete coverage with substantial endothelial disruption (D, E). (C, F) H&E-stained cross-sections revealed the extent of neointimal formation above the stent struts (black arrows). The EV group (C) demonstrated significantly reduced intimal thickening compared with the pronounced hyperplasia observed in the DPBS group (F). (G–H) Statistical analysis confirmed that EV treatment significantly increased endothelial coverage (G) and suppressed intimal hyperplasia thickness (H). (I–K) EV treatment significantly upregulated the expression of the angiogenic factor VEGF (I), the endothelial marker CD31 (J), and the proliferation marker PCNA (K), confirming accelerated vascular repair. (L–N) EV treatment prevented phenotypic switching and matrix accumulation, as evidenced by reduced levels of the contractile/hyperplasia marker α-SMA (L). Furthermore, the EV group showed decreased expression of matrix metalloproteinases MMP-2 and MMP-9 (M) and beneficial modulation of collagen composition, with increased Collagen I and the Collagen I/III ratio (N). (O–P) The EV group exhibited significantly downregulated levels of the profibrotic factor TGF-β1 (O) and the inflammatory cytokine IL-6 (P). N = 5 (G and H), and n = 3 (I-P). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.000.

Article Snippet: Proliferation and remodeling markers: PCNA (1:1000, ab29, Abcam), IL-6 (1:1000, A0286, ABclonal), TGF-β1 (1:1000, A2124, ABclonal), MMP-2 (1:1000, A6247, ABclonal), and MMP-9 (1:1000, A2095, ABclonal).

Techniques: In Vivo, Inhibition, Disruption, Staining, Expressing, Marker

Journal: Clinical and Translational Medicine

Article Title: Non‐canonical function of transferrin receptor‐1 promotes breast cancer metastasis by activating HCK‒STAT3‒MMP9 signalling

doi: 10.1002/ctm2.70731

Figure Lengend Snippet: Matrix metalloproteinase 9 (MMP9) is a central downstream executor in transferrin receptor 1 (TfR‐1)‐promoted breast cancer cells mobility. (A) Differentially expressed genes between mock and TfR‐1‐overexpressed MDA‐MB‐231/4175 cells were analysed by Gene Ontology (GO) enrichment. (B) Heatmap depicting gene expression in positive regulation of cell migration pathways for mock versus TfR‐1‐overexpressing MDA‐MB‐231/4175 cells. (C) Core genes in migration‐related pathways were evaluated using degree, betweenness and closeness algorithms. (D) Pearson correlation analysis revealed strong positive correlation between TFRC and MMP9 expression ( R = .991, p < .001). (E) Expression of MMP9 was detected by immunohistochemical (IHC) in 74 non‐metastatic and 66 metastatic breast cancer tissue samples. (F) The expression of MMP9 in the breast cancer tissue microarray was quantified based on staining intensity and extent. (G) Correlation analysis was performed to evaluate the relationship between the expression levels of TfR‐1 and MMP9 in breast cancer tissues. (H) Relative mRNA expression levels of MMP9 in MDA‐MB‐231 and MDA‐MB‐231/4175 mock or TfR‐1‐overexpressing cells were determined by real‐time quantitative PCR (RT‐qPCR). (I) Western blot (WB) analysis of total STAT3, pSTAT3 and MMP9 in MDA‐MB‐231 and MDA‐MB‐231/4175 mock or TfR‐1‐overexpressing cells. (J) MMP9 secretion in culture supernatants was measured by enzyme‐linked immunosorbent assay (ELISA) in MDA‐MB‐231 and MDA‐MB‐231/4175 mock or TfR‐1‐overexpressing cells. (K) ELISA analysis of MMP9 secretion in supernatants from TfR‐1‐overexpressing MDA‐MB‐231 and MDA‐MB‐231/4175 cells treated with or without OKT9. (L) RT‐qPCR analysis of MMP9 mRNA in TfR‐1‐overexpressing cells treated with or without STAT3 inhibitor BP‐1‐102. (M) WB analysis of MMP9, pSTAT3, STAT3 and TfR‐1 in MDA‐MB‐231 and MDA‐MB‐231/4175 TfR‐1‐overexpressing cells with or without BP‐1‐102. (N) ELISA measurement of MMP9 secretion in TfR‐1‐overexpressing MDA‐MB‐231 and MDA‐MB‐231/4175 cells treated with or without BP‐1‐102. Data represent mean ± standard deviation (SD) from at least three independent experiments. Statistical significance was determined by unpaired, two‐tailed Student's t ‐test, * p < .05, ** p < .01, *** p < .001, with comparisons made to relevant controls in each experiment.

Article Snippet: MMP9 in cell culture supernatants was measured using the MMP9 enzyme‐linked immunosorbent assay (ELISA) kit (Abclonal, #RK00217).

Techniques: Gene Expression, Migration, Expressing, Immunohistochemical staining, Microarray, Staining, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Standard Deviation, Two Tailed Test

Journal: Clinical and Translational Medicine

Article Title: Non‐canonical function of transferrin receptor‐1 promotes breast cancer metastasis by activating HCK‒STAT3‒MMP9 signalling

doi: 10.1002/ctm2.70731

Figure Lengend Snippet: STAT3‒matrix metalloproteinase 9 (MMP9) signalling mediates the pro‐metastatic effects of transferrin receptor 1 (TfR‐1) in breast cancer. (A) Western blot (WB) analysis of TfR‐1 and MMP9 expression in MMP9 depletion breast cancer cells. (B) Enzyme‐linked immunosorbent assay (ELISA) analysis of secreted MMP9 levels after siMMP9 transfection. (C) Transwell assays comparing siNC‐ or siMMP9‐treated cells. (D) ELISA analysis of secreted MMP9 in mock versus TfR‐1‐overexpressing breast cancer cells transfected with siNC or siMMP9. (E) Transwell assays of mock versus TfR‐1‐overexpressing cells transfected with siNC or siMMP9. (F) Effects of MMP9 knockdown and STAT3 inhibition (BP‐1‐102, 10 µM, 24 h) on MMP9 secretion. (G) Transwell assays of siNC‐ and siMMP9‐treated cells with or without STAT3 inhibitor BP‐1‐102 (10 µM, 24 h). Data are shown as mean ± standard deviation (SD) from at least three independent experiments. Statistical significance was determined by unpaired, two‐tailed Student's t ‐test, * p < .05, ** p < .01, *** p < .001, with comparisons made to relevant controls in each experiment. (H) Schematic summary of TfR‐1‐induced haematopoietic cell kinase (HCK) axis activation promoting breast cancer metastasis.

Article Snippet: MMP9 in cell culture supernatants was measured using the MMP9 enzyme‐linked immunosorbent assay (ELISA) kit (Abclonal, #RK00217).

Techniques: Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Transfection, Knockdown, Inhibition, Standard Deviation, Two Tailed Test, Activation Assay