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37 results for “elastase”
ADAM17 protects against elastase-induced emphysema by suppressing CD62L+ leukocyte infiltration in mice
<p>Pulmonary emphysema is a major manifestation of chronic obstructive pulmonary disease and is associated with chronic pulmonary inflammation caused by cigarette smoking, with contributions from immune cells such as neutrophils, macrophages, and lymphocytes. Although matrix metalloproteinases are well-known to contribute to emphysema progression, the role of a disintegrin and metalloproteinase (ADAM) family proteins, other major metalloproteinases, in disease pathogenesis is largely unknown. ADAM17 is a major sheddase that cleaves various cell surface proteins, including CD62L, an adhesion molecule that plays a critical role in promoting the migration of immune cells to the site of inflammation. In the present study, we aimed to investigate the potential role of ADAM17 and CD62L in the development of elastase-induced emphysema. Eight-to-ten-week-old control and <i>Adam17<sup>flox/flox</sup>/Mx1-Cre</i> (<i>Adam17<sup>ΔMx1</sup></i>) mice were intratracheally injected with 5 U of porcine pancreas elastase and monitored for 35 days after injection. Lung alveolar destruction was evaluated by analyzing the mean linear intercepts of lung tissue specimens and by histopathological examination. Mean linear intercepts data indicated that the degree of elastase-induced emphysema was significantly more severe in <i>Adam17<sup>ΔMx1</sup></i> mice. Further, flow cytometry showed that CD62L<sup>+</sup> neutrophil, CD62L<sup>+</sup> macrophage, and CD62L<sup>+ </sup>B lymphocyte numbers were significantly increased in <i>Adam17<sup>ΔMx1</sup></i> mice. Moreover, the pharmacological depletion of CD62L<sup>+</sup> cells with a CD62L-neutralizing antibody ameliorated the extent of emphysema in <i>Adam17<sup>ΔMx1</sup></i> mice. Collectively, these results suggest that ADAM17 possibly suppresses the progression of emphysema by proteolytically processing CD62L in immune cells and that ADAM17 and CD62L could be novel therapeutic targets for treating pulmonary emphysema.</p>
ADAM17 protects against elastase-induced emphysema by suppressing CD62L+ leukocyte infiltration in mice
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Fig. 2. rCeEI-4 in Bioengineering of an elastase inhibitor from Caesalpinia echinata (Brazil wood) seeds
Fig. 2. rCeEI-4 and rCeEI-5 amino acid sequences and molecular models. (A) Multiple alignment of rCeEI-4 and rCeEI-5 amino acid sequences with other Kunitz type inhibitors. Protein Data Base (PDB) codes are shown in the figure. 1avw_B: trypsin inhibitor from Glycine max; 1tie_A: trypsin inhibitor from Erythrina caffra seeds; 1eyl_A: winged bean chymotrypsin inhibitor; 4an6_B: trypsin inhibitor from Tamarindus indica; 4j2k_B: trypsin inhibitor from Enterolobium contortisiliquum; rCeEI-4 and rCeEI-5: putative elastase inhibitors from C. echinata. The cysteine residues are in black boxes. Residues at P1 and P1′ positions of the putative reactive site are in blue boxes. The Weblogo shows the consensus among the sequences. Theoretical models of (B) rCeEI-4 and (C) rCeEI-5. In both models the beta sheet is shown in red, turns in green, coils in cyan, cysteines involved in the disulfide bonds are in yellow and the putative reactive site in grey. The figures were obtained by the YASARA program. (D) Structural alignment of rCeEI-4 (blue) and rCeEI-5 (green) theoretical models. The disulfide bonds are shown in yellow and putative reactive sites in cyan. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 1 in Bioengineering of an elastase inhibitor from Caesalpinia echinata (Brazil wood) seeds
Fig. 1. Nucleotide and amino acid sequences of (A) rCeEI-4 and (B) rCeEI-5. The amino acid residues of inhibitors are shown in bold black. Amino acid numbers are presented in blue and the stop codon is in green. The N-terminal sequence of CeEI is highlighted in yellow. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 3 in Bioengineering of an elastase inhibitor from Caesalpinia echinata (Brazil wood) seeds
Fig. 3. Determination of rCeEI-based peptides inhibitory constants (Ki) for HNE. The enzyme was pre-incubated with rCeEI-36 (A) or rCeEI-46 (B) in different concentrations. The residual activity of the enzymes was determined using the synthetic substrate MeO-Suc-Ala-Ala-Pro-Val-pNan. The release of the ρ-nitroaniline was followed at 405 nm. Ki values were determined by adjusting the experimental data to the equation for slow tight binding using a non-linear regression.
Fig. 4. Sequences and theoretical 3D in Bioengineering of an elastase inhibitor from Caesalpinia echinata (Brazil wood) seeds
Fig. 4. Sequences and theoretical 3D model of rCeEIbased peptides. (A) Alignment of amino acid sequences of rCeEI-36, rCeEI-46 and rCeEI-55. The cysteine residues are in black box, and residues at P1 and P1′ positions of the putative reactive site are highlighted in green. The peptides (B) rCeEI-36 and (C) rCeEI-46 are in green and red, respectively. The putative reactive site is in cyan and the disulfide bond in rCeEI-36 is shown in yellow. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Effects of a Composition on the Oral Microbiome, pH, Nitrite/Nitrate Ratio, Elastases and Inflammation in Oral Dysbiosis
ClinicalTrials.gov study NCT05463484. IPD Sharing: NO. Countries: 1. Publications: 5.
Effect of Neutrophil Elastase Inhibitor on Lung Injury After Esophagectomy
ClinicalTrials.gov study NCT01170845. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Neutrophil Elastase Inhibitor in Treatment of ARDS Patients With Mechanical Ventilation Caused by Sepsis
ClinicalTrials.gov study NCT05672472. IPD Sharing: NO. Countries: 0. Publications: 1.
Neutrophil Elastase, Elastase Alpha-1 Proteinase, Periodontitis, Gingival Crevicular Fluid and Acute Coronary Syndrome
ClinicalTrials.gov study NCT04785235. IPD Sharing: NO. Countries: 0. Publications: 5.
Transcriptomic profiling of murine aneurysm formation after porcine pancreatic elastase infusion
GEO Series GSE153097. Mus musculus. 12 samples. Type: Expression profiling by high throughput sequencing.
Effect of in utero nicotine exposure and elastase instillation on transcriptomic profile at post-elastase day 21 in mice
GEO Series GSE167568. Mus musculus. 21 samples. Type: Expression profiling by high throughput sequencing.
Long-term effects of Elastase inhibition on human islets at single-cell resolution
GEO Series GSE190447. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.
Macrophage elastase (MMP12) critically contributes to the development of subretinal fibrosis
GEO Series GSE189555. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Effect of in utero nicotine exposure and elastase instillation on transcriptomic profile at post-elastase day 3 in mice
GEO Series GSE167567. Mus musculus. 14 samples. Type: Expression profiling by high throughput sequencing.
Creon Use in Coeliac Patients With Low Faecal Pancreatic Elastase
ClinicalTrials.gov study NCT01865695. IPD Sharing: Not stated. Countries: 1. Publications: 0.
The Roles of Neutrophil Elastase in Lung Cancer
ClinicalTrials.gov study NCT01360931. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Alvelestat (MPH966), an Oral Neutrophil Elastase Inhibitor, in Bronchiolitis Obliterans Syndrome After Allogeneic Hematopoietic Stem Cell Transplantation
ClinicalTrials.gov study NCT02669251. IPD Sharing: YES. Countries: 1. Publications: 0.
New Predictive Marker for Pancreatic Cancer Using CA19-9 and Fecal Elastase
ClinicalTrials.gov study NCT05923567. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Pancreatic Cancer Screening Through the Detection of Elastase-1 Combined With Other Examinations
ClinicalTrials.gov study NCT06041009. IPD Sharing: NO. Countries: 1. Publications: 0.
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