Ask about this productRelated genes to: DNASE1 Blocking Peptide
- Gene:
- DNASE1 NIH gene
- Name:
- deoxyribonuclease 1
- Previous symbol:
- DNL1
- Synonyms:
- -
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-07-08
- Date modifiied:
- 2016-07-18
Related products to: DNASE1 Blocking Peptide
Related articles to: DNASE1 Blocking Peptide
- After musculoskeletal injury, a considerable proportion of patients develop heterotopic ossification (HO), the formation of bone at ectopic sites. Traumatic HO is a disabling condition, potentially resulting in loss of joint function and compression of neurovascular structures. Available treatment options are often unsuccessful, frequently necessitating surgical resection of HO lesions with a high risk of recurrence. Given that myeloid cells, including neutrophils and macrophages, are among the first cell types to infiltrate injured tissue, the present study explored the relationship of extracellular traps (ETs) with HO formation in humans and mice. Human HO sample analysis revealed the presence of different stages of ETosis, which are clinically associated with increased ET concentrations in the blood. Experimentally, genetic impairment of ET resolution through combined and deficiency led to increased traumatic HO in mice, whereas HO was strongly attenuated by additional deletion of the ET generator . Neutrophil depletion impaired local ET formation, reduced HO formation, and blunted genotype-specific differences in HO outcome. In osteogenic precursors, ETs promoted matrix mineralization, and inhibition of ETosis or degradation of cell-free DNA, a major ET component, resulted in reduced osteogenesis. Pharmacological facilitation of ET clearance by dornase alfa, a US Food and Drug Administration-approved recombinant DNase1, or inhibition of ETs by the PADI4 inhibitor GSK484, resulted in inhibition of traumatic HO formation in mice without adversely affecting systemic bone remodeling. Together, our clinical and experimental findings demonstrate that traumatic HO is mediated by targetable neutrophil-dependent mechanisms, with altered ET formation contributing to these effects. - Source: PubMed
Publication date: 2026/05/06
Jiang ShanEis-Janzyk GesineAugustin RubenKleinertz HolgerSchröder SaskiaSevecke JanXie WeixinPan HaoyanBehrens IsabellWeisselberg SamiraAlbertsen Lilly-CharlotteMüller Elenavon Kroge SimonAlimy Assil-RaminFal MiladAmling MichaelTolosa EvaRenné ThomasFrosch Karl-HeinzMader KonradRolvien TimBaranowsky AnkeKeller Johannes - Oral mucosa regeneration represents a significant clinical challenge due to the limited availability of autologous grafts and associated morbidity. This study focused on developing and characterizing decellularized matrices decellularized extracellular matrix porcine skeletal muscle (dECM-pSM) for their potential use in oral mucosa restoration. A perfusion decellularization protocol was implemented on pSM segments, utilizing a combination of physical (perfusion), chemical (SDS), and enzymatic (DNase-1) agents over 18 d. The effectiveness of the process was evaluated macroscopically, through histological stains (H&E, DAPI, Masson's Trichrome), scanning electron microscopy, DNA quantification, and Fourier transform infrared spectroscopy. The thermal properties (TGA, DSC), swelling (S), and biocompatibility of the dECM-pSM with human gingiva fibroblast cells (HGF) were analyzed, including adhesion and viability assays. The results showed successful decellularization, with significant removal of nuclear material (0.7 ng mgresidual DNA) with preservation of the three-dimensional architecture of ECMs and physicochemical properties, as confirmed by histological integrity of the fiber and porous structures, preserved characteristic bands of amide groups, and stable thermal properties after the decellularization process. The dECM-pSM maintained their Scapacity (300% after 5 min) and demonstrated desirablebiocompatibility, promoting the adhesion at 92% after 2 d, and viability of 80% after 4 d of HGF compared to the control, without evidence of cytotoxicity. These results suggest that the developed protocol yields decellularized matrices with suitable properties for tissue engineering applications. - Source: PubMed
Publication date: 2026/05/08
Macouzet-Garduño JimenaCruz-Maya IriczalliSerrano-Bello JanethBarba María Cristina PiñaAlvarez-Perez Marco Antonio - : Recombinant human deoxyribonuclease I (rhDNase) cleaves DNA in mucus, facilitating increased mucociliary clearance of purulent sputum. In cystic fibrosis (CF), rhDNase improves pulmonary function and decreases exacerbations. Conversely, rhDNase use in non-CF bronchiectasis (NCFB) patients has not yielded similarly effective results. We explored the safety and feasibility of rhDNase in patients with bronchiectasis due to primary ciliary dyskinesia (PCD). : In this real-life pilot study, patients with PCD received rhDNase to treat viscous mucus. We compared pulmonary function tests and pulmonary exacerbations for these patients over six months of use of rhDNase. : Eight PCD patients with symptomatic bronchiectasis commenced use of rhDNase at variable dosing (ranging from at least twice weekly to a full 2.5 mg dose daily). Over a six-month period, pulmonary function tests, as measured by mean FVC and FEV, remained relatively stable compared to prior to commencing rhDNase. Mean pulmonary exacerbations decreased from 3.1 to 2.3 in the six-month period after commencing rhDNase, as compared to the six-month period prior to rhDNase. : Use of rhDNase in PCD patients was safe and did not adversely impact lung function or increase pulmonary exacerbations, in contrast to earlier trial results in NCFB patients with heterogeneous etiologies. Further clinical data is required to identify the population of PCD patients who can benefit from rhDNase, as well as the appropriate dosing and timing. - Source: PubMed
Publication date: 2026/03/12
Heching MosheSlomianksy LioraNaamany EviatarWeinberg JoelKramer Mordechai R - Neutrophil extracellular traps (NETs) contribute to chronic obstructive pulmonary disease (COPD) pathogenesis by amplifying airway inflammation. Gasdermin D (GSDMD)-mediated pyroptosis is a critical driver of COPD progression. This study provides insights into COPD pathogenesis and provides a theoretical basis for potential therapeutic targets. Mice were exposed to cigarette smoke (CS) for 16 weeks to establish a COPD model. In vitro, alveolar macrophages (AMs) (MH-S) and alveolar epithelial cells (MLE-12) were treated with cigarette smoke extract (CSE). Subsequently, NETs were isolated from phorbol-12-myristate-13-acetate (PMA)-stimulated neutrophils. Lung histopathology, inflammatory markers, and pyroptosis-related proteins were analyzed. Co-immunoprecipitation analysis was used to verify the binding of GSDMD and ubiquitin molecules in cells. Interventions included DNase1 to degrade NET and GSDMD knockdown. In CS-exposed mice, NETs increased the levels of proinflammatory cells and mediators, and lung structure was further disrupted. Pyroptosis of AMs was increased, while phagocytosis of AMs was inhibited. However, treatment with DNAse1 partially reversed the results caused by CS exposure and NET induction. Consistently, NETs aggravated inflammatory response and pyroptosis in the CSE-induced MH-S cell model. Furthermore, NETs significantly caused an increase in ROS, which promoted the activation of GSDMD deubiquitination and subsequent pyroptosis pathway in AMs. DNase1 treatment or GSDMD silencing attenuated pyroptosis, reduced inflammatory mediators, and improved lung function. NETs aggravated CS-induced lung inflammation and injury by activating GSDMD to promote pyroptosis in AMs. Targeting GSDMD or NETs represents a novel therapeutic strategy for COPD. © 2026 The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/03/13
Lu JunjuanSong RouxiYang HonghuiLiu Caihong - In multiple sclerosis (MS), functional network abnormalities arise as structural damage accumulates. However their biological basis and spatial distribution remain unclear. This study investigated the associations between MS-related functional network abnormalities and physiological gene expression using the Allen Human Brain Atlas (AHBA). Five-hundred fifty-eight MS patients and 214 healthy controls (HC) underwent neurological assessment and 3 T MRI; 491 patients also completed a neuropsychological evaluation. Resting-state functional MRI was used to generate degree centrality maps to identify network topography alterations. Spatial correlations between centrality abnormalities (p < 0.01 uncorrected) and the expression of 3634 MS-related genes was evaluated using AHBA and the Multimodal Environment for Neuroimaging and Genomic Analysis. Genes showing significant associations (p < 0.001, R ≥ 0.15) underwent pathway enrichment analysis (p < 0.05, Bonferroni-corrected). Compared to HC, MS patients showed higher centrality mainly in the default-mode network (DMN), linked to genes regulating inflammation resolution and immune functions, and lower centrality in regions mostly located in the salience network and cerebellum, associated with genes implicated in cytokine response. Compared to HC and relapsing-remitting MS, progressive MS patients showed higher centrality in DMN and cerebellar regions, correlating with genes related to epigenetic and mitochondrial functions. Of the MS cohort, 144 (29.3%) patients were cognitively impaired. Compared to cognitively preserved MS and HC, they showed higher centrality in DMN and mesial temporal lobe regions, negatively correlated with expression of DNASE1, regulating DNA degradation, and CP, encoding ceruloplasmin, involved in iron homeostasis and potentially iron-driven neurodegeneration. Physiological regional gene expression spatially correlates with MS-related functional network alterations. Biological factors may shape regional vulnerability or resilience to MS pathology, influencing functional reorganization. - Source: PubMed
Publication date: 2026/03/03
Preziosa PaoloAzzimonti MatteoStorelli LoredanaValsasina PaolaTedone NicolòMargoni MonicaFilippi MassimoRocca Maria A