Ask about this productRelated genes to: DNASE1 antibody
- 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 antibody
Related articles to: DNASE1 antibody
- 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 (dECM-pSM) for their potential use in oral mucosa restoration. A perfusion decellularization protocol was implemented on porcine skeletal muscle segments, utilizing a combination of physical (perfusion), chemical (SDS), and enzymatic (DNase-1) agents over 18 days. The effectiveness of the process was evaluated macroscopically, through histological stains (H&E, DAPI, Masson's Trichrome), scanning electron microscopy (SEM), DNA quantification, and FTIR spectroscopy. The thermal properties (TGA, DSC), swelling, and biocompatibility of the dECM-pSM with human gingiva fibroblast cells (HGF) were analyzed, including adhesion and proliferation assays. The results showed successful decellularization, with significant removal of nuclear material (0.7 ng/mg residual 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 swelling capacity (300% after 5 minutes) and demonstrated excellent biocompatibility, promoting the adhesion at 92% after 2 days, and proliferation of 80% after 4 days 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: 2026/04/24
Macouzet-Garduño JimenaCruz-Maya IriczalliSerrano-Bello JanethPiña-Barba María CristinaAlvarez-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 - Sepsis-associated acute kidney injury (SAKI) remains a life-threatening condition with limited therapeutic options, primarily driven by rampant oxidative stress, inflammatory dysregulation. Importantly, aberrant formation of neutrophil extracellular traps (NETs) and sustained innate immune activation further exacerbate renal injury, highlighting the need for strategies that precisely modulate these intertwined pathological mechanisms. Here, we present neutrophil-mimetic nanoscavengers (MD@NM) that comprise a catalytic core of DNase-1-loaded MnO nanozymes enveloped by a neutrophil membrane engineered to actively target and simultaneously disrupt multiple pathological circuits in SAKI. The neutrophil membrane confers chemokine-receptor (e.g., CXCR2) mediated homing to injured kidneys, while the MnO nanozymes catalytically scavenge ROS and the loaded DNase-1 enzymatically degrades NETs-derived extracellular DNA, thereby suppressing the cGAS-STING pathway and skewing macrophage polarization toward an M2 reparative phenotype. In a murine model of LPS-induced SAKI, MD@NM treatment facilitated robust renal targeting, attenuated neutrophilic infiltration, resolved cytokine storm, and ameliorated structural kidney damage. Collectively, this biomimetic platform represents a novel strategy for precision immunomodulation and multi-mechanistic therapy against SAKI by integrating antioxidative, NETs-scavenging, and anti-inflammatory functions into a single nanotherapeutic agent. - Source: PubMed
Publication date: 2026/02/15
Zhang ZeningZhang ChenxiLuo RanranWu QiuchiRen PengchenLiu XinyuLuo YingyingXu ZhongshengHe XiaojingLiu Yun