Browse
Submit Data
Databases
API
Help

Dataset Information

29 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MOFs-Based Nitric Oxide Therapy for Tendon Regeneration.

ABSTRACT: Tendon regeneration is still a great challenge due to its avascular structure and low self-renewal capability. The nitric oxide (NO) therapy emerges as a promising treatment for inducing the regeneration of injured tendon by angiogenesis. Here, in this study, a system that NO-loaded metal-organic frameworks (MOFs) encapsulated in polycaprolactone (PCL)/gelatin (Gel) aligned coaxial scaffolds (NMPGA) is designed and prepared for tendon repair. In this system, NO is able to be released in vitro at a slow and stable average speed of 1.67 nM h^-1 as long as 15 d without a burst release stage in the initial 48 h. Furthermore, NMPGA can not only improve the tubular formation capability of endothelial cells in vitro but also obviously increase the blood perfusion near the injured tendon in vivo, leading to accelerating the maturity of collagen and recovery of biomechanical strength of the regenerated tendon tissue. As a NO-loaded MOFs therapeutic system, NMPGA can promote tendon regeneration in a shorter healing period with better biomechanical properties in comparison with control group by angiogenesis. Therefore, this study not only provides a promising scaffold for tendon regeneration, but also paves a new way to develop a NO-based therapy for biomedical application in the future.

SUBMITTER: Chen J

PROVIDER: S-EPMC8187533 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

Tuning the nitric oxide release from CPO-27 MOFs.

Project description:Nitric oxide (NO) storage and release measurements have been recorded for Ni-doped CPO-27 (Mg) and CPO-27 (Zn), and the biological effect of the released NO was assessed in porcine coronary artery relaxation tests. The results indicate that the doping strategy leads to increased levels of NO storage and delivery compared to the parent materials and that the NO dosage and biological response can be tuned via this approach to suit the requirements of particular applications.

| S-EPMC4786954 | biostudies-literature

Can nitric oxide-based therapy prevent bronchopulmonary dysplasia?

Project description:A growing understanding of endogenous nitric oxide (NO) biology is helping to explain how and when exogenous NO may confer benefit or harm; this knowledge is also helping to identify new better-targeted NO-based therapies. In this review, results of the bronchopulmonary dysplasia clinical trials that used inhaled NO in the preterm population are placed in context, the biologic basis for novel NO therapeutics is considered, and possible future directions for NO-focused clinical and basic research in developmental lung disease are identified.

| S-EPMC3437658 | biostudies-other

Addition of nitric oxide through nitric oxide-paracetamol enhances healing rat achilles tendon.

Project description:Nitric oxide is an important messenger molecule in many physiological processes. The addition of NO via NO-flurbiprofen enhances the material properties of healing tendon, however, flurbiprofen has a detrimental effect on healing. We asked if NO delivered by a cyclooxygenase 3 inhibitor (paracetamol/acetaminophen) would enhance healing in a rat Achilles tendon healing model. Rats were injected subcutaneously daily with NO-paracetamol, paracetamol or vehicle from two days before surgery to the day of tissue harvesting. Paracetamol had no effect on tendon healing compared with vehicle alone. NO-paracetamol did not change the failure load, but did decrease the water content, enhance the collagen content, reduce the cross-sectional area and improve the ultimate stress of healing tendon compared with paracetamol and vehicle. The collagen organization of the healing tendon in the NO-paracetamol group, as determined by polarized light microscopy, was enhanced. Our data suggests NO-paracetamol increases the total collagen content and enhances organization while decreasing the cross-sectional area of healing rat Achilles tendon and is consistent with human clinical trials where NO has improved the symptoms and signs of tendinopathy.

| S-EPMC2505261 | biostudies-other

Cost of nitric oxide therapy in neonates.

Project description:A retrospective observational cohort study was performed to review the cost of inhaled nitric oxide (iNO) therapy in a UK neonatal intensive care setting over a 4-year period. 188 neonates with a median (IQR) gestational age and birth weight of 27 (24-37) weeks and 980 (695-2812) g, respectively, were treated with iNO. The median (IQR) duration of iNO therapy was 60 (22-129) hours. The mean cost of iNO therapy was approximately £820 per baby treated equivalent to £8.50 per hour of therapy. Alternative pricing models suggested a calculated cost of iNO therapy of between approximately £950 and £1350 per baby.

| S-EPMC7554454 | biostudies-literature

Home Nitric Oxide Therapy for COVID-19.

Project description: Not available

| S-EPMC7328337 | biostudies-literature

Role of nitric oxide and nitric oxide synthase isoforms in pulmonary emphysema.

Project description:The purpose of this study is to comprehensively elucidate the role of nitric oxide and nitric oxide synthase isoforms in pulmonary emphysema using cap analysis of gene expression (CAGE) sequencing.

2021-01-18 | GSE164521 | GEO

Nitric Oxide (NO) and NO Synthases (NOS)-Based Targeted Therapy for Colon Cancer.

Project description:Colorectal cancer (CRC) is one of the most lethal malignancies worldwide and CRC therapy remains unsatisfactory. In recent decades, nitric oxide (NO)-a free-radical gas-plus its endogenous producer NO synthases (NOS), have attracted considerable attention. NO exerts dual effects (pro- and anti-tumor) in cancers. Endogenous levels of NO promote colon neoplasms, whereas exogenously sustained doses lead to cytotoxic functions. Importantly, NO has been implicated as an essential mediator in many signaling pathways in CRC, such as the Wnt/?-catenin and extracellular-signal-regulated kinase (ERK) pathways, which are closely associated with cancer initiation, metastasis, inflammation, and chemo-/radio-resistance. Therefore, NO/NOS have been proposed as promising targets in the regulation of CRC carcinogenesis. Clinically relevant NO-donating agents have been developed for CRC therapy to deliver a high level of NO to tumor sites. Notably, inducible NOS (iNOS) is ubiquitously over-expressed in inflammatory-associated colon cancer. The development of iNOS inhibitors contributes to targeted therapies for CRC with clinical benefits. In this review, we summarize the multifaceted mechanisms of NO-mediated networks in several hallmarks of CRC. We review the clinical manifestation and limitations of NO donors and NOS inhibitors in clinical trials. We also discuss the possible directions of NO/NOS therapies in the immediate future.

| S-EPMC7408898 | biostudies-literature

Nitric oxide-releasing hyperbranched polyaminoglycosides for antibacterial therapy.

Project description:Hyperbranched polyaminoglycosides were prepared by the polymerization of kanamycin, gentamicin, and neomycin, and N,N'-methylenebis(acrylamide) via a one-pot reaction. The secondary amines at the linear units of the hyperbranched polymers were subsequently reacted with NO gas at high pressure under alkaline conditions to form N-diazeniumdiolate NO donors. The resulting NO-releasing hyperbranched polyaminoglycosides exhibited a wide range of NO payloads (~0.4-1.3 µmol mg-1) and release kinetics (half-lives ~70-180 min). The therapeutic utility of these materials was evaluated by examining their bactericidal activity against common dental pathogens and toxicity to human gingival fibroblast cells. The antibacterial efficacy of NO-releasing hyperbranched polyaminoglycosides was dependent on specific physiochemical properties, with greater degrees of branching and aminoglycoside terminal groups correlating to enhanced action. Nitric oxide-releasing hyperbranched polykanamycin and polyneomycin elicited the least cytotoxicity at bactericidal concentrations, indicating the greatest therapeutic index for future biomedical applications.

| S-EPMC7164780 | biostudies-literature

Nitric Oxide Synthase Regulates Growth Coordination During Drosophila melanogaster Imaginal Disc Regeneration.

Project description:Mechanisms that coordinate growth during development are essential for producing animals with proper organ proportion. Here we describe a pathway through which tissues communicate to coordinate growth. During Drosophila melanogaster larval development, damage to imaginal discs activates a regeneration checkpoint through expression of Dilp8. This both produces a delay in developmental timing and slows the growth of undamaged tissues, coordinating regeneration of the damaged tissue with developmental progression and overall growth. Here we demonstrate that Dilp8-dependent growth coordination between regenerating and undamaged tissues, but not developmental delay, requires the activity of nitric oxide synthase (NOS) in the prothoracic gland. NOS limits the growth of undamaged tissues by reducing ecdysone biosynthesis, a requirement for imaginal disc growth during both the regenerative checkpoint and normal development. Therefore, NOS activity in the prothoracic gland coordinates tissue growth through regulation of endocrine signals.

| S-EPMC4574233 | biostudies-literature

Bacterial Heme-Based Sensors of Nitric Oxide.

Project description:SIGNIFICANCE:The molecule nitric oxide (NO) has been shown to regulate behaviors in bacteria, including biofilm formation. NO detection and signaling in bacteria is typically mediated by hemoproteins such as the bis-(3',5')-cyclic dimeric adenosine monophosphate-specific phosphodiesterase YybT, the transcriptional regulator dissimilative nitrate respiration regulator, or heme-NO/oxygen binding (H-NOX) domains. H-NOX domains are well-characterized primary NO sensors that are capable of detecting nanomolar NO and influencing downstream signal transduction in many bacterial species. However, many bacteria, including the human pathogen Pseudomonas aeruginosa, respond to nanomolar concentrations of NO but do not contain an annotated H-NOX domain, indicating the existence of an additional nanomolar NO-sensing protein (NosP). Recent Advances: A newly discovered bacterial hemoprotein called NosP may also act as a primary NO sensor in bacteria, in addition to, or in place of, H-NOX. NosP was first described as a regulator of a histidine kinase signal transduction pathway that is involved in biofilm formation in P. aeruginosa. CRITICAL ISSUES:The molecular details of NO signaling in bacteria are still poorly understood. There are still many bacteria that are NO responsive but do encode either H-NOX or NosP domains in their genomes. Even among bacteria that encode H-NOX or NosP, many questions remain. FUTURE DIRECTIONS:The molecular mechanisms of NO regulation in many bacteria remain to be established. Future studies are required to gain knowledge about the mechanism of NosP signaling. Advancements on structural and molecular understanding of heme-based sensors in bacteria could lead to strategies to alleviate or control bacterial biofilm formation or persistent biofilm-related infections.

| S-EPMC6217740 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data