ArticleMolecular and cellular biochemistry2019
PARP-1 inhibition provides protection against elastase-induced emphysema by mitigating the expression of matrix metalloproteinases.
Article in Molecular and cellular biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Excessive poly(ADP)-ribosylation in the inflamed mucosa of pediatric celiac disease points to a novel inflammatory mechanism and therapeutic target.Molecular and cellular pediatrics · 2026Article
- The poly (ADP-ribose) polymerase inhibitor olaparib attenuates established pulmonary fibrosis in a large animal model.BMC pulmonary medicine · 2025Article
- Dynamics of Inflammatory and Pathological Changes Induced by Single Exposure of Particulate Matter (PMCell biochemistry and biophysics · 2024Article
- Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway.iScience · 2024Article
- Advanced models for respiratory disease and drug studies.Medicinal research reviews · 2023Review
- PARPs and ADP-Ribosylation in Chronic Inflammation: A Focus on Macrophages.Pathogens (Basel, Switzerland) · 2023Review
- Gallic acid suppresses inflammation and oxidative stress through modulating Nrf2-HO-1-NF-κB signaling pathways in elastase-induced emphysema in rats.Environmental science and pollution research international · 2021Article
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- DNA Damage Response and Immune Defense.International journal of molecular sciences · 2020Review
- Gallic acid protects against the COPD-linked lung inflammation and emphysema in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- The impact of PARPs and ADP-ribosylation on inflammation and host-pathogen interactions.Genes & development · 2020Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In our previous study, we have shown that PARP-1 inhibition (genetic or pharmacological) ameliorates elastase-induced inflammation and emphysema. Since matrix metalloproteinases (MMPs) particularly MMP-2 and MMP-9 are known to play a critical role in emphysema development, the present work was designed to evaluate the effects of PARP-1 inhibition on their expression utilizing elastase-induced mouse model of emphysema. Our data show that olaparib administration at a dose of 5 mg/kg b.wt. (daily) significantly prevented the elastase-induced inflammation as indicated by decreased inflammatory cells particularly macrophages in BALF at 1 week post-injury. In addition, the drug restored the altered redox balance in the lungs of elastase-treated mice toward normal. Further, PCR data show that olaparib administration ameliorates the elastase-induced expression of MMP-2 and MMP-9 without having much effect on the expressions of their inhibitors TIMP-1 and TIMP-2. Next, our data on immunoblot, gelatin zymography, and immunohistochemical analysis indeed confirm that olaparib reduced the elastase-induced expression of MMP-2 and MMP-9. Reduction in the expression of metalloproteinases correlate well with the PARP activity as olaparib treatment suppressed the elastase-induced expression of PAR modified proteins markedly. Overall, our data strongly suggest that PARP-1 inhibition blunts elastase-induced MMP-2 and MMP-9 expression, which may be partly responsible for prevention of emphysema.
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