PARP1 promotes NLRP3 activation via blocking TFEB-mediated autophagy in rotenone-induced neurodegeneration DOI Creative Commons
He Zhang,

Zhefan Xie,

Yongming Peng

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2023, Volume and Issue: 252, P. 114630 - 114630

Published: Feb. 8, 2023

Rotenone, a widely used pesticide, causes dopaminergic neurons loss and increase the risk of Parkinson's disease (PD). However, few studies link role PARP1 to neuroinflammatory response autophagy dysfunction in rotenone-induced neurodegeneration. Here, we identified that overactivation caused by rotenone led NLRP3-mediated inflammation. Further results showed inhibition could reduce inflammation, which was effectively eliminated TFEB knockdown. Moreover, poly(ADP-ribosyl)ated reduced autophagy. Of note, rescue loss. Overall, our study revealed blocks through poly (ADP-ribosyl)ating inhibited NLRP3 degradation, suggests intervention PARP1-TFEB-NLRP3 signaling can be new treatment strategy for

Language: Английский

Dual function of HPF1 in the modulation of PARP1 and PARP2 activities DOI Creative Commons
Tatyana A. Kurgina, Nina Moor, Mikhail M. Kutuzov

et al.

Communications Biology, Journal Year: 2021, Volume and Issue: 4(1)

Published: Nov. 3, 2021

Abstract Poly(ADP-ribosyl)ation catalyzed by poly(ADP-ribose) polymerases (PARPs) is one of the immediate cellular responses to DNA damage. The histone PARylation factor 1 (HPF1) discovered recently form a joint active site with PARP1 and PARP2 was shown limit activity PARPs stimulate their NAD + -hydrolase activity. Here we demonstrate that HPF1 can DNA-dependent DNA-independent autoPARylation as well heteroPARylation histones in complex nucleosome. stimulatory action detected defined range concentrations at which no HPF1-dependent enhancement hydrolytic consumption occurs. PARP2, comparing PARP1, more efficiently stimulated reaction than automodification, suggesting specific role ADP-ribosylation-dependent modulation chromatin structure. Possible dual function maintaining PARP discussed.

Language: Английский

Citations

26

Extracellular vesicles derived from HuMSCs alleviate daunorubicin-induced cardiac microvascular injury via miR-186-5p/PARP9/STAT1 signal pathway DOI Creative Commons
Shule Zhang, Dong Li, Linghong Liu

et al.

Regenerative Therapy, Journal Year: 2024, Volume and Issue: 25, P. 320 - 330

Published: Feb. 2, 2024

It is essential to acknowledge that the cardiovascular toxicity associated with anthracycline drugs can be partially attributed damage inflicted on blood vessels and endothelial cells. Extracellular vesicles (EVs) derived from mesenchymal stem cells (MSCs) have potential repair cellular processes promote tissue regeneration through transfer of signaling molecules such as miRNAs. In present study, we investigated effects MSC-EVs daunorubicin (DNR)-damaged human cardiac microvascular (HCMEC) developing Chicken Chorioallantoic Membrane (CAM) in vivo.

Language: Английский

Citations

3

Current status and progress in using radiolabelled PARP-1 inhibitors for imaging PARP-1 expression in tumours DOI

Qianna Wang,

Junbo Zhang

European Journal of Medicinal Chemistry, Journal Year: 2022, Volume and Issue: 242, P. 114690 - 114690

Published: Aug. 18, 2022

Language: Английский

Citations

15

Targeting NAD Metabolism for the Therapy of Age-Related Neurodegenerative Diseases DOI Creative Commons
Feifei Li, Chou Wu, Gelin Wang

et al.

Neuroscience Bulletin, Journal Year: 2023, Volume and Issue: 40(2), P. 218 - 240

Published: May 31, 2023

Abstract As the aging population continues to grow rapidly, age-related diseases are becoming an increasing burden on healthcare system and a major concern for well-being of elderly individuals. While is inevitable process all humans, it can be slowed down treated or alleviated. Nicotinamide adenine dinucleotide (NAD) critical coenzyme cofactor that plays central role in metabolism involved various cellular processes including maintenance metabolic homeostasis, post-translational protein modifications, DNA repair, immune responses. individuals age, their NAD levels decline, this decrease has been suggested contributing factor development numerous diseases, such as cancer, diabetes, cardiovascular neurodegenerative diseases. In pursuit healthy aging, researchers have investigated approaches boost maintain levels. Here, we provide overview summarize recent progress strategies target treatment particularly

Language: Английский

Citations

8

PARP1 promotes NLRP3 activation via blocking TFEB-mediated autophagy in rotenone-induced neurodegeneration DOI Creative Commons
He Zhang,

Zhefan Xie,

Yongming Peng

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2023, Volume and Issue: 252, P. 114630 - 114630

Published: Feb. 8, 2023

Rotenone, a widely used pesticide, causes dopaminergic neurons loss and increase the risk of Parkinson's disease (PD). However, few studies link role PARP1 to neuroinflammatory response autophagy dysfunction in rotenone-induced neurodegeneration. Here, we identified that overactivation caused by rotenone led NLRP3-mediated inflammation. Further results showed inhibition could reduce inflammation, which was effectively eliminated TFEB knockdown. Moreover, poly(ADP-ribosyl)ated reduced autophagy. Of note, rescue loss. Overall, our study revealed blocks through poly (ADP-ribosyl)ating inhibited NLRP3 degradation, suggests intervention PARP1-TFEB-NLRP3 signaling can be new treatment strategy for

Language: Английский

Citations

7