Doxorubicin suppresses chondrocyte differentiation by stimulating ROS production

Author(s):  
Cheng Wu ◽  
Jiayi Luo ◽  
Yuanxin Liu ◽  
Jiannan Fan ◽  
Xianwen Shang ◽  
...  
Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1703-P
Author(s):  
SVETLANA MICHURINA ◽  
IURII STAFEEV ◽  
IGOR SKLYANIK ◽  
EKATERINA SHESTAKOVA ◽  
ANATOLIY YURASOV ◽  
...  

Pharmaceutics ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 942
Author(s):  
Helen Yarimet Lorenzo-Anota ◽  
Diana G. Zarate-Triviño ◽  
Jorge Alberto Uribe-Echeverría ◽  
Andrea Ávila-Ávila ◽  
José Raúl Rangel-López ◽  
...  

(1) Background: Chitosan-coated gold nanoparticles (CH-AuNPs) have important theranostic applications in biomedical sciences, including cancer research. However, although cell cytotoxicity has been studied in cancerous cells, little is known about their effect in proliferating primary leukocytes. Here, we assessed the effect of CH-AuNPs and the implication of ROS on non-cancerous endothelial and fibroblast cell lines and in proliferative lymphoid cells. (2) Methods: The Turkevich method was used to synthetize gold nanoparticles. We tested cell viability, cell death, ROS production, and cell cycle in primary lymphoid cells, compared with non-cancer and cancer cell lines. Concanavalin A (ConA) or lipopolysaccharide (LPS) were used to induce proliferation on lymphoid cells. (3) Results: CH-AuNPs presented high cytotoxicity and ROS production against cancer cells compared to non-cancer cells; they also induced a different pattern of ROS production in peripheral blood mononuclear cells (PBMCs). No significant cell-death difference was found in PBMCs, splenic mononuclear cells, and bone marrow cells (BMC) with or without a proliferative stimuli. (4) Conclusions: Taken together, our results highlight the selectivity of CH-AuNPs to cancer cells, discarding a consistent cytotoxicity upon proliferative cells including endothelial, fibroblast, and lymphoid cells, and suggest their application in cancer treatment without affecting immune cells.


2020 ◽  
Author(s):  
Consiglia Longobardi ◽  
Emanuela Andretta ◽  
Vincenzo Romano ◽  
Chiara Lauritano ◽  
Giuseppina Avantaggiato ◽  
...  
Keyword(s):  

2021 ◽  
Author(s):  
Mei Zheng ◽  
Jingchen Lin ◽  
Xingbei Liu ◽  
Wei Chu ◽  
Jinpeng Li ◽  
...  

Abstract Polyploidy occurs prevalently and plays an important role during plant speciation and evolution. This phenomenon suggests polyploidy could develop novel features that enable them to adapt wider range of environmental conditions compared with diploid progenitors. Bread wheat (Triticum aestivum L., BBAADD) is a typical allohexaploid species and generally exhibits greater salt tolerance than its tetraploid wheat progenitor (BBAA). However, little is known about the underlying molecular basis and the regulatory pathway of this trait. Here, we show that the histone acetyltransferase TaHAG1 acts as a crucial regulator to strengthen salt tolerance of hexaploid wheat. Salinity-induced TaHAG1 expression was associated with tolerance variation in polyploidy wheat. Overexpression, silencing and CRISPR-mediated knockout of TaHAG1 validated the role of TaHAG1 in salinity tolerance of wheat. TaHAG1 contributed to salt tolerance by modulating ROS production and signal specificity. Moreover, TaHAG1 directly targeted a subset of genes that are responsible for hydrogen peroxide production, and enrichment of TaHAG1 triggered increased H3 acetylation and transcriptional upregulation of these loci under salt stress. In addition, we found the salinity-induced TaHAG1-mediated ROS production pathway is involved in salt tolerance difference of wheat accessions with varying ploidy. Our findings provide insight into the molecular mechanism of how an epigenetic regulatory factor facilitates adaptability of polyploidy wheat and highlights this epigenetic modulator as a strategy for salt tolerance breeding in bread wheat.


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