A pocket-escaping design to prevent the common interference with near-infrared fluorescent probes in vivo

Xing, Panfei; Niu, Yiming; Mu, Ruoyu; Wang, Zhenzhen; Xie, Daping; Huanling, L; Dong, Lei; Wang, Chunming

doi:10.1038/s41467-020-15323-8

Cited by 43 publications

(32 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Mice were treated with Vehicle, CCl 4 , VA-Lip-control-vector + CCl 4 +Erastin, VA-Lip-Mettl4-shRNA + CCl 4 +Erastin, VA-Lip-Fto-plasmid + CCl 4 +Erastin, VA-Lip- Ythdf1-shRNA + CCl 4 +Erastin, respectively. A mixture of olive oil and carbon tetrachloride (CCl 4 ) (9:1 (v/v)) was used to trigger liver fibrosis in mouse model by intraperitoneal injection (0.1 ml/20 g body weight), according to our previous reports [ 23 ]. Erastin was dissolved according to the instructions and given once every other day for 2 weeks by intraperitoneal injection (30 mg/kg) after the CCl 4 treatment.…”

Section: Methodsmentioning

confidence: 99%

N6-methyladenosine modification regulates ferroptosis through autophagy signaling pathway in hepatic stellate cells

et al. 2021

View full text Add to dashboard Cite

Ferroptosis is a recently identified non-apoptotic form of cell death characterized by iron-dependent lipid peroxidation. However, the underlying exact mechanisms remain poorly understood. Here, we report that the total levels of N 6 -methyladenosine (m 6 A) modification are evidently increased upon exposure to ferroptosis-inducing compounds due to the upregulation of methylase METTL4 and the downregulation of demethylase FTO. Interestingly, RNA-seq shows that m 6 A modification appears to trigger autophagy activation by stabilizing BECN1 mRNA, which may be the potential mechanism for m 6 A modification-enhanced HSC ferroptosis. Importantly, YTHDF1 is identified as a key m 6 A reader protein for BECN1 mRNA stability, and knockdown of YTHDF1 could prevent BECN1 plasmid-induced HSC ferroptosis. Noteworthy, YTHDF1 promotes BECN1 mRNA stability and autophagy activation via recognizing the m 6 A binding site within BECN1 coding regions. In mice, erastin treatment alleviates liver fibrosis by inducing HSC ferroptosis. HSC-specific inhibition of m 6 A modification could impair erastin-induced HSC ferroptosis in murine liver fibrosis. Moreover, we retrospectively analyzed the effect of sorafenib on HSC ferroptosis and m 6 A modification in advanced fibrotic patients with hepatocellular carcinoma (HCC) receiving sorafenib monotherapy. Attractively, the m 6 A modification upregulation, autophagy activation, and ferroptosis induction occur in human HSCs. Overall, these findings reveal novel signaling pathways and molecular mechanisms of ferroptosis, and also identify m 6 A modification-dependent ferroptosis as a potential target for the treatment of liver fibrosis.

show abstract

Section: Methodsmentioning

confidence: 99%

N6-methyladenosine modification regulates ferroptosis through autophagy signaling pathway in hepatic stellate cells

et al. 2021

View full text Add to dashboard Cite

show abstract

“…24). 34 BNLBN contained a hydrazine unit that was introduced into the probe as an allysine-responsive moiety. The initial fluorescence of BNLBN was weak, presumably due to an acceptor-photoinduced electron transfer (a-PeT) effect; however, addition of allysine negates this a-PeT effect resulting in enhanced fluorescence.…”

Section: Small Molecule-based Fluorescent Probes For Liver Fibrosismentioning

confidence: 99%

Small-molecule fluorescence-based probes for interrogating major organ diseases

et al. 2021

View full text Add to dashboard Cite

show abstract

“…In consideration of the spatial inversion of the ligands, we chose the graphical user interface CDOCKER protocol, a CHARMm force field based molecular docking tool using a half‐flexible receptor, to implement the simulation consulting our previous work. [ 24 ] The conformations were ranked according to the energy index.…”

Section: Methodsmentioning

confidence: 99%

A “Bridge‐Building” Glycan Scaffold Mimicking Microbial Invasion for In Situ Endothelialization

Zhang

Yan

et al. 2021

Advanced Materials

Self Cite

View full text Add to dashboard Cite

The globally high prevalence of peripheral artery diseases poses a pressing need for biomaterials grafts to rebuild vasculature. When implanted, they should promote endothelial cells (ECs) adhesion both profoundly and selectively—but the latter expectation remains unfulfilled. Here, this work is inspired by fungi that invade blood vessels via the “bridge” of galectins that, secreted by ECs, can simultaneously bind carbohydrates on fungal surface and integrin receptors on ECs. A glucomannan decanoate (GMDE) substrate mimicking fungal carbohydrates that highly and preferentially supports ECs adhesion while rejecting several other cell types is designed. Electrospun GMDE scaffolds efficiently sequester endogenous galectin‐1—which bridges ECs to the scaffolds as it functions in fungal invasions—and promote blood perfusion in a murine limb ischemic model. Meanwhile, the application of GMDE requires no exogenous pro‐angiogenic agents and causes no organ toxicity or adverse inflammation in mice, highlighting its high safety of potential translation. This glycan material, uniquely mimicking a microbial action and harnessing a secreted protein as a “bridge,” represents an effective, safe, and different strategy for ischemic vascular therapy.

show abstract

A pocket-escaping design to prevent the common interference with near-infrared fluorescent probes in vivo

Cited by 43 publications

References 50 publications

N6-methyladenosine modification regulates ferroptosis through autophagy signaling pathway in hepatic stellate cells

N6-methyladenosine modification regulates ferroptosis through autophagy signaling pathway in hepatic stellate cells

Small-molecule fluorescence-based probes for interrogating major organ diseases

A “Bridge‐Building” Glycan Scaffold Mimicking Microbial Invasion for In Situ Endothelialization

Contact Info

Product

Resources

About