Hydrogen sulfide donor AP123 restores endothelial nitric oxide-dependent vascular function in hyperglycemia via a CREB-dependent pathway

Montanaro, Rosangela; Vellecco, Valentina; Torregrossa, Roberta; Casillo, Gian Marco; Manzo, Onorina Laura; Mitidieri, Emma; Bucci, Mariarosaria; Castaldo, Sigismondo; Sorrentino, Raffaella; Whiteman, Matthew; Smimmo, Martina; Carriero, Flavia; Terrazzano, Giuseppe; Cirino, Giuseppe; Bianca, Roberta d’Emmanuele di Villa; Brancaleone, Vincenzo

doi:10.1016/j.redox.2023.102657

Cited by 14 publications

(8 citation statements)

References 80 publications

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“…The interplay between H 2 S and NO pathways plays a crucial role in the vasoactive function during vascular lesions . To verify the synergistic effect of NO and H 2 S, CCK-8 was used to detect the cell viability of HUVECs and HUASMCs on PLCL/KS//PLCL-SH-Cu bilayer mats in the presence of individual components of GSNO or GSH, and the mixture of GSNO and GSH, respectively.…”

Section: Resultsmentioning

confidence: 99%

“…The interplay between H 2 S and NO pathways plays a crucial role in the vasoactive function during vascular lesions. 44 To verify the synergistic effect of NO and H 2 S, CCK-8 was used to detect the cell viability of HUVECs and HUASMCs on PLCL/ KS//PLCL-SH-Cu bilayer mats in the presence of individual components of GSNO or GSH, and the mixture of GSNO and GSH, respectively. Compared with PLCL/KS//PLCL-SH-Cu bilayer mats without GSNO and GSH, the proliferation of HUVECs was promoted, while the proliferation of HUASMCs was suppressed with the addition of a single-component GSNO or GSH (Figure 2J,K).…”

Section: ■ Results and Discussionmentioning

confidence: 99%

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Endothelium-Mimicking Bilayer Vascular Grafts with Dual-Releasing of NO/H₂S for Anti-Inflammation and Anticalcification

Wang,

Liang,

Shang

et al. 2023

ACS Appl. Mater. Interfaces

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Vascular complications caused by diabetes impair the activities of endothelial nitric oxide synthase (eNOS) and cystathionine γ-lyase (CSE), resulting in decreased physiological levels of nitric oxide (NO) and hydrogen sulfide (H 2 S). The low bioavailability of NO and H 2 S hinders the endothelialization of vascular grafts. In this study, endothelium-mimicking bilayer vascular grafts were designed with spatiotemporally controlled dual releases of NO and H 2 S for in situ endothelialization and angiogenesis. Keratinbased H 2 S donor was synthesized and electrospun with poly(L-lactide-co-εcaprolactone) (PLCL) as the outer layer of the graft to release H 2 S. Hyaluronic acid, one of the major glycosaminoglycans in endothelial glycocalyx, was complexed with Cu ions as the inner layer to mimic glutathione peroxidase (GPx) and maintain long-term physiological NO flux. The synergistic effects of NO and H 2 S of bilayer grafts selectively promoted the regeneration and migration of human umbilical vascular endothelial cells (HUVECs), while inhibiting the overproliferation of human umbilical artery smooth muscle cells (HUASMCs). Bilayer grafts could effectively prevent vascular calcification, reduce inflammation, and alleviate endothelial dysfunction. The in vivo study in a rat abdominal aorta replacement model for 1 month showed that the graft had a good patency rate and had potential for vascular remodeling in situ.

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Section: Resultsmentioning

confidence: 99%

Section: ■ Results and Discussionmentioning

confidence: 99%

Endothelium-Mimicking Bilayer Vascular Grafts with Dual-Releasing of NO/H₂S for Anti-Inflammation and Anticalcification

Wang,

Liang,

Shang

et al. 2023

ACS Appl. Mater. Interfaces

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“…In addition to its direct effects on eNOS, H 2 S has been shown to modulate eNOS activity by regulating signaling pathways involved in eNOS activation. H 2 S has been reported to activate the PI3K/Akt pathway, which leads to the phosphorylation and activation of eNOS [114]. H 2 S has also been shown to activate the AMP-activated protein kinase (AMPK) pathway, which plays a critical role in regulating eNOS activity [115].…”

Section: Main Outlines Limitations and Future Directionsmentioning

confidence: 99%

Hydrogen Sulfide and Oxygen Homeostasis in Atherosclerosis: A Systematic Review from Molecular Biology to Therapeutic Perspectives

Munteanu

2023

IJMS

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Atherosclerosis is a complex pathological condition marked by the accumulation of lipids in the arterial wall, leading to the development of plaques that can eventually rupture and cause thrombotic events. In recent years, hydrogen sulfide (H2S) has emerged as a key mediator of cardiovascular homeostasis, with potential therapeutic applications in atherosclerosis. This systematic review highlights the importance of understanding the complex interplay between H2S, oxygen homeostasis, and atherosclerosis and suggests that targeting H2S signaling pathways may offer new avenues for treating and preventing this condition. Oxygen homeostasis is a critical aspect of cardiovascular health, and disruption of this balance can contribute to the development and progression of atherosclerosis. Recent studies have demonstrated that H2S plays an important role in maintaining oxygen homeostasis by regulating the function of oxygen-sensing enzymes and transcription factors in vascular cells. H2S has been shown to modulate endothelial nitric oxide synthase (eNOS) activity, which plays a key role in regulating vascular tone and oxygen delivery to tissues. The comprehensive analysis of the current understanding of H2S in atherosclerosis can pave the way for future research and the development of new therapeutic strategies for this debilitating condition. PROSPERO ID: 417150.

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“…Several H 2 S-releasing molecules have been identified or developed, including e.g. non-targeted sodium hydrosulfide (NaSH), 4-hydroxythiobenzamide, GYY4137, esterase-sensitive BW-HS platform or mitochondria-targeted AP39 or AP123 molecules [ [17] , [18] , [19] , [20] , [21] , [22] ]. Recently in vitro studies showed that GYY4137 affected oxygen consumption in endothelial cells due to the modulation of mitochondrial activity [ 23 ].…”

Section: Introductionmentioning

confidence: 99%

The mitochondria-targeted sulfide delivery molecule attenuates drugs-induced gastropathy. Involvement of heme oxygenase pathway.

et al. 2023

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Hydrogen sulfide donor AP123 restores endothelial nitric oxide-dependent vascular function in hyperglycemia via a CREB-dependent pathway

Cited by 14 publications

References 80 publications

Endothelium-Mimicking Bilayer Vascular Grafts with Dual-Releasing of NO/H₂S for Anti-Inflammation and Anticalcification

Endothelium-Mimicking Bilayer Vascular Grafts with Dual-Releasing of NO/H₂S for Anti-Inflammation and Anticalcification

Hydrogen Sulfide and Oxygen Homeostasis in Atherosclerosis: A Systematic Review from Molecular Biology to Therapeutic Perspectives

The mitochondria-targeted sulfide delivery molecule attenuates drugs-induced gastropathy. Involvement of heme oxygenase pathway.

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Hydrogen sulfide donor AP123 restores endothelial nitric oxide-dependent vascular function in hyperglycemia via a CREB-dependent pathway

Cited by 14 publications

References 80 publications

Endothelium-Mimicking Bilayer Vascular Grafts with Dual-Releasing of NO/H2S for Anti-Inflammation and Anticalcification

Endothelium-Mimicking Bilayer Vascular Grafts with Dual-Releasing of NO/H2S for Anti-Inflammation and Anticalcification

Hydrogen Sulfide and Oxygen Homeostasis in Atherosclerosis: A Systematic Review from Molecular Biology to Therapeutic Perspectives

The mitochondria-targeted sulfide delivery molecule attenuates drugs-induced gastropathy. Involvement of heme oxygenase pathway.

Contact Info

Product

Resources

About

Endothelium-Mimicking Bilayer Vascular Grafts with Dual-Releasing of NO/H₂S for Anti-Inflammation and Anticalcification

Endothelium-Mimicking Bilayer Vascular Grafts with Dual-Releasing of NO/H₂S for Anti-Inflammation and Anticalcification