Signaling by S-nitrosylation in the heart

Abstract

Nitric oxide is a gaseous signaling molecule that is well-known for the Nobel prize-winning research that defined nitric oxide as a physiological regulator of blood pressure in the cardiovascular system. Nitric oxide can signal via the classical pathway involving activation of guanylyl cyclase or by a post-translational modification, referred to as S-nitrosylation (SNO) that can occur on cysteine residues of proteins. As proteins with cysteine residues are common, this allows for amplification of the nitric oxide signaling. This review will focus on the possible mechanisms through which SNO can alter protein function in cardiac cells, and the role of SNO occupancy in these mechanisms. The specific mechanisms that regulate protein SNO, including redox-dependent processes, will also be discussed.

Effect of Nitric Oxide on Cardiac Functions: Review

“…Protein S-nitrozilasyonu, dinitrojen trioksit veya nitrozonyum iyonu eklenmesi gibi mekanizmalarla da gerçekleşebilmektedir. 32 S-nitrozilasyon'un NF-κB, hipoksiyle indüklenebilen faktör "hypoxia inducible factor (HIF)" gibi transkripsiyon faktörleri, kaspazlar, N-metil-D-aspartik asit (NMDA) reseptör iyon kanalları, G protein Ras ailesi, matriks metalloproteinazları ve riyanodin reseptörleri (RyR) nin düzenlenmesinde önemli olduğu bilinmektedir. 24 sGC'nin S-nitrozilasyonu ile inhibisyonu da gerçekleşebilmektedir.…”

“…32 3 3) ) N Ni it tr ra as sy yo on n İ İl le e O Ok ks si id da as sy yo on n: : Bir nitrozo (NO 2 ) grubunun, hedef molekülün aromatik karbonlarına bağlanması "nitrasyon" olarak bilinmektedir. Proteinler gibi lipitler ve alkoller de nitrasyona uğra-yabilmektedir.…”

Peroxiredoxin-2 nitrosylation facilitates cardiomyogenesis of mouse embryonic stem cells via XBP-1s/PI3K pathway

“…Nitrosylation can affect proteins from many aspects, such as stability, enzymatic activity and interactions with other proteins [8,9]. Notably, the redox-dependent signaling via S-nitrosylation in the Contents lists available at ScienceDirect journal homepage: www.elsevier.com/locate/freeradbiomed heart has been indicated as two enzyme systems in particular, the glutathione/S-nitrosoglutathione reductase (GSH/GSNOR) and the thioredoxin/thioredoxin reductase (Trx/TrxR) [10]. However, whether their downstream reductases, peroxiredoxin (Prdx) family, also take role in the heart is so far not elucidated.…”

Cytoprotective approaches to protect myocardium against ischemia/reperfusion injury

“…It typically exerts its physiological functions by binding directly to ferrous iron of heme proteins or indirectly by S-nitrosylation of protein thiol groups [51]. NO is synthesized at low physiological levels by NO synthase (NOS) enzymes.…”

“…51,[53][54][55][56][57]. However, excess of NO in the presence of the co-existing free radicals have detrimental effect on cell survival.…”