scholarly journals Post-genomic insight into thylakoid membrane lateral heterogeneity and redox balance

FEBS Letters ◽  
2012 ◽  
Vol 586 (18) ◽  
pp. 2911-2916 ◽  
Author(s):  
Mikko Tikkanen ◽  
Marjaana Suorsa ◽  
Peter J. Gollan ◽  
Eva-Mari Aro
2021 ◽  
Vol 22 (11) ◽  
pp. 5937
Author(s):  
David Bode ◽  
Lukas Semmler ◽  
Christian U. Oeing ◽  
Alessio Alogna ◽  
Gabriele G. Schiattarella ◽  
...  

Atrial fibrillation (AF) is the most common sustained (atrial) arrhythmia, a considerable global health burden and often associated with heart failure. Perturbations of redox signalling in cardiomyocytes provide a cellular substrate for the manifestation and maintenance of atrial arrhythmias. Several clinical trials have shown that treatment with sodium-glucose linked transporter inhibitors (SGLTi) improves mortality and hospitalisation in heart failure patients independent of the presence of diabetes. Post hoc analysis of the DECLARE-TIMI 58 trial showed a 19% reduction in AF in patients with diabetes mellitus (hazard ratio, 0.81 (95% confidence interval: 0.68–0.95), n = 17.160) upon treatment with SGLTi, regardless of pre-existing AF or heart failure and independent from blood pressure or renal function. Accordingly, ongoing experimental work suggests that SGLTi not only positively impact heart failure but also counteract cellular ROS production in cardiomyocytes, thereby potentially altering atrial remodelling and reducing AF burden. In this article, we review recent studies investigating the effect of SGLTi on cellular processes closely interlinked with redox balance and their potential effects on the onset and progression of AF. Despite promising insight into SGLTi effect on Ca2+ cycling, Na+ balance, inflammatory and fibrotic signalling, mitochondrial function and energy balance and their potential effect on AF, the data are not yet conclusive and the importance of individual pathways for human AF remains to be established. Lastly, an overview of clinical studies investigating SGLTi in the context of AF is provided.


Lipids ◽  
2000 ◽  
Vol 35 (7) ◽  
pp. 739-744 ◽  
Author(s):  
Sylvie Duchêne ◽  
Paul-André Siegenthaler

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Bin Yin ◽  
Jiaxue Zhang ◽  
Yadi Liu ◽  
Xiang Pan ◽  
Zhijing Zhao ◽  
...  

AbstractPlant mitochondria are important energy-producing structure and ROS are generated as byproducts. APX is one enzyme of the AsA-GSH cycle to reduces H2O2 to water. We identified both PtomtAPX and PtosAPX are located in mitochondria of Populus tomentosa Carr. PtomtAPX is specifically targeted to mitochondria, while PtosAPX is dual targeted to both chloroplast and mitochondria. The expression of PtomtAPX in mitochondria was 60-fold that of PtosAPX by ELISA and qPCR analysis. Under high light stress, the expression levels of PtosAPX increased, while that of PtomtAPX only slightly changed. Compared to the WT, the antisense transgenic PtomtAPX cell lines showed slowed growth, smaller cells impaired mitochondria in MS medium under normal growth. RNA-seq results showed 3121 genes significantly altered expression in the antisense cells, and most of them are important for mitochondrial function, particularly in oxidative phosphorylation. Our findings demonstrates a mitochondrial location for one APX isoform, and provide valuable insight into the mechanism which ROS balance is modulated by AsA-GSH cycle in mitochondria.


2021 ◽  
Vol 22 (20) ◽  
pp. 11010
Author(s):  
Daniel J. Torres ◽  
Matthew W. Pitts ◽  
Lucia A. Seale ◽  
Ann C. Hashimoto ◽  
Katlyn J. An ◽  
...  

The role of the essential trace element selenium in hypothalamic physiology has begun to come to light over recent years. Selenium is used to synthesize a family of proteins participating in redox reactions called selenoproteins, which contain a selenocysteine residue in place of a cysteine. Past studies have shown that disrupted selenoprotein expression in the hypothalamus can adversely impact energy homeostasis. There is also evidence that selenium supports leptin signaling in the hypothalamus by maintaining proper redox balance. In this study, we generated mice with conditional knockout of the selenocysteine tRNA[Ser]Sec gene (Trsp) in an orexigenic cell population called agouti-related peptide (Agrp)-positive neurons. We found that female TrspAgrpKO mice gain less weight while on a high-fat diet, which occurs due to changes in adipose tissue activity. Female TrspAgrpKO mice also retained hypothalamic sensitivity to leptin administration. Male mice were unaffected, however, highlighting the sexually dimorphic influence of selenium on neurobiology and energy homeostasis. These findings provide novel insight into the role of selenoproteins within a small yet heavily influential population of hypothalamic neurons.


2020 ◽  
Author(s):  
Marta Hammerstad ◽  
Ingvild Gudim ◽  
Hans-Petter Hersleth

AbstractLow G+C Gram-positive Firmicutes, such as the clinically important pathogens Staphylococcus aureus and Bacillus cereus, use the low-molecular weight (LMW) thiol bacillithiol (BSH) as a defense mechanism to buffer the intracellular redox environment and counteract oxidative stress encountered by human neutrophils during infections. The protein YpdA has recently been shown to function as an essential NADPH-dependent reductase of oxidized bacillithiol disulfide (BSSB) resulting from stress responses and is crucial in maintaining the reduced pool of BSH and cellular redox balance. In this work, we present the first crystallographic structures of YpdAs, namely from S. aureus and B. cereus. Our analyses reveal a uniquely organized biological tetramer; however, the monomeric subunit has high structural similarity to other flavin disulfide reductases. The absence of a redox active cysteine in the vicinity of the FAD isoalloxazine ring implies a new direct disulfide reduction mechanism, which is backed by the presence of a potentially gated channel, serving as a putative binding site for BSSB in proximity to the FAD cofactor. We also report enzymatic activity for both YpdAs, which along with the structures presented in this work provide important structural and functional insight into a new class of FAD-containing NADPH-dependent oxidoreductases, related to the emerging fight against pathogenic bacteria.


2012 ◽  
Vol 367 (1608) ◽  
pp. 3384-3388 ◽  
Author(s):  
Jan M. Anderson

The concept that the two photosystems of photosynthesis cooperate in series, immortalized in Hill and Bendall's Z scheme, was still a black box that defined neither the structural nor the molecular organization of the thylakoid membrane network into grana and stroma thylakoids. The differentiation of the continuous thylakoid membrane into stacked grana thylakoids interconnected by single stroma thylakoids is a morphological reflection of the non-random distribution of photosystem II/light-harvesting complex of photosystem II, photosystem I and ATP synthase, which became known as lateral heterogeneity.


2015 ◽  
Vol 119 (1) ◽  
pp. 1-15 ◽  
Author(s):  
Aastha Mishra ◽  
Ghulam Mohammad ◽  
Tsering Norboo ◽  
John H. Newman ◽  
M. A. Qadar Pasha

Hypobaric hypoxia at high altitude (HA) results in reduced blood arterial oxygen saturation, perfusion of organs with hypoxemic blood, and direct hypoxia of lung tissues. The pulmonary complications in the cells of the pulmonary arterioles due to hypobaric hypoxia are the basis of the pathophysiological mechanisms of high-altitude pulmonary edema (HAPE). Some populations that have dwelled at HA for thousands of years have evolutionarily adapted to this environmental stress; unadapted populations may react with excessive physiological responses that impair health. Individual variations in response to hypoxia and the mechanisms of HA adaptation provide insight into physiological responses. Adaptive and maladaptive responses include alterations in pathways such as oxygen sensing, hypoxia signaling, K+- and Ca2+-gated channels, redox balance, and the renin-angiotensin-aldosterone system. Physiological imbalances are linked with genetic susceptibilities, and nonhomeostatic responses in gene regulation that occur by small RNAs, histone modification, and DNA methylation predispose susceptible humans to these HA illnesses. Elucidation of the interaction of these factors will lead to a more comprehensive understanding of HA adaptations and maladaptations and will lead to new therapeutics for HA disorders related to hypoxic lungs.


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