bims-polyam 2022-01-09 papers

Issue of 2022–01–09
five papers selected by
Sebastian J. Hofer, University of Graz

Chin J Physiol. 2021 Nov-Dec;64(6):64(6): 281-288

A study of the cardioprotective effect of spermidine: A novel inducer of autophagy.

Eman Magdy Omar, Rasha Said Omar, Mai Said Shoela, Norhan Sobhy El Sayed.

Acute myocardial infarction (AMI) is an instant death of cardiomyocytes that ends in a large mortality worldwide. Thus, there is a great interest to come up with novel protective approaches for AMI to mount cardiomyocyte survival, enhance postinfarcted cardiac function, and countermand the process of cardiac remodeling. Spermidine has vital roles in vast cellular processes under pathophysiological circumstances. This study aims to enhance our comprehension of the role of autophagy as a possible protective sequel of spermidine supplementation on postinfarction ventricular dysfunction in a rat model of AMI induced by isoproterenol (ISO). Thirty male rats were divided into three groups (control, AMI, and spermidine + AMI). AMI was induced by subcutaneous ISO injections for two consecutive days. Rats were pretreated with spermidine by intraperitoneal injection before induction of AMI. Electrocardiogram (ECG) was recorded in all rats 24 h after the second dose of ISO. Rats were sacrificed after ECG recording, and samples were taken for biochemical assessments. Spermidine intake before induction of AMI in rats significantly attenuated cardiac dysfunction where cardiac enzymes are decreased, and ECG changes induced by ISO are reversed in cardiomyocytes. Spermidine affects the autophagic flux of autophagy-related protein expression (LC3-II, TFEP, and p62). Furthermore, it increased the total antioxidant capacity.

Keywords: Acute myocardial infarction; autophagy; oxidative stress; spermidine

DOI: https://doi.org/10.4103/cjp.cjp_76_21

Anim Nutr. 2022 Mar;8(1): 135-143

Spermine protects intestinal barrier integrity through ras-related C3 botulinum toxin substrate 1/phospholipase C-γ1 signaling pathway in piglets.

Guangmang Liu, Xiaomei Xu, Caimei Wu, Gang Jia, Hua Zhao, Xiaoling Chen, Gang Tian, Jingyi Cai, Jing Wang.

Weaning stress can cause tight junctions damage and intestinal permeability enhancement, which leads to intestinal imbalance and growth retardation, thereby causing damage to piglet growth and development. Spermine can reduce stress. However, the mechanism of spermine modulating the intestinal integrity in pigs remains largely unknown. This study aims to examine whether spermine protects the intestinal barrier integrity of piglets through ras-related C3 botulinum toxin substrate 1 (Rac1)/phospholipase C-γ1 (PLC-γ1) signaling pathway. In vivo, 80 piglets were categorised into 4 control groups and 4 spermine groups (10 piglets per group). The piglets were fed with normal saline or spermine at 0.4 mmol/kg BW for 7 h and 3, 6 and 9 d. In vitro, we investigated whether spermine protects the intestinal barrier after a tumor necrosis factor α (TNF-α) challenge through Rac1/PLC-γ1 signaling pathway. The in vivo study found that spermine supplementation increased tight junction protein mRNA levels and Rac1/PLC-γ1 signaling pathway gene expression in the jejunum of piglets. The serum D-lactate content was significantly decreased after spermine supplementation (P < 0.05). The in vitro study found that 0.1 μmol/L spermine increased the levels of tight junction protein expression, Rac1/PLC-γ1 signaling pathway and transepithelial electrical resistance, and decreased paracellular permeability (P < 0.05). Further experiments demonstrated that spermine supplementation enhanced the levels of tight junction protein expression, Rac1/PLC-γ1 signaling pathway and transepithelial electrical resistance, and decreased paracellular permeability compared with the NSC-23766 and U73122 treatment with spermine after TNF-α challenge (P < 0.05). Collectively, spermine protects intestinal barrier integrity through Rac1/PLC-γ1 signaling pathway in piglets.

Keywords: Intestinal barrier; Intestinal integrity; Rac1/PLC-γ1 signaling pathway; Spermine

DOI: https://doi.org/10.1016/j.aninu.2021.06.016

Mol Oral Microbiol. 2022 Jan 06.

Spermidine enhances the survival of Streptococcus pyogenes M3 under oxidative stress.

Rajashri Banerji, Parvati Iyer, Sunil D Saroj.

Streptococcus pyogenes, a host-restricted gram-positive pathogen during infection, initially adheres to the epithelia of the nasopharynx and respiratory tract of the human host; followed by disseminating to other organs and evading the host immune system. Upon phagocytosis, S. pyogenes encounters oxidative stress inside the macrophages. The role of polyamines in regulating various physiological functions, including stress resistance in bacteria have been reported widely. Since S. pyogenes lacks the machinery for the biosynthesis of polyamines, the study aimed to understand the role of extracellular polyamines in the survival of S. pyogenes under oxidative stress environments. S. pyogenes being a catalase-negative organism, we report that its survival within the macrophages and H2 O2 is enhanced by the presence of spermidine. The increased survival can be attributed to the upregulation of oxidative stress response genes like sodM, npx, and mtsABC. In addition, spermidine influences the upregulation of virulence factors such as sagA, slo, and hasA. Also, spermidine leads to a decrease in hydrophobicity of the cell membrane and an increase in hyaluronic acid. This report suggests a role for extracellular spermidine in the survival of S. pyogenes under oxidative stress environments. Recognizing the factors that modulate S. pyogenes survival and virulence under stress will assist in understanding its interactions with the host. This article is protected by copyright. All rights reserved.

Keywords: adhesion; gene expression; pathogenesis; polyamines; virulence

DOI: https://doi.org/10.1111/omi.12360

PLoS One. 2022 ;17(1): e0262099

Exogenous putrescine attenuates the negative impact of drought stress by modulating physio-biochemical traits and gene expression in sugar beet (Beta vulgaris L.).

Md Jahirul Islam, Md Jalal Uddin, Mohammad Anwar Hossain, Robert Henry, Mst Kohinoor Begum, Md Abu Taher Sohel, Masuma Akter Mou, Juhee Ahn, Eun Ju Cheong, Young-Seok Lim.

Drought tolerance is a complex trait controlled by many metabolic pathways and genes and identifying a solution to increase the resilience of plants to drought stress is one of the grand challenges in plant biology. This study provided compelling evidence of increased drought stress tolerance in two sugar beet genotypes when treated with exogenous putrescine (Put) at the seedling stage. Morpho-physiological and biochemical traits and gene expression were assessed in thirty-day-old sugar beet seedlings subjected to drought stress with or without Put (0.3, 0.6, and 0.9 mM) application. Sugar beet plants exposed to drought stress exhibited a significant decline in growth and development as evidenced by root and shoot growth characteristics, photosynthetic pigments, antioxidant enzyme activities, and gene expression. Drought stress resulted in a sharp increase in hydrogen peroxide (H2O2) (89.4 and 118% in SBT-010 and BSRI Sugar beet 2, respectively) and malondialdehyde (MDA) (35.6 and 27.1% in SBT-010 and BSRI Sugar beet 2, respectively). These changes were strongly linked to growth retardation as evidenced by principal component analysis (PCA) and heatmap clustering. Importantly, Put-sprayed plants suffered from less oxidative stress as indicated by lower H2O2 and MDA accumulation. They better regulated the physiological processes supporting growth, dry matter accumulation, photosynthetic pigmentation and gas exchange, relative water content; modulated biochemical changes including proline, total soluble carbohydrate, total soluble sugar, and ascorbic acid; and enhanced the activities of antioxidant enzymes and gene expression. PCA results strongly suggested that Put conferred drought tolerance mostly by enhancing antioxidant enzymes activities that regulated homeostasis of reactive oxygen species. These findings collectively provide an important illustration of the use of Put in modulating drought tolerance in sugar beet plants.

DOI: https://doi.org/10.1371/journal.pone.0262099

Nat Metab. 2022 Jan 06.

Oxidative ornithine metabolism supports non-inflammatory C. difficile colonization.

Kali M Pruss, Fatima Enam, Eric Battaglioli, Mary DeFeo, Oscar R Diaz, Steven K Higginbottom, Curt R Fischer, Andrew J Hryckowian, William Van Treuren, Dylan Dodd, Purna Kashyap, Justin L Sonnenburg.

The enteric pathogen Clostridioides difficile (Cd) is responsible for a toxin-mediated infection that causes more than 200,000 recorded hospitalizations and 13,000 deaths in the United States every year1. However, Cd can colonize the gut in the absence of disease symptoms. Prevalence of asymptomatic colonization by toxigenic Cd in healthy populations is high; asymptomatic carriers are at increased risk of infection compared to noncolonized individuals and may be a reservoir for transmission of Cd infection2,3. Elucidating the molecular mechanisms by which Cd persists in the absence of disease is necessary for understanding pathogenesis and developing refined therapeutic strategies. Here, we show with gut microbiome metatranscriptomic analysis that mice recalcitrant to Cd infection and inflammation exhibit increased community-wide expression of arginine and ornithine metabolic pathways. To query Cd metabolism specifically, we leverage RNA sequencing in gnotobiotic mice infected with two wild-type strains (630 and R20291) and isogenic toxin-deficient mutants of these strains to differentiate inflammation-dependent versus -independent transcriptional states. A single operon encoding oxidative ornithine degradation is consistently upregulated across non-toxigenic Cd strains. Combining untargeted and targeted metabolomics with bacterial and host genetics, we demonstrate that both diet- and host-derived sources of ornithine provide a competitive advantage to Cd, suggesting a mechanism for Cd persistence within a non-inflammatory, healthy gut.

DOI: https://doi.org/10.1038/s42255-021-00506-4