PECTOPLATE: the simultaneous phenotyping of pectin methylesterases, pectinases and oligogalacturonides in plants during biotic stresses

Degradation of pectin, a major component of plant cell wall, is important for fungal necrotrophs to achieve a successful infection. The activities of pectin methylesterases (PMEs) from both plants and pathogens and the degree and pattern of pectin methylesterification are critical for the outcome of plant–pathogen interaction. Partial degradation of pectin by pectin degrading enzymes releases oligogalacturonides (OGs), elicitors of plant defense responses. Few analytical techniques are available to monitor pectin methylesterification-modulating machineries and OGs produced during plant pathogen interaction. In the present study, ruthenium red is presented as useful dye to monitor both Botrytis cinerea mycelium growth and the induction of PME activity in plant tissue during fungal infection. Moreover a simple, inexpensive and sensitive method, named PECTOPLATE, is proposed that allows a simultaneous phenotyping of PME and pectinase activities expressed during pathogen infection and of pectinase potential in generating OGs. The results in the manuscript also indicate that PME inhibitors can be used in PECTOPLATE as a tool to discriminate the activities of plant PMEs from those of pathogen PMEs expressed during pathogenesis

Prometheus’s Heart: what lies beneath

A heart attack kills off many cells in the heart. Parts of the heart become thin and fail to contract properly following the replacement oflost cells by scar tissue. However, the notion that the same adult cardiomyocytes beat throughout the lifespan of the organ and organism,without the need for a minimum turnover, gives way to a fascinating investigations. Since the late 1800s, scientists and cardiologistswanted to demonstrate that the cardiomyocytes cannot be generated after the perinatal period in human beings. This curiosity hasbeen passed down in subsequent years and has motivated more and more accurate studies in an attempt to exclude the presence ofrenewed cardiomyocytes in the tissue bordering the ischaemic area, and then to confirm the dogma of the heart as terminally differentiated organ. Conversely, peri-lesional mitosis of cardiomyocytes were discovered initially by light microscopy and subsequently confirmed by more sophisticated technologies. Controversial evidence of mechanisms underlying myocardial regeneration has shown that adult cardiomyocytes are renewed through a slow turnover, even in the absence of damage. This turnover is ensured by the activationof rare clusters of progenitor cells interspersed among the cardiac cells functionally mature. Cardiac progenitor cells continuously interactwith each other, with the cells circulating in the vessels of the coronary microcirculation and myocardial cells in auto-/paracrine manner. Much remains to be understood; however, the limited functional recovery in human beings after myocardial injury clearly demonstrates weak regenerative potential of cardiomyocytes and encourages the development of new approaches to stimulate this process

Pectic enzymes as potential enhancers of ascorbic acid production through the D-galacturonate pathway in Solanaceae

The increase of L-Ascorbic Acid (AsA) content in tomato (Solanum lycopersicum) is a common goal in breeding programs due to its beneficial effect on human health. To shed light into the regulation of fruit AsA content, we exploited a Solanum pennellii introgression line (IL12-4-SL) harbouring one quantitative trait locus that increases the content of total AsA in the fruit. Biochemical and transcriptomic analyses were carried out in fruits of IL12-4-SL in comparison with the cultivated line M82 at different stages of ripening. AsA content was studied in relation with pectin methylesterase (PME) activity and the degree of pectin methylesterification (DME). Our results indicated that the increase of AsA content in IL12-4-SL fruits was related with pectin de-methylesterification/degradation. Specific PME, polygalacturonase (PG) and UDP-D-glucuronic-acid-4-epimerase (UGlcAE) isoforms were proposed as components of the D-galacturonate pathway leading to AsA biosynthesis. The relationship between AsA content and PME activity was also exploited in PMEI tobacco plants expressing a specific PME inhibitor (PMEI). Here we report that tobacco PMEI plants, altered in PME activity and degree of pectin methylesterification, showed a reduction in low methylesterified pectic domains and exhibited a reduced AsA content. Overall, our results provide novel biochemical and genetic traits for increasing antioxidant content by marker-assisted selection in the Solanaceae family

how resident stem cells communicate with cardiac cells in beatingheart

The adult myocardium is a dynamic tissue with different functions which normally adapts to endless mechanical loads throughout life. The complexity and diversity of myocardial responses to different conditions imply the coexistence of different cell types within a hierarchically ordered architecture. Rare stem/progenitor cells have been detected interspersed within the interstitium and/or adherent to the wall of the capillaries forming the myocardial microcirculation. The origin of these cells is still debated. Multipotent and self-renewing cells resident into the heart survive to a mechanically and biochemically active environment without acquiring a cardiac phenotype. The persistence of an intense physical and biochemical stress do not affect the gene profyle of these cells in beating heart. Otherwise, differentiated cardiac cells continually release humoral factors preserving the fate of stem/progenitor cells. It is conceivable that undifferentiated cardiac cells have a different bio-mechanical response threshold compared to cells resident in other tissue. The codification of the language adopted by cardiac stem/progenitor cells to communicate with each other and other myocardial cells will help the cardiovascular therapy to fulfill its true potential

Plant cell wall dynamics and wall-related susceptibility in plant–pathogen interactions

The cell wall is a dynamic structure that often determines the outcome of the interactions between plants and pathogens. It is a barrier that pathogens need to breach to colonize the plant tissue. While fungal necrotrophs extensively destroy the integrity of the cell wall through the combined action of degrading enzymes, biotrophic fungi require a more localized and controlled degradation of the cell wall in order to keep the host cells alive and utilize their feeding structures. Also bacteria and nematodes need to degrade the plant cell wall at a certain stage of their infection process, to obtain nutrients for their growth. Plants have developed a system for sensing pathogens and monitoring the cell wall integrity, upon which they activate defense responses that lead to a dynamic cell wall remodeling required to prevent the disease. Pathogens, on the other hand, may exploit the host cell wall metabolism to support the infection. We review here the strategies utilized by both plants and pathogens to prevail in the cell wall battleground

the unexpected cardioprotection by epigenetic foods

Epigenetic changes affect the gene expression profile of cells without altering the DNA sequence in response to different environmental stimuli, such as the diet. Several dietary plant compounds have the epigenetic ability to prevent both the onset and the progression of different diseases, including cardiovascular diseases that are one of the most common in the world. Heart failure following perioperative myocardial infarction is a complex clinical syndrome without cure, also affecting high-risk patients undergoing non-cardiac surgery. It is characterized by serious decay of cardiac pump function as a result of ongoing remodelling of the myocardium. Despite the increasing use of conventional medications has reduced the mortality of patients with myocardial infarction, the outcome remains unpredictable so far. The past three decades have witnessed incessant research aimed at protecting the adult myocardium against ischemic injury, but the development of effective strategies to prevent the maladaptive tissue remodelling is still a desirable achievement. Recent findings reveal that the dietary intake of natural bioactive components with known antioxidant activity improves the intercellular communication and increases the tolerance of both cardiomyocytes and coronary endothelial cells against the ischemic microenvironment. The Epigenetic activation of rescue genes prevents the decay of function of the abovementioned cardiac cells. Consequently, this scenario would reduce the myocardial accumulation of collagen responsible for the tightening of the heart walls. Whereas the noninvasive delivery of cardioprotectant epigenetic compounds through diet is a promising approach, regulatory mechanisms need to be unravelled

Planetary health: an interdisciplinary perspective

This paper addresses the issue of planetary health under a multidisciplinary profile. It starts with defining the scope of planetary health, retracing its most salient historical points. It then reflects on the socio-political changes needed to achieve transformational change in society. The concepts of health literacy and environmental health literacy are explored as a useful means of disseminating and raising awareness about planetary health. Finally, a case study related to heart disease is explored to demonstrate why this approach is more necessary today than ever

Diet impact on Mitochondrial Bioenergetics and Dynamics

Diet induced obesity is associated with impaired mitochondrial function and dynamic behavior. Mitochondria are highly dynamic organelles and the balance in fusion/fission is strictly associated with their bioenergetics. Fusion processes are associated with the optimization of mitochondrial function, whereas fission processes are associated with the removal of damaged mitochondria. In diet-induced obesity, impaired mitochondrial function and increased fission processes were found in liver and skeletal muscle. Diverse dietary fat sources differently affect mitochondrial dynamics and bioenergetics. In contrast to saturated fatty acids, omega 3 polyunsaturated fatty acids induce fusion processes and improve mitochondrial function. Moreover, the pro-longevity effect of caloric restriction has been correlated with changes in mitochondrial dynamics leading to decreased cell oxidative injury. Noteworthy, emerging findings revealed an important role for mitochondrial dynamics within neuronal populations involved in central regulation of body energy balance. In conclusion, mitochondrial dynamic processes with their strict interconnection with mitochondrial bioenergetics are involved in energy balance and diet impact on metabolic tissues

Late plasma exosome microRNA-21-5p depicts magnitude of reverse ventricular remodeling after early surgical repair of primary mitral valve regurgitation

Introduction: Primary mitral valve regurgitation (MR) results from degeneration of mitral valve apparatus. Mechanisms leading to incomplete postoperative left ventricular (LV) reverse remodeling (Rev–Rem) despite timely and successful surgical mitral valve repair (MVR) remain unknown. Plasma exosomes (pEXOs) are smallest nanovesicles exerting early postoperative cardioprotection. We hypothesized that late plasma exosomal microRNAs (miRs) contribute to Rev–Rem during the late postoperative period. Methods: Primary MR patients (n = 19; age, 45–71 years) underwent cardiac magnetic resonance imaging and blood sampling before (T0) and 6 months after (T1) MVR. The postoperative LV Rev–Rem was assessed in terms of a decrease in LV end-diastolic volume and patients were stratified into high (HiR-REM) and low (LoR-REM) LV Rev–Rem subgroups. Isolated pEXOs were quantified by nanoparticle tracking analysis. Exosomal microRNA (miR)-1, –21–5p, –133a, and –208a levels were measured by RT-qPCR. Anti-hypertrophic effects of pEXOs were tested in HL-1 cardiomyocytes cultured with angiotensin II (AngII, 1 μM for 48 h). Results: Surgery zeroed out volume regurgitation in all patients. Although preoperative pEXOs were similar in both groups, pEXO levels increased after MVR in HiR-REM patients (+0.75-fold, p = 0.016), who showed lower cardiac mass index (–11%, p = 0.032). Postoperative exosomal miR-21-5p values of HiR-REM patients were higher than other groups (p < 0.05). In vitro, T1-pEXOs isolated from LoR-REM patients boosted the AngII-induced cardiomyocyte hypertrophy, but not postoperative exosomes of HiR-REM. This adaptive effect was counteracted by miR-21-5p inhibition. Summary/Conclusion: High levels of miR-21-5p-enriched pEXOs during the late postoperative period depict higher LV Rev–Rem after MVR. miR-21-5p-enriched pEXOs may be helpful to predict and to treat incomplete LV Rev–Rem after successful early surgical MVR