Heat Stress-induced Damage Research Articles

Rice responses to rising temperatures--challenges, perspectives and future directions.

Phenotypic plasticity in overcoming heat stress-induced damage across hot tropical rice-growing regions is predominantly governed by relative humidity. Expression of transpiration cooling, an effective heat-avoiding mechanism, will diminish with the transition from fully flooded paddies to water-saving technologies, such as direct-seeded and aerobic rice cultivation, thus further aggravating stress damage. This change can potentially introduce greater sensitivity to previously unaffected developmental stages such as floral meristem (panicle) initiation and spikelet differentiation, and further intensify vulnerability at the known sensitive gametogenesis and flowering stages. More than the mean temperature rise, increased variability and a more rapid increase in nighttime temperature compared with the daytime maximum present a greater challenge. This review addresses (1) the importance of vapour pressure deficit under fully flooded paddies and increased vulnerability of rice production to heat stress or intermittent occurrence of combined heat and drought stress under emerging water-saving rice technologies; (2) the major disconnect with high night temperature response between field and controlled environments in terms of spikelet sterility; (3) highlights the most important mechanisms that affect key grain quality parameters, such as chalk formation under heat stress; and finally (4), we model and estimate heat stress-induced spikelet sterility taking South Asia as a case study.

Sodium hydrosulfide induces systemic thermotolerance to strawberry plants through transcriptional regulation of heat shock proteins and aquaporin

BackgroundTemperature extremes represent an important limiting factor to plant growth and productivity. The present study evaluated the effect of hydroponic pretreatment of strawberry (Fragaria x ananassa cv. ‘Camarosa’) roots with an H2S donor, sodium hydrosulfide (NaHS; 100 μM for 48 h), on the response of plants to acute heat shock treatment (42°C, 8 h).ResultsHeat stress-induced phenotypic damage was ameliorated in NaHS-pretreated plants, which managed to preserve higher maximum photochemical PSII quantum yields than stressed plants. Apparent mitigating effects of H2S pretreatment were registered regarding oxidative and nitrosative secondary stress, since malondialdehyde (MDA), H2O2 and nitric oxide (NO) were quantified in lower amounts than in heat-stressed plants. In addition, NaHS pretreatment preserved ascorbate/glutathione homeostasis, as evidenced by lower ASC and GSH pool redox disturbances and enhanced transcription of ASC (GDH) and GSH biosynthetic enzymes (GS, GCS), 8 h after heat stress imposition. Furthermore, NaHS root pretreatment resulted in induction of gene expression levels of an array of protective molecules, such as enzymatic antioxidants (cAPX, CAT, MnSOD, GR), heat shock proteins (HSP70, HSP80, HSP90) and aquaporins (PIP).ConclusionOverall, we propose that H2S root pretreatment activates a coordinated network of heat shock defense-related pathways at a transcriptional level and systemically protects strawberry plants from heat shock-induced damage.

Ursolic acid prevents endoplasmic reticulum stress-mediated apoptosis induced by heat stress in mouse cardiac myocytes

Heat stress causes serious physiological dysfunction of cardiac myocytes and is associated with several types of cardiovascular diseases. However, the underlying mechanisms and therapeutic strategies to alleviate heat stress-induced myocardial damage are not available. The objective of this study was to (1) investigate the functional role of endoplasmic reticulum (ER) stress-mediated apoptosis in heat exposure-induced myocardial damage, and (2) to evaluate the effects of ursolic acid on the myocardial apoptosis as well as the underlying mechanisms in mouse cardiac myocytes. We show here that heat stress-induced apoptosis is predominantly mediated by the activation of PERK-eIF2α-CHOP unfolded protein response which up-regulates the protein expression of Puma, and by the modulation of cellular redox state. Intriguingly, the myocardial apoptosis is markedly attenuated by ursolic acid treatment. Mechanistically, the protective effects of ursolic acid are mediated, at least partly, by reestablishing the intracellular redox state and inducing the expression of the anti-apoptotic protein Mcl-1, which, in turn, inactivating CHOP-induced Puma up-regulation. The striking finding that ursolic acid has both anti-apoptotic and antioxidative activities against ER stress-associated myocardial damage suggests that supplementation of ursolic acid might be a potential strategy to reduce the detrimental effects of heat stress in cardiomyocytes.

Saikosaponin-D attenuates heat stress-induced oxidative damage in LLC-PK1 cells by increasing the expression of anti-oxidant enzymes and HSP72.

Heat stress stimulates the production of reactive oxygen species (ROS), which cause oxidative damage in the kidney. This study clarifies the mechanism by which saikosaponin-d (SSd), which is extracted from the roots of Bupleurum falcatum L, protects heat-stressed pig kidney proximal tubular (LLC-PK1) cells against oxidative damage. SSd alone is not cytotoxic at concentrations of 1 or 3 μg/mL as demonstrated by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. To assess the effects of SSd on heat stress-induced cellular damage, LLC-PK1 cells were pretreated with various concentrations of SSd, heat stressed at 42°C for 1 h, and then returned to 37°C for 9 h. DNA ladder and MTT assays demonstrated that SSd helped to prevent heat stress-induced cellular damage when compared to untreated cells. Additionally, pretreatment with SSd increased the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) but decreased the concentration of malondialdehyde (MDA) in a dose-dependent manner when compared to controls. Furthermore, real-time PCR and Western blot analysis demonstrated that SSd significantly increased the expression of copper and zinc superoxide dismutase (SOD-1), CAT, GPx-1 and heat shock protein 72 (HSP72) at both the mRNA and protein levels. In conclusion, these results are the first to demonstrate that SSd ameliorates heat stress-induced oxidative damage by modulating the activity of anti-oxidant enzymes and HSP72 in LLC-PK1 cells.

The polyamine spermine protects Arabidopsis from heat stress-induced damage by increasing expression of heat shock-related genes

It is known that the polyamine (PA) biosynthetic pathway is modulated at the transcriptional level during abiotic stresses. Here we studied the expression of PA biosynthetic pathway genes upon exposure to heat shock (HS) in Arabidopsis and showed that the spermine (Spm) synthase gene (SPMS) and S-adenosylmethionine decarboxylase 2 gene are induced at the earliest stage, followed by the induction of the arginine decarboxylase 2 gene. Correspondingly, Spm content increased linearly upon HS, and putrescine (Put) and spermidine (Spd) content also increased but not thermospermine (T-Spm) content. Exogenously applied Spm had a potential to protect Arabidopsis plants from HS-induced damage. Such protection was also observed to the same extent with T-Spm and by Spd to a lesser extent but not by Put. Then we tested whether altered endogenous Spm content affects sensitivity to HS using both transgenic plants overexpressing SPMS and a Spm deficient (spms) mutant plant. The result revealed that the higher the Spm content the higher the thermotolerance. Even in the spms plant, representative genes encoding heat shock proteins (HSPs) and heat shock transcription factors were upregulated upon HS, while the expression of such genes was increased in a positively correlated manner with Spm content. Furthermore four kinds of HSPs (HSP101, HSP90, HSP70 and HSP17.6) were detected proportionally with the levels of their respective transcripts upon HS. We propose that Spm increases the HS response at transcriptional and translational levels and protects host plants from HS-induced damage.

Involvement of oxidative stress and mitogen-activated protein kinase signaling pathways in heat stress-induced injury in the rat small intestine

Extreme heat stress-induced gastrointestinal injury and dysfunction may occur during summer. We investigated possible mechanisms of heat stress-induced damage in the small intestine using male Sprague-Dawley rats subjected to 2 h of heat stress (40°C, 60% relative humidity) daily for 10 consecutive days. Rats were killed at specific times immediately following heat treatment to determine: morphological changes by optical and electron microscopy; intestinal permeability using fluorescein isothiocyanate–dextran; production of reactive oxygen species (ROS), malondialdehyde (MDA), and activities of superoxide-dismutase and glutathione-peroxidase by specific assays; phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) by immunocytochemistry and western-blot analysis. The rat intestinal epithelial cell line (IEC-6) and specific MAPK inhibitors were used for in vitro investigation of effects of activation of MAPKs by heat stress. Heat stress caused marked morphological damage to the small intestine and significantly increased intestinal permeability. Heat stress increased ROS and MDA production, and significantly reduced anti-oxidase activity. MAPK activity in small intestine was increased by heat stress. In vitro, heat stress caused damage and apoptosis in IEC-6 cells; inhibition of ERK1/2 activation (by U0126) exacerbated these effects, which were attenuated by inhibition of JNK (by SP600125) and p38 (by SB203580) activation. Hence, heat stress caused severe small intestine injury, increased oxidative stress, and activated MAPK signaling pathways. The in vitro studies indicated that ERK1/2 activation is anti-apoptotic, and JNK and p38 activation are pro-apoptotic in heat stressed intestinal epithelial cells.

Overexpression of GASA5 increases the sensitivity of Arabidopsis to heat stress

Basal thermotolerance is very important for plant growth and development when plants are subjected to heat stress. However, little is known about the functional mechanism of gibberellins (GAs) in the basal thermotolerance of plants. In the present work, we provide molecular evidence that a member of the gene family encoding the GA- stimulated Arabidopsis (GASA) peptides, namely GASA5, is involved in the regulation of seedling thermotolerance. The GASA5-overexpressing plants displayed a weak thermotolerance, with a faster cotyledon-yellowing rate, lower seedling-survival rate, and slower hypocotyl elongation, in comparison to the wild-type and GASA5 null-mutant ( gasa5-1) plants, after heat-stress treatment. The short-hypocotyl phenotype of GASA5-overexpressing plants could be rescued by the exogenous application of salicylic acid (SA), the hormone found to protect plants from heat stress-induced damage. GASA5 expression was inhibited by heat stress but unaffected by the application of exogenous SA. However, expression of the gene encoding the noexpresser of PR genes 1 ( NPR1), a key component of the SA-signaling pathway, was downregulated by GASA5 overexpression. Importantly, when different GASA5-genotype plants were treated with heat stress, several genes encoding heat-shock proteins, including HSP101, HSP70B, HSP90.1, HSP17.6-C1, and HSP60, were inhibited by GASA5 overexpression. Meanwhile, hydrogen peroxide was accumulated at high levels in heat stress-treated GASA5-overexpressing plants. These results suggest that the Arabidopsis GASA5 gene acts as a negative regulator in thermotolerance by regulating both SA signaling and heat shock-protein accumulation.

Involvement of ERK1/2 signalling and growth-related molecules’ expression in response to heat stress-induced damage in rat jejunum and IEC-6 cells

Our previous studies found small intestine epithelial tissues from several different animals (including rats, pigs and chickens) became significantly damaged following exposure to extreme heat. However, damaged tissue was rapidly repaired or regenerated in the following few days. Growth-related molecules are critical for cellular survival and promote endothelial cell proliferation and migration. The ERK1/2 signalling pathway is reported to regulate the growth and adaptation of endothelial cells to both physiological and pathological stimuli. However, little information is available concerning both growth-related molecules and ERK1/2 in response to heat stress. Herein, we employed both live rats and rat IEC-6 cells to investigate growth-related molecule expression and ERK1/2 activation in heat stress. Heat stress caused significant morphological damage to rat intestinal tissue and IEC-6 cells, reduced cell growth and proliferation, induced apoptosis, altered growth-related molecule mRNA expression and increased ERK1/2 phosphorylation. Addition of U0126 (a selective inhibitor of MEK kinase responsible for ERK phosphorylation) combined with heat stress exacerbated the morphological damage and apoptosis. With the addition of U0126, further up- or down-regulation of Egfr, Ctgf, Tgif, Vegfa, Okl38 and Gdf15 in response to heat stress was observed. In conclusion, extreme heat stress caused obvious damage to rat jejunum and IEC-6 cells. Both growth-related molecule expression and ERK1/2 phosphorylation were involved in response to heat stress. ERK1/2 inhibition exacerbated apoptosis and affected growth factor mRNA expression in heat stress.

Effect of heat stress on the porcine small intestine: A morphological and gene expression study

With the presence of global warming, the occurrence of extreme heat is becoming more common, especially during the summer, increasing pig susceptibility to severe heat stress. The aim of the current study was to investigate changes in morphology and gene expression in the pig small intestine in response to heat stress. Forty eight Chinese experimental mini pigs ( Sus scrofa) were subjected to 40 °C for 5 h each day for 10 successive days. Pigs were euthanized at 1, 3, 6, and 10 days after heat treatment and sections of the small intestine epithelial tissue were excised for morphological examination and microarray analyses. After heat treatment, the pig rectal temperature, the body surface temperature and serum cortisol levels were all significantly increased. The duodenum and jejunum displayed significant damage, most severe after 3 days of treatment. Microarray analysis found 93 genes to be up-regulated and 110 genes to be down-regulated in response to heat stress. Subsequent bioinformatic analysis (including gene ontology and KEGG pathway analysis) revealed the genes altered in response to heat stress related to unfolded protein, regulation of translation initiation, regulation of cell proliferation, cell migration and antioxidant regulation. Heat stress caused significant damage to the pig small intestine and altered gene expression in the pig jejunum. The results of the bioinformatic analysis from the present study will be beneficial to further investigate the underlying mechanisms involved in heat stress-induced damage in the pig small intestine.