scholarly journals Cytogenetic and Transcriptomic Analysis of Human Endometrial MSC Retaining Proliferative Activity after Sublethal Heat Shock

Cells ◽  
2018 ◽  
Vol 7 (11) ◽  
pp. 184 ◽  
Author(s):  
Mariia Shilina ◽  
Tatiana Grinchuk ◽  
Olga Anatskaya ◽  
Alexander Vinogradov ◽  
Larisa Alekseenko ◽  
...  
Keyword(s):  
Heat Stress ◽  
Heat Shock ◽  
Replicative Senescence ◽  
Molecular Karyotyping ◽  
Irreversible Processes ◽  
Long Term Effects ◽  
Oncogene Expression ◽  
New Therapeutic Approaches ◽  
Karyotype Instability

Temperature is an important exogenous factor capable of leading to irreversible processes in the vital activity of cells. However, the long-term effects of heat shock (HS) on mesenchymal stromal cells (MSC) remain unstudied. We investigated the karyotype and DNA repair drivers and pathways in the human endometrium MSC (eMSC) survived progeny at passage 6 after sublethal heat stress (sublethal heat stress survived progeny (SHS-SP)). G-banding revealed an outbreak of random karyotype instability caused by chromosome breakages and aneuploidy. Molecular karyotyping confirmed the random nature of this instability. Transcriptome analysis found homologous recombination (HR) deficiency that most likely originated from the low thermostability of the AT-rich HR driving genes. SHS-SP protection from transformation is provided presumably by low oncogene expression maintained by tight co-regulation between thermosensitive HR drivers BRCA, ATM, ATR, and RAD51 (decreasing expression after SHS), and oncogenes mTOR, MDM2, KRAS, and EGFR. The cancer-related transcriptomic features previously identified in hTERT transformed MSC in culture were not found in SHS-SP, suggesting no traits of malignancy in them. The entrance of SHS-SP into replicative senescence after 25 passages confirms their mortality and absence of transformation features. Overall, our data indicate that SHS may trigger non-tumorigenic karyotypic instability due to HR deficiency and decrease of oncogene expression in progeny of SHS-survived MSC. These data can be helpful for the development of new therapeutic approaches in personalized medicine.

scholarly journals Evaluation of Lasting Effects of Heat Stress on Sperm Profile and Oxidative Status of Ram Semen and Epididymal Sperm

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Thais Rose dos Santos Hamilton ◽  
Camilla Mota Mendes ◽  
Letícia Signori de Castro ◽  
Patrícia Monken de Assis ◽  
Adriano Felipe Perez Siqueira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heat Stress ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Treated Group ◽  
Epididymal Sperm ◽  
Long Term Effects ◽  
Stressed Cells

Higher temperatures lead to an increase of testicular metabolism that results in spermatic damage. Oxidative stress is the main factor responsible for testicular damage caused by heat stress. The aim of this study was to evaluate lasting effects of heat stress on ejaculated sperm and immediate or long-term effects of heat stress on epididymal sperm. We observed decrease in motility and mass motility of ejaculated sperm, as well as an increase in the percentages of sperm showing major and minor defects, damaged plasma and acrosome membranes, and a decrease in the percentage of sperm with high mitochondrial membrane potential in the treated group until one spermatic cycle. An increased enzymatic activity of glutathione peroxidase and an increase of stressed cells were observed in ejaculated sperm of the treated group. A decrease in the percentage of epididymal sperm with high mitochondrial membrane potential was observed in the treated group. However, when comparing immediate and long-term effects, we observed an increase in the percentage of sperm with low mitochondrial membrane potential. In conclusion, testicular heat stress induced oxidative stress that led to rescuable alterations after one spermatic cycle in ejaculated sperm and also after 30 days in epididymal sperm.

scholarly journals Worldwide reef surveys highlight different adaptive responses to heat between coral taxa

2021 ◽  
Author(s):  
Oliver Selmoni ◽  
Gael Lecellier ◽  
Veronique Berteaux-Lecellier ◽  
Stephane Joost
Keyword(s):  
Heat Stress ◽  
Heat Waves ◽  
Coral Cover ◽  
Heat Exposure ◽  
Negative Association ◽  
Conservation Strategies ◽  
Long Term Effects ◽  
Thermal Anomalies ◽  
Adaptive Processes

Coral reefs around the world are under threat due to widespread decline of hard corals caused by anomalous heat waves. Coral taxa of different morphologies are known to have different sensitivities to heat stress. However, little is known about how long-term effects of heat exposure differ between coral taxa, nor in particular how such effects might drive adaptive processes. Here, we combined worldwide reef survey data with remotely sensed thermal anomalies to evaluate how local rates of taxa-specific coral cover were associated with heat stress. We found a negative association between coral cover and heat stress, where associations were weaker for corals with boulder-like morphology (massive corals), intermediate for corals with arborescent morphology (branching corals) and stronger for corals with encrusting or laminar morphology (plating corals). Additionally, we found that the negative association between branching coral cover and recent exposure to heat stress (measured as the year before a survey) was mitigated by the effect of long-term heat stress (measured since 1985), suggesting that adaptive processes occurred. In contrast, this "mitigating effect" of past heat-stress was not observed for either massive or plating corals. We hypothesize that these different responses to recent and past heat stress mirror different life history traits of coral taxa. For instance, branching corals are known to show higher sensitivities to heat stress and faster growth rates, two characteristics that might boost adaptive rates via evolutionary processes, when compared with other taxa. The results of this work suggest that all coral taxa, regardless of their morphology, will be "losers" of coral bleaching, and that conservation strategies should be adjusted to match taxa-specific responses to heat stress.

scholarly journals Molecular Genetic Analysis of Human Endometrial Mesenchymal Stem Cells That Survived Sublethal Heat Shock

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
A. E. Vinogradov ◽  
M. A. Shilina ◽  
O. V. Anatskaya ◽  
L. L. Alekseenko ◽  
I. I. Fridlyanskaya ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Heat Shock ◽  
Replicative Senescence ◽  
Molecular Genetic ◽  
Interaction Network ◽  
Molecular Genetic Analysis ◽  
Molecular Karyotyping ◽  
Sequencing Data ◽  
Oncogenic Signaling

High temperature is a critical environmental and personal factor. Although heat shock is a well-studied biological phenomenon, hyperthermia response of stem cells is poorly understood. Previously, we demonstrated that sublethal heat shock induced premature senescence in human endometrial mesenchymal stem cells (eMSC). This study aimed to investigate the fate of eMSC-survived sublethal heat shock (SHS) with special emphasis on their genetic stability and possible malignant transformation using methods of classic and molecular karyotyping, next-generation sequencing, and transcriptome functional analysis. G-banding revealed random chromosome breakages and aneuploidy in the SHS-treated eMSC. Molecular karyotyping found no genomic imbalance in these cells. Gene module and protein interaction network analysis of mRNA sequencing data showed that compared to untreated cells, SHS-survived progeny revealed some difference in gene expression. However, no hallmarks of cancer were found. Our data identified downregulation of oncogenic signaling, upregulation of tumor-suppressing and prosenescence signaling, induction of mismatch, and excision DNA repair. The common feature of heated eMSC is the silence of MYC, AKT1/PKB oncogenes, and hTERT telomerase. Overall, our data indicate that despite genetic instability, SHS-survived eMSC do not undergo transformation. After long-term cultivation, these cells like their unheated counterparts enter replicative senescence and die.

Long-Term Effects of Prior Heat Shock on Neuronal Potassium Currents Recorded in a Novel Insect Ganglion Slice Preparation

1999 ◽  
Vol 81 (2) ◽  
pp. 795-802 ◽  
Author(s):  
J. M. Ramirez ◽  
F. P. Elsen ◽  
R. M. Robertson
Keyword(s):  
Steady State ◽  
Heat Shock ◽  
Outward Current ◽  
Potassium Currents ◽  
Respiratory Neurons ◽  
Long Term Effects ◽  
Slice Preparation ◽  
Population Activity ◽  
Steady State Current

Long-term effects of prior heat shock on neuronal potassium currents recorded in a novel insect ganglion slice preparation. Brief exposure to high temperatures (heat shock) induces long-lasting adaptive changes in the molecular biology of protein interactions and behavior of poikilotherms. However, little is known about heat shock effects on neuronal properties. To investigate how heat shock affects neuronal properties we developed an insect ganglion slice from locusts. The functional integrity of neuronal circuits in slices was demonstrated by recordings from rhythmically active respiratory neurons and by the ability to induce rhythmic population activity with octopamine. Under these “functional” in vitro conditions we recorded outward potassium currents from neurons of the ventral midline of the A1 metathoracic neuromere. In control neurons, voltage steps to 40 mV from a holding potential of −60 mV evoked in control neurons potassium currents with a peak current of 10.0 ± 2.5 nA and a large steady state current of 8.5 ± 2.6 nA, which was still activated from a holding potential of −40 mV. After heat shock most of the outward current inactivated rapidly (peak amplitude: 8.4 ± 2.4 nA; steady state: 3.6 ± 2.0 nA). This current was inactivated at a holding potential of −40 mV. The response to temperature changes was also significantly different. After changing the temperature from 38 to 42°C the amplitude of the peak and steady-state current was significantly lower in neurons obtained from heat-shocked animals than those obtained from controls. Our study indicates that not only heat shock can alter neuronal properties, but also that it is possible to investigate ion currents in insect ganglion slices.

scholarly journals Effect of long term heat stress and dietary restriction on the expression of small heat shock protein (sHSP) genes in rat liver tissue

2016 ◽  
Vol 32 (3) ◽  
pp. 161-161
Author(s):  
Faruk Bozkaya ◽  
Mehmet Osman Atlı ◽  
Aydin Guzeloglu ◽  
Seyit Ali Kayis ◽  
Mehmet Salih Kaya ◽  
...  
Keyword(s):  
Heat Stress ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Rat Liver ◽  
Dietary Restriction ◽  
Liver Tissue ◽  
Small Heat Shock Protein
Sign in / Sign up

Export Citation Format

Share Document