Protective effect and mechanism of mesenchymal stem cells on heat stroke induced intestinal injury

Wang, Lu; Deng, Zihui; Yuan, Rui; Zhao, Yan; Hu, Jie; Li, Yun; Zhou, Feihu; Kang, Hongjun

doi:10.3892/etm.2020.9051

Cited by 3 publications

(4 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The primary IAV host is aquatic birds, with virus replications occurring in the gastrointestinal tract that commonly are asymptomatic. However, mammalian IAV strains replicate in respiratory tissues and produce symptoms that range from mild cases to severe and sometimes fatal (13). Owing to the high mutation rates and the genetic recombination thereof, IAV is commonly associated with epidemics (22).…”

Section: Zbp1 In Influenza a Virusmentioning

confidence: 99%

“…When heat stress persists, the blood flow is redistributed, which is manifested as a decreased visceral blood flow and an increased blood flow to the skin and vital organs, so as to meet the needs of heat dissipation. These factors lead to intestinal ischemia, which induces the generation of intestinal free radicals and intestinal mucosal edema and increases intestinal permeability, all of which promote intestinal disruption and lead to the release of a large number of intestinal toxins into the blood circulation (13,109,(151)(152)(153)(154)(155)(156)(157)(158). Renal failure is a common complication of heatstroke that is mainly manifested as tubular necrotizing acute renal failure and can be caused by massive protein deposition in the renal tubular epithelial cells after hemolysis and rhabdomyolysis (13,21,(158)(159)(160)(161)(162)(163)(164)(165)(166).…”

Section: Tissue Injury Responsesmentioning

confidence: 99%

“…These factors lead to intestinal ischemia, which induces the generation of intestinal free radicals and intestinal mucosal edema and increases intestinal permeability, all of which promote intestinal disruption and lead to the release of a large number of intestinal toxins into the blood circulation (13,109,(151)(152)(153)(154)(155)(156)(157)(158). Renal failure is a common complication of heatstroke that is mainly manifested as tubular necrotizing acute renal failure and can be caused by massive protein deposition in the renal tubular epithelial cells after hemolysis and rhabdomyolysis (13,21,(158)(159)(160)(161)(162)(163)(164)(165)(166). Liver dysfunction in patients with heatstroke and in animal models is considerably common, with the liver injury mainly occurring in the recovery period of heatstroke (167)(168)(169)(170)(171)(172)(173)(174).…”

Section: Tissue Injury Responsesmentioning

confidence: 99%

See 2 more Smart Citations

ZBP1 and heatstroke

Deng²,

He³

et al. 2023

Front. Immunol.

View full text Add to dashboard Cite

Heatstroke, which is associated with circulatory failure and multiple organ dysfunction, is a heat stress-induced life-threatening condition characterized by a raised core body temperature and central nervous system dysfunction. As global warming continues to worsen, heatstroke is expected to become the leading cause of death globally. Despite the severity of this condition, the detailed mechanisms that underlie the pathogenesis of heatstroke still remain largely unknown. Z-DNA-binding protein 1 (ZBP1), also referred to as DNA-dependent activator of IFN-regulatory factors (DAI) and DLM-1, was initially identified as a tumor-associated and interferon (IFN)-inducible protein, but has recently been reported to be a Z-nucleic acid sensor that regulates cell death and inflammation; however, its biological function is not yet fully understood. In the present study, a brief review of the main regulators is presented, in which the Z-nucleic acid sensor ZBP1 was identified to be a significant factor in regulating the pathological characteristics of heatstroke through ZBP1-dependent signaling. Thus, the lethal mechanism of heatstroke is revealed, in addition to a second function of ZBP1 other than as a nucleic acid sensor.

show abstract

Section: Zbp1 In Influenza a Virusmentioning

confidence: 99%

Section: Tissue Injury Responsesmentioning

confidence: 99%

Section: Tissue Injury Responsesmentioning

confidence: 99%

See 1 more Smart Citation

ZBP1 and heatstroke

Deng²,

He³

et al. 2023

Front. Immunol.

View full text Add to dashboard Cite

show abstract

“…Although many key genes and pathways that respond to acute thermal stress were identified in these studies, only a few genes were common across tissues, suggesting a high level of tissue specificity in the cellular response to thermal stress. Additionally, although short preconditioning with temperatures above the standard has been shown to prevent or reverse age related impairment and significantly improve the regenerative potential and therapeutic potential of human MSCs [16,[28][29][30][31][32], other studies have shown reduced proliferative and regenerative abilities [22,33,34]. This inconsistency is possibly due to the different treatment protocols (namely, different temperatures and durations of heat stress) and the origin of MSCs used but could also be attributed to the intrinsic heterogeneity of MSCs.…”

Section: Introductionmentioning

confidence: 99%

Short heat shock has a long-term effect on mesenchymal stem cells’ transcriptome

Ribarski-Chorev

Schudy

Strauss

et al. 2022

Preprint

View full text Add to dashboard Cite

Background: Mesenchymal stem cells (MSCs) are multipotent stromal, non-hematopoietic cells with self-renewal and differentiation properties and are therefore a preferred source for cellular therapies. However, a better understanding of culture techniques is required to harness their full potential. Here we aim to compare the effects of short and long heat shock (HS) on the transcriptomic landscape of MSCs. Methods: MSCs were extracted from the umbilical cord of a bovine fetus, cultured, and validated as MSCs. Early passage cells were exposed to 40.5°C for six hours or three days. RNA sequencing and bioinformatics analysis were performed to systematically examine the transcriptional changes following each treatment and to identify specific biological features and processes. Results: The data indicates that while long heat stress influences many cell processes, such as immune response, cell cycle, and differentiation, the short HS mostly upregulates the cellular stress response. Once normothermia is resumed the long-term effects of the short HS can be revealed: although most genes revert to their original expression levels, a subgroup of epigenetically marked genes termed bivalent genes, maintains high expression levels. These genes are known to support cell lineage specification and are carefully regulated by a group of chromatin modifiers. One family of those chromatin modifiers, called MLL genes, is highly over-represented in the transiently upregulated cluster after six hours of HS. Therefore, our data provide a mechanistic explanation for the long-term phenotype of short HS on development-related genes and could be used to predict the long-term effect of HS on cell identity. Conclusions: Understanding the influence of culture conditions on morphology, phenotype, proliferative capacity, and fate decision of MSCs is needed to optimize culture conditions suitable for clinical or commercial use. Here, we suggest that simple and short stress can alter the cell's proliferation and differentiation capacities and, therefore, following future optimizations, be used to shift the cells toward a more desirable functionality.

show abstract

The mechanisms behind heatstroke-induced intestinal damage

Sun,

Li,

Zou

et al. 2024

Cell Death Discov.

View full text Add to dashboard Cite

With the frequent occurrence of heatwaves, heatstroke (HS) is expected to become one of the main causes of global death. Being a multi-organized disease, HS can result in circulatory disturbance and systemic inflammatory response, with the gastrointestinal tract being one of the primary organs affected. Intestinal damage plays an initiating and promoting role in HS. Multiple pathways result in damage to the integrity of the intestinal epithelial barrier due to heat stress and hypoxia brought on by blood distribution. This usually leads to intestinal leakage as well as the infiltration and metastasis of toxins and pathogenic bacteria in the intestinal cavity, which will eventually cause inflammation in the whole body. A large number of studies have shown that intestinal damage after HS involves the body’s stress response, disruption of oxidative balance, disorder of tight junction proteins, massive cell death, and microbial imbalance. Based on these damage mechanisms, protecting the intestinal barrier and regulating the body’s inflammatory and immune responses are effective treatment strategies. To better understand the pathophysiology of this complex process, this review aims to outline the potential processes and possible therapeutic strategies for intestinal damage after HS in recent years.

show abstract

Protective effect and mechanism of mesenchymal stem cells on heat stroke induced intestinal injury

Cited by 3 publications

References 51 publications

ZBP1 and heatstroke

ZBP1 and heatstroke

Short heat shock has a long-term effect on mesenchymal stem cells’ transcriptome

The mechanisms behind heatstroke-induced intestinal damage

Contact Info

Product

Resources

About