Liver isoform of phosphofructokinase (PFKL)-Mediated Hypoxic Preconditioned Bone Marrow-Derived Mesenchymal Stem Cells Attenuate Cardiac Arrest-Induced Pyroptosis in Rat Cortical Neurons by Protecting Mitochondrial Function from Oxidative Damage DOI Creative Commons
Xiahong Tang, Nan Zheng, Zheng Gong

et al.

Research Square (Research Square), Journal Year: 2023, Volume and Issue: unknown

Published: Nov. 11, 2023

Abstract Introduction : Cardiac arrest (CA) often leads to severe neurological dysfunction due inflammation, mitochondrial dysfunction, and post-cardiopulmonary resuscitation (CPR) damage. Bone marrow-derived mesenchymal stem cells (BMSCs) show promise for diseases, but optimizing their therapeutic potential neuroregulation post-CA remains unclear. Methods We established an in vitro co-culture model with BMSCs post-oxygen-glucose deprivation (OGD) primary neurons, confirming that hypoxic preconditioning enhances BMSCs' resistance neuronal pyroptosis. induced 8-minute CA through asphyxia induction assessed preconditioned bone (HP-BMSCs) on post-resuscitation oxidative stress pyroptosis using deficit scores (NDS), brain tissue markers, apoptosis-related proteins, area, damage markers. Mechanistic studies knocked down PFKL expression HP-BMSCs via si-RNA, verifying mechanisms animals cells. Results Hypoxic boosted neuroprotective effect against pyroptosis, possibly MAPK NF-κB pathway inhibition. Consequently, we pursued as a neuroprotection strategy, RNA sequencing suggesting liver isoform of phosphofructokinase (PFKL) regulatory molecule. significantly reduced stress, by CA. This manifested improved decreased protein levels, enhanced cell membrane structures, Transfection PFKL-targeted si-RNA into weakened protective effects. also confirm HP-BMSCs' role improving energy metabolism following OGD. lowered levels markers neurons. Intracellular reactive oxygen species (ROS) dropped, detected DCFH-DA MitoSOX probes. Notably, knocking reversed these Conclusion In conclusion, offer promising approach injury reducing mediated ROS, potentially linked elevated preconditioning.

Language: Английский

Modes of Brain Cell Death Following Intracerebral Hemorrhage DOI Creative Commons
Yan Zhang, Suliman Khan, Yang Liu

et al.

Frontiers in Cellular Neuroscience, Journal Year: 2022, Volume and Issue: 16

Published: Feb. 3, 2022

Intracerebral hemorrhage (ICH) is a devastating form of stroke with high rates mortality and morbidity. It induces cell death that responsible for neurological deficits postinjury. There are no therapies effectively mitigate to treat ICH. This review aims summarize our knowledge ICH-induced focus on apoptosis necrosis. We also discuss the involvement ICH in recently described modes including necroptosis, pyroptosis, ferroptosis, autophagy, parthanatos. treatment strategies brain injury based particular pathways after

Language: Английский

Citations

55

Recent advances in pre-conditioned mesenchymal stem/stromal cell (MSCs) therapy in organ failure; a comprehensive review of preclinical studies DOI Creative Commons
Mohammad Saeed Kahrizi, Elnaz Mousavi, Armin Khosravi

et al.

Stem Cell Research & Therapy, Journal Year: 2023, Volume and Issue: 14(1)

Published: June 7, 2023

Abstract Mesenchymal stem/stromal cells (MSCs)‐based therapy brings the reassuring capability to regenerative medicine through their self‐renewal and multilineage potency. Also, they secret a diversity of mediators, which are complicated in moderation deregulated immune responses, yielding angiogenesis vivo. Nonetheless, MSCs may lose biological performance after procurement prolonged expansion vitro. following transplantation migration target tissue, encounter harsh milieu accompanied by death signals because lack proper tensegrity structure between matrix. Accordingly, pre-conditioning is strongly suggested upgrade performances vivo, leading more favored efficacy medicine. Indeed, ex vivo hypoxia, inflammatory stimulus, or other factors/conditions stimulate survival, proliferation, migration, exosome secretion, pro-angiogenic anti-inflammatory characteristics In this review, we deliver an overview methods that considered strategy for improving therapeutic organ failures, particular, renal, heart, lung, liver.

Language: Английский

Citations

25

Research progress on ferroptosis in cerebral hemorrhage DOI

Niping Mao,

Min Zhang, Mingyue Shen

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2025, Volume and Issue: 185, P. 117932 - 117932

Published: Feb. 26, 2025

Language: Английский

Citations

1

Perspectives on the mechanism of pyroptosis after intracerebral hemorrhage DOI Creative Commons
Dengpan Song, Chi‐Tai Yeh, Jian Wang

et al.

Frontiers in Immunology, Journal Year: 2022, Volume and Issue: 13

Published: Sept. 5, 2022

Intracerebral hemorrhage (ICH) is a highly harmful neurological disorder with high rates of mortality, disability, and recurrence. However, effective therapies are not currently available. Secondary immune injury cell death the leading causes brain poor prognosis. Pyroptosis recently discovered form programmed that differs from apoptosis necrosis mediated by gasdermin proteins. caused multiple pathways eventually pores in membrane, facilitating release inflammatory substances causing to rupture die. occurs neurons, glial cells, endothelial cells after ICH. Furthermore, pyroptosis releases factors such as interleukin (IL)-1β IL-18, secondary immune-inflammatory response further damage. The NOD-like receptor protein 3 (NLRP3)/caspase-1/gasdermin D (GSDMD) pathway plays most critical role can be inhibited directly targeting NLRP3 or its upstream molecules, interfering caspase-1 expression GSDMD formation, thus significantly improving prognosis present review discusses key pathological regulatory mechanisms ICH suggests possible intervention strategies mitigate dysfunction

Language: Английский

Citations

36

Mesenchymal Stem Cell Application and Its Therapeutic Mechanisms in Intracerebral Hemorrhage DOI Creative Commons
Guoqiang Yang, Xuehui Fan, Maryam Mazhar

et al.

Frontiers in Cellular Neuroscience, Journal Year: 2022, Volume and Issue: 16

Published: June 13, 2022

Intracerebral hemorrhage (ICH), a common lethal subtype of stroke accounting for nearly 10–15% the total disease and affecting two million people worldwide, has high mortality disability rate and, thus, major socioeconomic burden. However, there is no effective treatment available currently. The role mesenchymal stem cells (MSCs) in regenerative medicine well known owing to simplicity acquisition from various sources, low immunogenicity, adaptation autogenic allogeneic systems, immunomodulation, self-recovery by secreting extracellular vesicles (EVs), repair, antioxidative stress. MSC therapy provides an increasingly attractive therapeutic approach ICH. Recently, functions MSCs such as neuroprotection, anti-inflammation, improvement synaptic plasticity have been widely researched human rodent models transplantation proven improve ICH-induced injury, including damage nerve oligodendrocytes, activation microglia astrocytes, destruction blood vessels. recovery neurological ICH were demonstrated via mechanisms neurogenesis, angiogenesis, anti-apoptosis, plasticity. Here, we discuss pathological following MSC-based unravel new cues future strategies. Furthermore, some potential strategies enhancing function also suggested.

Language: Английский

Citations

19

Mesenchymal stem cells (MSCs) and MSC‐derived exosomes in animal models of central nervous system diseases: Targeting the NLRP3 inflammasome DOI
Shahrzad Nazari, Seyed Mahmoud Pourmand, Elahe Motevaseli

et al.

IUBMB Life, Journal Year: 2023, Volume and Issue: 75(10), P. 794 - 810

Published: June 6, 2023

Abstract The NLRP3 (NOD‐, LRR‐, and pyrin domain‐containing protein 3) inflammasome is a multimeric complex that engaged in the innate immune system plays vital role inflammatory reactions. Activation of subsequent release proinflammatory cytokines can be triggered by microbial infection or cellular injury. has been implicated pathogenesis many disorders affecting central nervous (CNS), ranging from stroke, traumatic brain injury, spinal cord injury to Alzheimer's disease, Parkinson's epilepsy, multiple sclerosis, depression. Furthermore, emerging evidence suggested mesenchymal stem cells (MSCs) their exosomes may modulate activation way might promising for therapeutic management CNS diseases. In present review, particular focus placed on highlighting discussing recent scientific regarding regulatory effects MSC‐based therapies potential counteract responses pyroptotic cell death CNS, thereby achieving neuroprotective impacts improvement behavioral impairments.

Language: Английский

Citations

12

Regulating pyroptosis by mesenchymal stem cells and extracellular vesicles: A promising strategy to alleviate intervertebral disc degeneration DOI Open Access
Sheng Yang, Yongbo Zhang, Qing Peng

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2023, Volume and Issue: 170, P. 116001 - 116001

Published: Dec. 20, 2023

Intervertebral disc degeneration (IVDD) is a main cause of low back pain (LBP), which can lead to disability and thus generate heavy burden on society. IVDD characterized by decrease in nucleus pulposus cells (NPCs) endogenous mesenchymal stem (MSCs), degradation the extracellular matrix, macrophage infiltration, blood vessel nerve ingrowth. To date, therapeutic approaches regarding mainly include conservative treatment surgical intervention. However, both only relieve symptoms rather than stop or revert progression IVDD, since pathogenesis not yet clear. Pyroptosis, Caspase family dependence conducted Gasdermin family, newly discovered mode programmed cell death. Pyroptosis has been observed NPCs, annulus fibrosus (AFCs), chondrocytes, MSCs, macrophages, vascular endothelial neurons may contribute IVDD. MSCs are kind pluripotent that be found almost all tissues. have strong ability secrete vesicles (EVs), contain exosomes, microvesicles apoptotic bodies. EVs derived from play an important role pyroptosis regulation could beneficial for alleviating This review focuses clarifying improve MSCs.

Language: Английский

Citations

12

SENP1 facilitates OM-MSC differentiation through activating OPTN-mediated mitophagy to mitigate the neurologic impairment following ICH DOI Creative Commons
Jun He, Jun Peng,

You Li

et al.

iScience, Journal Year: 2024, Volume and Issue: 27(6), P. 109865 - 109865

Published: April 30, 2024

Previous studies have indicated the neuroprotective effect of olfactory mucosa mesenchymal stem cells (OM-MSCs) on brain injury. Intracerebral hemorrhage (ICH) models were established in rats by injecting autologous blood. SENP1 expression was enhanced neurons but decreased astrocytes compared to that OM-MSCs. Overexpression promoted proliferation and neuronal differentiation, while inhibiting astrocytic differentiation Conversely, its knockdown had opposite effect. Moreover, OM-MSCs reduced neurological dysfunction after ICH, could be further overexpression. In addition, mitophagy, which might related SENP1-mediated OPTN deSUMOylation. Furthermore, through mitophagy mediated OPTN. Similar SENP1, transfection remission OM-MSC ICH rats. OPTN-mediated improve deficits

Language: Английский

Citations

4

Priming mesenchymal stem cells to develop “super stem cells” DOI
Khawaja Husnain Haider

World Journal of Stem Cells, Journal Year: 2024, Volume and Issue: 16(6), P. 623 - 640

Published: June 24, 2024

The stem cell pre-treatment approaches at cellular and sub-cellular levels encompass physical manipulation of cells to growth factor treatment, genetic manipulation, chemical pharmacological each strategy having advantages limitations. Most these protocols are non-combinative. This editorial is a continuum Li

Language: Английский

Citations

4

Toona sinensis fruit polyphenols alleviate cerebral ischemia-reperfusion injury in rats by inhibiting MAPK signaling pathways and NLRP3 inflammasome/pyroptosis DOI
Ke Wang,

Hang Zhao,

Jing Chen

et al.

Journal of Ethnopharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 119375 - 119375

Published: Jan. 1, 2025

Language: Английский

Citations

0