Moderate hypothermia induces protein SUMOylation in bone marrow stromal cells and enhances their tolerance to hypoxia

Ren, Wenbo; Ma, Xiaofang; Liu, Xiaozhi; Li, Yanxia; Jiang, Zhongmin; Zhao, Yan; Li, Chen; Li, Xin

doi:10.3892/mmr.2017.7425

Cited by 3 publications

(2 citation statements)

References 36 publications

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“…were high in all organs tested (Yang et al, 2009). Moderate hypothermia-induced SUMO conjugation also reduced damage to bone marrow stromal cells (BMSCs) following OGD and improved BMSC survival following transplantation into the penumbra (Liu et al, 2017;Ren et al, 2017). Similarly, hibernation-like hypothermia induced by opioid receptor agonists protected the brain from ischemic injury FIGURE 9 | Effect of hypothermia on VDAC3 mRNA expression in microglial cells.…”

Section: Discussionmentioning

confidence: 97%

Hypothermia-Induced Ubiquitination of Voltage-Dependent Anion Channel 3 Protects BV2 Microglia Cells From Cytotoxicity Following Oxygen-Glucose Deprivation/Recovery

Xiao

Cui

Gong

et al. 2020

Front. Mol. Neurosci.

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Background: Hypothermia attenuates microglial activation and exerts a potential neuroprotective effect against cerebral ischemic-reperfusion (I/R) injury. However, the underlying mechanism remains to be elucidated. In this in vitro study, a model of oxygen-glucose deprivation, followed by recovery (OGD/R), was used to investigate whether hypothermia exerts anti-inflammatory and anti-apoptosis properties via enhanced ubiquitination and down-regulation of voltage-dependent anion channel 3 (VDAC3) expression. Methods: BV2 microglia were cultured under OGD for 4 h following reperfusion with or without hypothermia for 2, 4, or 8 h. M1 and M2 microglia markers [inducible nitric oxide synthase (iNOS) and arginase (Arg)1] were detected using immunofluorescence. The levels of pro-inflammatory cytokines [tumor necrosis factor (TNF) α, interleukin (IL)-1β], and anti-inflammatory factor (IL-10) were determined using enzyme-linked immunosorbent assay (ELISA). Mitochondrial membrane potential (m) was assayed by JC-1 staining using a flow cytometer. Expression of caspase-3, cleaved caspase-3, and VDAC3 were assessed using western blot analysis. The cellular locations and interactions of ubiquitin and VDAC3 were identified using double immunofluorescence staining and immunoprecipitation (IP) assay. Also, the level of the VDAC3 mRNA was determined using a quantitative polymerase chain reaction (qPCR). Results: Hypothermia inhibited the OGD/R-induced microglia activation and differentiation into the M1 type with pro-inflammatory effect, whereas it promoted differentiation to the M2 type with anti-inflammatory effect. Hypothermia attenuated OGD/R-induced loss of ∆Ψm, as well as the expression of apoptosis-associated

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Section: Discussionmentioning

confidence: 97%

Hypothermia-Induced Ubiquitination of Voltage-Dependent Anion Channel 3 Protects BV2 Microglia Cells From Cytotoxicity Following Oxygen-Glucose Deprivation/Recovery

Xiao

Cui

Gong

et al. 2020

Front. Mol. Neurosci.

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“…Moderate hypothermia promotes bone marrow stromal cell resistance to hypoxia through enhancing protein SUMOylation. Therefore, bone marrow stromal cell transplantation along with moderate hypothermia is supposed to be a promising candidate for the treatment of ischemic stroke [58].…”

Section: 42mentioning

confidence: 99%

The Role of Ubiquitin-Proteasome Pathway and Autophagy-Lysosome Pathway in Cerebral Ischemia

Chen

Qin

Tan

et al. 2020

Oxidative Medicine and Cellular Longevity

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The ubiquitin-proteasome pathway and autophagy-lysosome pathway are two major routes for clearance of aberrant cellular components to maintain protein homeostasis and normal cellular functions. Accumulating evidence shows that these two pathways are impaired during cerebral ischemia, which contributes to ischemic-induced neuronal necrosis and apoptosis. This review aims to critically discuss current knowledge and controversies on these two pathways in response to cerebral ischemic stress. We also discuss molecular mechanisms underlying the impairments of these protein degradation pathways and how such impairments lead to neuronal damage after cerebral ischemia. Further, we review the recent advance on the understanding of the involvement of these two pathways in the pathological process during many therapeutic approaches against cerebral ischemia. Despite recent advances, the exact role and molecular mechanisms of these two pathways following cerebral ischemia are complex and not completely understood, of which better understanding will provide avenues to develop novel therapeutic strategies for ischemic stroke.

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SUMO‐modified bone marrow mesenchymal stem cells promoted the repair of articular cartilage in rats

Liu

Yin

et al. 2019

Cell Biology International

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Articular cartilage damage can lead to joint deformity, pain, and severe dysfunction. However, due to the lack of blood vessels and nerves in articular cartilage, the self‐healing capacity of damaged cartilage is limited. In this study, we overexpressed small ubiquitin‐like modifier (SUMO)1, SUMO2/3, and SUMO1/2/3 in bone marrow mesenchymal stem cells (BMSCs). Then, these cells were inoculated on surfaces of different hardness, and their differentiation into chondrocytes, hypoxic tolerance ability, and inflammatory response was detected. Finally, BMSCs were transplanted into the injured knee joint cavity of the rats, and the repair was evaluated. We found that BMSCs overexpressing SUMO1 were more likely to differentiate into articular cartilage along with the hardness of the surface, while BMSCs overexpressing SUMO2/3 could reduce inflammation response and improve the damaged cartilage microenvironment. In the rat model, BMSCs overexpressing SUMO1/2/3 transplanted on injured articular cartilage surface showed better survival, less inflammatory response, and improved tissue repair capability. In conclusion, BMSCs overexpressing SUMO are more tolerant to hypoxia conditions, and have stronger repair ability for damaged chondrocytes in vitro and for articular cartilage injury model in rats, and are excellent seed cells for repairing articular cartilage.

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Moderate hypothermia induces protein SUMOylation in bone marrow stromal cells and enhances their tolerance to hypoxia

Cited by 3 publications

References 36 publications

Hypothermia-Induced Ubiquitination of Voltage-Dependent Anion Channel 3 Protects BV2 Microglia Cells From Cytotoxicity Following Oxygen-Glucose Deprivation/Recovery

Hypothermia-Induced Ubiquitination of Voltage-Dependent Anion Channel 3 Protects BV2 Microglia Cells From Cytotoxicity Following Oxygen-Glucose Deprivation/Recovery

The Role of Ubiquitin-Proteasome Pathway and Autophagy-Lysosome Pathway in Cerebral Ischemia

SUMO‐modified bone marrow mesenchymal stem cells promoted the repair of articular cartilage in rats

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