Oxidative Stress Enhances Autophagy-Mediated Death Of Stem Cells Through Erk1/2 Signaling Pathway – Implications For Neurotransplantations

Prakash, Ravi; Fauzia, Eram; Siddiqui, Abu Junaid; Yadav, Santosh Kumar; Kumari, Neha; Singhai, Atin; Khan, Mohsin Ali; Janowski, Mirosław; Bhutia, Sujit K.; Raza, Syed Shadab

doi:10.1007/s12015-021-10212-z

Cited by 18 publications

(8 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The oxidative stress-induced activation of the Nrf2/HO-1 pathway results in increased expression of downstream antioxidant enzymes including catalase. The phenomenon was in accordance with a previous study [ 55 ]. Considering that BMSC-EVs often function as antioxidants, we detected ROS and catalase levels in TSCs under oxidative stress.…”

Section: Discussionsupporting

confidence: 93%

Eugenol-Preconditioned Mesenchymal Stem Cell-Derived Extracellular Vesicles Promote Antioxidant Capacity of Tendon Stem Cells In Vitro and In Vivo

Shen

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Tendon stem cells (TSCs) are often exposed to oxidative stress at tendon injury sites, which impairs their physiological effect as well as therapeutic application. Recently, extracellular vesicles (EVs) derived from bone marrow mesenchymal stem cells (BMSCs) were shown to mediate cell protection and survival under stress conditions. The function of BMSC-EVs may be affected by pretreatment with various factors such as eugenol (EUG)—a powerful antioxidant. In our previous study, we found that H2O2 significantly impaired TSC proliferation and tenogenic differentiation capabilities. Apoptosis and intracellular ROS accumulation in TSCs were induced by H2O2. However, such H2O2-induced damage was prevented by treatment with EUG-BMSC-EVs. Furthermore, EUG-BMSC-EVs activated the Nrf2/HO-1 pathway to counteract H2O2-induced damage in TSCs. In a rat patellar tendon injury model, the ROS level was significantly higher than that in the normal tendon and TSCs not pretreated showed a poor therapeutic effect. However, EUG-BMSC-EV-pretreated TSCs significantly improved tenogenesis and matrix regeneration during tendon healing. Additionally, the EUG-BMSC-EV group had a significantly improved fiber arrangement. Overall, EUG-BMSC-EVs protected TSCs against oxidative stress and enhanced their functions in tendon injury. These findings provide a basis for potential clinical use of EUG-BMSC-EVs as a new therapeutic vehicle to facilitate TSC therapies for tendon regeneration.

show abstract

Section: Discussionsupporting

confidence: 93%

Eugenol-Preconditioned Mesenchymal Stem Cell-Derived Extracellular Vesicles Promote Antioxidant Capacity of Tendon Stem Cells In Vitro and In Vivo

Shen

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…Previous studies have suggested that excessive mitophagy can trigger endogenous apoptosis, while inhibition of mitophagy can reduce apoptosis ( Gao et al, 2017 ; Prakash et al, 2021 ), which seems to contradict our research results. However, more evidence shows that AEC apoptosis caused by mitochondrial dysfunction and mitophagy defects plays a key role in the pathogenesis of pulmonary fibrosis ( Bueno et al, 2015 ; Malsin and Kamp, 2018 ).…”

Section: Discussioncontrasting

confidence: 99%

Number 2 Feibi Recipe Inhibits H2O2-Mediated Oxidative Stress Damage of Alveolar Epithelial Cells by Regulating the Balance of Mitophagy/Apoptosis

Long

Wan

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

Reactive oxygen species (ROS)-mediated alveolar epithelial cell (AEC) injury and apoptosis are considered to be the initiating link of idiopathic pulmonary fibrosis (IPF), and protecting AECs can alleviate IPF. This study aimed to explore the protective effect of number 2 Feibi recipe (FBR-2) medicated serum on H2O2-mediated oxidative stress injury in AECs and further explore its mechanism. We found that FBR-2 can regulate downstream antioxidant enzymes expression by activating nuclear factor erythroid 2-related factor 2 (Nrf2), reducing the level of intracellular ROS, protecting mitochondrial function and improving cell survival. FBR-2 can also activate mitophagy through the PINK1/Parkin pathway. Moreover, FBR-2 can inhibit apoptosis by blocking the mitochondrial apoptosis mechanism. In summary, these data indicate that FBR-2 medicated serum can inhibit H2O2-mediated oxidative stress damage in AECs by regulating the balance of mitophagy/apoptosis. This study provides new evidence for the antifibrotic effect of FBR-2 and provides new drug candidates for the clinical treatment of IPF.

show abstract

“…In summary, when compared to the control, the OGD+M-PMPL@Tf nanomicelle-treated cells showed less viability, while the supplementation with OGD+M-PMPL@Tf nanomicelles reversed the outcome in the OGD-treated group. These findings were consistent with previous research using the MTT test TUNEL assay, and Trypan blue staining …”

Section: Resultssupporting

confidence: 93%

NLRP3 Inflammasome-Targeting Nanomicelles for Preventing Ischemia–Reperfusion-Induced Inflammatory Injury

et al. 2023

Self Cite

View full text Add to dashboard Cite

Ischemia−reperfusion (I/R) injury is a disease process that affects several vital organs. There is widespread agreement that the NLRP3 inflammasome pathway plays a crucial role in the development of I/R injury. We have developed transferrinconjugated, pH-responsive nanomicelles for the entrapment of MCC950 drug. These nanomicelles specifically bind to the transferrin receptor 1 (TFR1) expressed on the cells of the blood−brain barrier (BBB) and thus help the cargo to cross the BBB. Furthermore, the therapeutic potential of nanomicelles was assessed using in vitro, in ovo, and in vivo models of I/R injury. Nanomicelles were injected into the common carotid artery (CCA) of a middle cerebral artery occlusion (MCAO) rat model to achieve maximum accretion of nanomicelles into the brain as blood flows toward the brain in the CCA. The current study reveals that the treatment with nanomicelles significantly alleviates the levels of NLRP3 inflammasome biomarkers which were found to be increased in oxygen−glucose deprivation (OGD)-treated SH-SY5Y cells, the I/Rdamaged right vitelline artery (RVA) of chick embryos, and the MCAO rat model. The supplementation with nanomicelles significantly enhanced the overall survival of MCAO rats. Overall, nanomicelles exerted therapeutic effects against I/R injury, which might be due to the suppression of the activation of the NLRP3 inflammasome.

show abstract

Oxidative Stress Enhances Autophagy-Mediated Death Of Stem Cells Through Erk1/2 Signaling Pathway – Implications For Neurotransplantations

Cited by 18 publications

References 66 publications

Eugenol-Preconditioned Mesenchymal Stem Cell-Derived Extracellular Vesicles Promote Antioxidant Capacity of Tendon Stem Cells In Vitro and In Vivo

Eugenol-Preconditioned Mesenchymal Stem Cell-Derived Extracellular Vesicles Promote Antioxidant Capacity of Tendon Stem Cells In Vitro and In Vivo

Number 2 Feibi Recipe Inhibits H2O2-Mediated Oxidative Stress Damage of Alveolar Epithelial Cells by Regulating the Balance of Mitophagy/Apoptosis

NLRP3 Inflammasome-Targeting Nanomicelles for Preventing Ischemia–Reperfusion-Induced Inflammatory Injury

Contact Info

Product

Resources

About