Lactoferrin Protects Human Mesenchymal Stem Cells from Oxidative Stress-Induced Senescence and Apoptosis

Park, Soon Yong; Jeong, Ae Jin; Kim, Geun Young; Jo, Ala; Lee, Joo Eon; Leem, Sun Hee; Yoon, Joung Hahn; Ye, Sang Kyu; Chung, Jin Woong

doi:10.4014/jmb.1707.07040

Cited by 62 publications

(31 citation statements)

References 31 publications

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“…Additional potential regulators: The AKT pathway plays an important role in the rejuvenation of features and functions of aged MSCs. This pathway can act via ERBB4/PI3K/AKT[ 112 ], lactoferrin/AKT[ 113 ], Vc/AKT/mTOR[ 114 ], and fucoidan/FAK-Akt-TWIST axes[ 115 ]. Administration of rapamycin, an inhibitor of the mTOR signaling pathway, raised the expression level of NANOG, postponed replicative arrest, and enhanced the lifespan increment of BM-MSCs[ 116 ].…”

Section: Cellular Rejuvenation Strategiesmentioning

confidence: 99%

Senescent mesenchymal stem/stromal cells and restoring their cellular functions

Meng¹,

Liu²,

Lu³

et al. 2020

WJSC

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Mesenchymal stem/stromal cells (MSCs) have various properties that make them promising candidates for stem cell-based therapies in clinical settings. These include self-renewal, multilineage differentiation, and immunoregulation. However, recent studies have confirmed that aging is a vital factor that limits their function and therapeutic properties as standardized clinical products. Understanding the features of senescence and exploration of cell rejuvenation methods are necessary to develop effective strategies that can overcome the shortage and instability of MSCs. This review will summarize the current knowledge on characteristics and functional changes of aged MSCs. Additionally, it will highlight cell rejuvenation strategies such as molecular regulation, non-coding RNA modifications, and microenvironment controls that may enhance the therapeutic potential of MSCs in clinical settings.

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Section: Cellular Rejuvenation Strategiesmentioning

confidence: 99%

Senescent mesenchymal stem/stromal cells and restoring their cellular functions

Meng¹,

Liu²,

Lu³

et al. 2020

WJSC

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“…Lactoferrin plays a role in iron homeostasis, anti-inflammation, and host defense against microbial infections. Recently, it has been shown that lactoferrin inhibits the production of intracellular ROS in human mesenchymal stem cells, which suggests a potential role of lactoferrin in the prevention of OS-related damage [ 58 ]. Several RCTs have explored the effectiveness of oral lactoferrin in the prevention of NEC in preterm neonates.…”

Section: Exploring the “Milky Way”: Reducing Oxidative Stress By Imentioning

confidence: 99%

Oxidative Stress and Necrotizing Enterocolitis: Pathogenetic Mechanisms, Opportunities for Intervention, and Role of Human Milk

Aceti

Beghetti

Martini

et al. 2018

Oxidative Medicine and Cellular Longevity

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This review will examine the role of oxidative stress (OS) in the pathogenesis of necrotizing enterocolitis (NEC) and explore potential preventive and therapeutic antioxidant strategies. Preterm infants are particularly exposed to OS as a result of several perinatal stimuli and constitutive defective antioxidant defenses. For this reason, OS damage represents a contributing factor to several complications of prematurity, including necrotizing enterocolitis (NEC). Being NEC a multifactorial disease, OS may act as downstream component of the pathogenetic cascade. To counteract OS in preterm infants with NEC, several antioxidant strategies have been proposed and different antioxidant compounds have been experimented. It is well known that human milk (HM) is an important source of antioxidants. At the same time, the role of an exclusive HM diet is well recognized in the prevention of NEC. However, donor HM (DHM) processing may impair antioxidant properties. As DHM is becoming a common nutritional intervention for high risk PI, the antioxidant status of preterm and DHM and potential ways to preserve its antioxidant capacity may merit further investigation.

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“…Research has reported that cells suffering from apoptosis involve endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and death receptors [ 9 , 10 ]. Furthermore, oxidative stress plays a crucial role in regulating cancer cell behavior, especially associated with cell apoptosis [ 11 ]. High ROS levels were reported to have damaged ER function, resulting in unfolded proteins accumulation and ER stress [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Aloe-Emodin Induces Endoplasmic Reticulum Stress-Dependent Apoptosis in Colorectal Cancer Cells

Cheng

Dong

2018

Med Sci Monit

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BackgroundRecently, colorectal cancer has become a more common type of tumor in the world. Research has reported that several kinds of single compounds of Chinese herbs have shown anti-tumor activity in colorectal cancer. Aloe-emodin (AE), a natural compound extract from Aloe Vera, has been discovered to suppress cell proliferation and accelerate apoptosis in a variety of tumor cells. Whether AE exerts an effect on colorectal cancer cells has not yet been investigated.Material/MethodsIn this study, we examined the impact of AE on SW620 and HT29 colorectal cancer cell lines. After treatment with various concentrations of AE (10, 20, and 40 μM), cell proliferation, cell apoptosis, reactive oxygen species (ROS) generation, cytosolic calcium level, and related gene expression were analyzed.ResultsOur results indicated that AE suppressed cell viability and induced cell apoptosis in SW620 and HT29 cell lines. Furthermore, both cell lines when exposed to AE generated ROS, which induces endoplasmic reticulum (ER) stress. We then detected the expression of ER stress-related proteins and cytosolic calcium levels. We found that cells exposure to AE had upregulation of unfolded protein response (UPR) proteins like glucose-related protein 78 (GRP78), phosphorylated protein kinase R (PKR)-like ER kinase (p-PERK), phosphorylated eukaryotic initiation factor-2α (p-eIF2α), and transcription factor C/EBP homologous protein (CHOP). Meanwhile, we detected an increased cytosolic calcium content followed by the upregulation of the calpain-1, calpain-2 and caspase-12. CHOP and caspase-12 are important regulatory factors leading to cell apoptosis.ConclusionsAE might serve as a candidate in the treatment of colorectal cancer through inducing ER stress-dependent apoptosis.

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Lactoferrin Protects Human Mesenchymal Stem Cells from Oxidative Stress-Induced Senescence and Apoptosis

Cited by 62 publications

References 31 publications

Senescent mesenchymal stem/stromal cells and restoring their cellular functions

Senescent mesenchymal stem/stromal cells and restoring their cellular functions

Oxidative Stress and Necrotizing Enterocolitis: Pathogenetic Mechanisms, Opportunities for Intervention, and Role of Human Milk

Aloe-Emodin Induces Endoplasmic Reticulum Stress-Dependent Apoptosis in Colorectal Cancer Cells

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