Lipocalin-2-mediated upregulation of various antioxidants and growth factors protects bone marrow-derived mesenchymal stem cells against unfavorable microenvironments

Halabian, Raheleh; Tehrani, Hossein Abdul; Jahanian-Najafabadi, Ali; Roudkenar, Mehryar Habibi

doi:10.1007/s12192-013-0430-2

Cited by 43 publications

(48 citation statements)

References 55 publications

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“…More recently, we also reported that engineering of hB-MSCs with lipocalin 2 granted them many protective properties including strengthening them to withstand oxidative, hypoxia, and serum-deprivation conditions, besides the induction of antioxidants and the up-regulation of some growth factors (Halabian et al 2013). According to the present study, another property might be added to the previous properties of Lcn2, which is its capability to decrease senescence in cells following their exposure to oxidative stress.…”

Section: Discussionsupporting

confidence: 60%

Lipocalin 2 decreases senescence of bone marrow-derived mesenchymal stem cells under sub-lethal doses of oxidative stress

Bahmani

Roudkenar

Halabian

et al. 2014

Cell Stress and Chaperones

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The regenerative potential of mesenchymal stem cells (MSCs) is impaired by cellular senescence, a multi factorial process that has various functions. However, pathways and molecules involved in senescence have not been fully identified. Lipocalin 2 (Lcn2) has been the subject of intensive research, due to its contribution to many physiological and pathophysiological conditions. The implication of Lcn2 has been reported in many conditions where senescence also occurs. In the present study, we evaluated the role of Lcn2 in the occurrence of senescence in human bone marrowderived mesenchymal stem cells (hB-MSCs) under oxidative conditions. When hB-MSCs were genetically engineered to over-express Lcn2 (MSC-Lcn2) and exposed to H 2 O 2 , the proliferation rate of the cells increased. However, the number of colonies and the number of cells that made up each colony in both MSC-V and MSC-Lcn2 cells decreased compared to those cultivated under normal conditions. Our results revealed that over-expression of recombinant Lcn2 in hB-MSCs decreases senescence induced by H 2 O 2 treatment. Senescent cells were observed in aged hB-MSCs; however, no alteration in the expression level of Lcn2 was detected compared to earlier passages. Finally, a higher amount of Lcn2 protein was detected in the plasma of the elderly than in young people.Our findings suggest that Lcn2 might restore the health and regeneration potential of MSCs by decreasing senescence.

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Section: Discussionsupporting

confidence: 60%

Lipocalin 2 decreases senescence of bone marrow-derived mesenchymal stem cells under sub-lethal doses of oxidative stress

Bahmani

Roudkenar

Halabian

et al. 2014

Cell Stress and Chaperones

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“…Moreover, Lcn2-treated cells showed SOD gene upregulation, increased proliferation, maintained pluripotency, and improved cellular adhesion to culture media upon H 2 O 2 exposure, in comparison to untreated cells [37]. Similarly, Fan and colleagues studied different methods for isolation of BMSCs, aiming at reducing the number of chromosomal abnormalities in isolated cells.…”

Section: Bone Marrow-derived Mesenchymal (Bmscs) and Hematopoieticmentioning

confidence: 99%

Effects of Antioxidant Supplements on the Survival and Differentiation of Stem Cells

Shaban

El-Husseny

Abushouk

et al. 2017

Oxidative Medicine and Cellular Longevity

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Although physiological levels of reactive oxygen species (ROS) are required to maintain the self-renewal capacity of stem cells, elevated ROS levels can induce chromosomal aberrations, mitochondrial DNA damage, and defective stem cell differentiation. Over the past decade, several studies have shown that antioxidants can not only mitigate oxidative stress and improve stem cell survival but also affect the potency and differentiation of these cells. Further beneficial effects of antioxidants include increasing genomic stability, improving the adhesion of stem cells to culture media, and enabling researchers to manipulate stem cell proliferation by using different doses of antioxidants. These findings can have several clinical implications, such as improving neurogenesis in patients with stroke and neurodegenerative diseases, as well as improving the regeneration of infarcted myocardial tissue and the banking of spermatogonial stem cells. This article reviews the cellular and molecular effects of antioxidant supplementation to cultured or transplanted stem cells and draws up recommendations for further research in this area.

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“…NGAL is clearly an important regulator in the microenvironment and can play protective roles [143]. Chemokine expression can be regulated by NGAL in certain microenvironments during ischemia and reperfusion [144].…”

Section: Mmp-9 and Ngal And The Tumor Microenvironmentmentioning

confidence: 99%

Roles of NGAL and MMP-9 in the tumor microenvironment and sensitivity to targeted therapy

Candido

Abrams

Steelman

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Various, diverse molecules contribute to the tumor microenvironment and influence invasion and metastasis. In this review, the roles of neutrophil gelatinase-associated lipocalin (NGAL) and matrix metalloproteinase-9 (MMP-9) in the tumor microenvironment and sensitivity to therapy will be discussed. The lipocalin family of proteins has many important functions. For example when NGAL forms a complex with MMP-9 it increases its stability which is important in cancer metastasis. Small hydrophobic molecules are bound by NGAL which can alter their entry into and efflux from cells. Iron transport and storage are also influenced by NGAL activity. Regulation of iron levels is important for survival in the tumor microenvironment as well as metastasis. Innate immunity is also regulated by NGAL as it can have bacteriostatic properties. NGAL and MMP-9 expression may also affect the sensitivity of cancer cells to chemotherapy as well as targeted therapy. Thus NGAL and MMP-9 play important roles in key processes involved in metastasis as well as response to therapy. This article is part of a Special Issue entitled: Tumor Microenvironment Regulation of Cancer Cell Survival, Metastasis, Inflammation, and Immune Surveillance edited by Peter Ruvolo and Gregg L. Semenza.

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Lipocalin-2-mediated upregulation of various antioxidants and growth factors protects bone marrow-derived mesenchymal stem cells against unfavorable microenvironments

Cited by 43 publications

References 55 publications

Lipocalin 2 decreases senescence of bone marrow-derived mesenchymal stem cells under sub-lethal doses of oxidative stress

Lipocalin 2 decreases senescence of bone marrow-derived mesenchymal stem cells under sub-lethal doses of oxidative stress

Effects of Antioxidant Supplements on the Survival and Differentiation of Stem Cells

Roles of NGAL and MMP-9 in the tumor microenvironment and sensitivity to targeted therapy

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