Human Adipose-Derived Stem Cells Ameliorate Cigarette Smoke-Induced Murine Myelosuppression via Secretion of TSG-6

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Abstract

Bone marrow-derived hematopoietic stem and progenitor cells (HSC/HPC) are critical to homeostasis and tissue repair. The aims of this study were to delineate the myelotoxicity of cigarette smoking (CS) in a murine model, to explore human adipose-derived stem cells (hASC) as a novel approach to mitigate this toxicity, and to identify key mediating factors for ASC activities.

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Rapid mobilization of murine and human hematopoietic stem and progenitor cells with AMD3100, a CXCR4 antagonist

Hal E. Broxmeyer, Christie M. Orschell, D. Wade Clapp … (2005)

Improving approaches for hematopoietic stem cell (HSC) and hematopoietic progenitor cell (HPC) mobilization is clinically important because increased numbers of these cells are needed for enhanced transplantation. Chemokine stromal cell derived factor-1 (also known as CXCL12) is believed to be involved in retention of HSCs and HPCs in bone marrow. AMD3100, a selective antagonist of CXCL12 that binds to its receptor, CXCR4, was evaluated in murine and human systems for mobilizing capacity, alone and in combination with granulocyte colony-stimulating factor (G-CSF). AMD3100 induced rapid mobilization of mouse and human HPCs and synergistically augmented G-CSF–induced mobilization of HPCs. AMD3100 also mobilized murine long-term repopulating (LTR) cells that engrafted primary and secondary lethally-irradiated mice, and human CD34+ cells that can repopulate nonobese diabetic-severe combined immunodeficiency (SCID) mice. AMD3100 synergized with G-CSF to mobilize murine LTR cells and human SCID repopulating cells (SRCs). Human CD34+ cells isolated after treatment with G-CSF plus AMD3100 expressed a phenotype that was characteristic of highly engrafting mouse HSCs. Synergy of AMD3100 and G-CSF in mobilization was due to enhanced numbers and perhaps other characteristics of the mobilized cells. These results support the hypothesis that the CXCL12-CXCR4 axis is involved in marrow retention of HSCs and HPCs, and demonstrate the clinical potential of AMD3100 for HSC mobilization.

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Human multipotent stromal cells attenuate lipopolysaccharide-induced acute lung injury in mice via secretion of tumor necrosis factor-α-induced protein 6

Svitlana D Danchuk, Joni Ylöstalo, Fokhrul Hossain … (2011)

Introduction Multipotent stromal cells (MSCs) are currently in clinical trials for a number of inflammatory diseases. Recent studies have demonstrated the ability of MSCs to attenuate inflammation in rodent models of acute lung injury (ALI) suggesting that MSCs may also be beneficial in treating ALI. Methods To better understand how human MSCs (hMSCs) may act in ALI, the lungs of immunocompetent mice were exposed to lipopolysaccharide (LPS) and four hours later bone marrow derived hMSCs were delivered by oropharyngeal aspiration (OA). The effect of hMSCs on lung injury was assessed by measuring the lung wet/dry weight ratio and total protein in bronchoalveolar lavage (BAL) fluid 24 or 48 h after LPS. BAL fluid was also analyzed for the presence of inflammatory cells and cytokine expression by multiplex immunoassay. Microarray analysis of total RNA isolated from treated and untreated lungs was performed to elucidate the mechanism(s) involved in hMSC modulation of lung inflammation. Results Administration of hMSCs significantly reduced the expression of pro-inflammatory cytokines, neutrophil counts and total protein in bronchoalveolar lavage. There was a concomitant reduction in pulmonary edema. The anti-inflammatory effects of hMSCs were not dependent on localization to the lung, as intraperitoneal administration of hMSCs also attenuated LPS-induced inflammation in the lung. Microarray analysis revealed significant induction of tumor necrosis factor (TNF)-α-induced protein 6 (TNFAIP6/TSG-6) expression by hMSCs 12 h after OA delivery to LPS-exposed lungs. Knockdown of TSG-6 expression in hMSCs by RNA interference abrogated most of their anti-inflammatory effects. In addition, intra-pulmonary delivery of recombinant human TSG-6 reduced LPS-induced inflammation in the lung. Conclusions These results show that hMSCs recapitulate the observed beneficial effects of rodent MSCs in animal models of ALI and suggest that the anti-inflammatory properties of hMSCs in the lung are explained, at least in part, by activation of hMSCs to secrete TSG-6.

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Cigarette smoking: an undertreated risk factor for cardiovascular disease.

Leif Erhardt (2009)

Smoking and other forms of tobacco use are major risk factors for cardiovascular disease. The effect of cigarette smoking on cardiovascular health is evident even at the lowest levels of exposure. Yet, the adverse effects of smoking are reversible, with cardiovascular risk decreasing substantially within the first 2 years of smoking cessation. Significantly, the mortality from coronary heart disease is reduced more through smoking cessation than by other secondary preventive therapies such as cholesterol lowering. Smoking cessation is a highly effective way to improve cardiovascular health in smokers and extremely cost-effective. However, smoking cessation therapies are not implemented maximally if they are implemented at all, perhaps because smoking is seen as a lifestyle choice or because smokers frequently relapse, as indicated by very low long-term quit rates. Too often, healthcare professionals, including lipidologists and cardiologists, do little to address their patients' smoking status, in spite of its impact on cardiovascular health. With the advent of new therapies to treat the nicotine addiction that results from smoking and other tobacco use, it is hoped that physicians will be more proactive in encouraging and implementing smoking cessation programs for their patients, with the goal of increasing long-term quit rates, and reducing the morbidity and mortality associated with cardiovascular disease.

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Journal

Title: STEM CELLS

Abbreviated Title: Stem Cells

Publisher: Wiley-Blackwell

ISSN: 10665099

Publication date Created: February 2015

Publication date (Print): February 22 2015

Volume: 33

Issue: 2

Pages: 468-478

Article

DOI: 10.1002/stem.1851

PMC ID: 4618797

PubMed ID: 25329668

SO-VID: 44dbb232-2a54-4294-bd7f-935a79e2191f

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http://doi.wiley.com/10.1002/tdm_license_1

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Human Adipose-Derived Stem Cells Ameliorate Cigarette Smoke-Induced Murine Myelosuppression via Secretion of TSG-6 : Adipose Stem Cells Ameliorate Smoking-Induced Myelosuppression Via TSG-6

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Most cited references 39

Rapid mobilization of murine and human hematopoietic stem and progenitor cells with AMD3100, a CXCR4 antagonist

Human multipotent stromal cells attenuate lipopolysaccharide-induced acute lung injury in mice via secretion of tumor necrosis factor-α-induced protein 6

Cigarette smoking: an undertreated risk factor for cardiovascular disease.

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