Induction of notochordal differentiation of bone marrow mesenchymal‑derived stem cells via the stimulation of notochordal cell‑rich nucleus pulposus tissue

Modulation of the RAS (renin–angiotensin system), in particular of the function of the hormones AngII (angiotensin II) and Ang-(1–7) [angiotensin-(1–7)], is an important target for pharmacotherapy in the cardiovascular system. In the classical view, such modulation affects cardiovascular cells to decrease hypertrophy, fibrosis and endothelial dysfunction, and improves diuresis. In this view, excessive stimulation of AT1 receptors (AngII type 1 receptors) fulfils a detrimental role, as it promotes cardiovascular pathogenesis, and this is opposed by stimulation of the AT2 receptor (angiotensin II type 2 receptor) and the Ang-(1–7) receptor encoded by the Mas proto-oncogene. In recent years, this view has been broadened with the observation that the RAS regulates bone marrow stromal cells and stem cells, thus involving haematopoiesis and tissue regeneration by progenitor cells. This change of paradigm has enlarged the field of perspectives for therapeutic application of existing as well as newly developed medicines that alter angiotensin signalling, which now stretches beyond cardiovascular therapy. In the present article, we review the role of AngII and Ang-(1–7) and their respective receptors in haematopoietic and mesenchymal stem cells, and discuss possible pharmacotherapeutical implications.

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Co-culturing nucleus pulposus mesenchymal stem cells with notochordal cell-rich nucleus pulposus explants attenuates tumor necrosis factor-α-induced senescence

Stem Cell Research & Therapy ◽

10.1186/s13287-018-0919-9 ◽

2018 ◽

Vol 9 (1) ◽

Cited By ~ 5

Author(s):

Xiao-Chuan Li ◽

Mao-Sheng Wang ◽

Wei Liu ◽

Cheng-Fan Zhong ◽

Gui-Bin Deng ◽

...

Keyword(s):

Stem Cells ◽

Mesenchymal Stem Cells ◽

Tumor Necrosis Factor ◽

Nucleus Pulposus ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Notochordal Cell ◽

Factor Α ◽

Necrosis Factor

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P616 TGFβ1 STIMULATION OF HUMAN BONE MARROW MESENCHYMAL STEM CELLS (MSC) ENHANCES THEIR HEPATIC ENGRAFTMENT AND THERAPEUTIC EFFECT IN INJURED LIVER VIA UPREGULATION OF CXCR3 FUNCTION

Journal of Hepatology ◽

10.1016/s0168-8278(14)60778-9 ◽

2014 ◽

Vol 60 (1) ◽

pp. S274

Author(s):

A. Garg ◽

N.J. Davies ◽

V. Aldridge ◽

A.L. King ◽

S.T. Ward ◽

...

Keyword(s):

Stem Cells ◽

Bone Marrow ◽

Mesenchymal Stem Cells ◽

Therapeutic Effect ◽

Human Bone ◽

Human Bone Marrow ◽

Marrow Mesenchymal Stem Cells ◽

Injured Liver ◽

Stimulation Of

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Growing, Tracking, and Directing Bone Marrow Derived Stem Cells From Two-Dimensional and Three-Dimensional Cell Culture Microenvironments

10.36227/techrxiv.11133059 ◽

2019 ◽

Author(s):

Tiffany Miller

Keyword(s):

Stem Cells ◽

Cell Culture ◽

Bone Marrow ◽

Stem Cell ◽

Three Dimensional ◽

Inflammatory Biomarkers ◽

Two Dimensional ◽

Cell Culturing ◽

Dimensional Cell ◽

Stimulation Of

<p>Bone marrow derived stem cells express biomarkers capable of facilitating adhesion to the cell culturing microenvironment, thereby, influencing their proliferation, migration, and differentiation. In particular, biological biomarkers of mesenchymal stem cells include, but are not limited to, CD14-, CD19-, CD34-, CD45-, CD29, CD44, CD73+, CD90+, CD105+, CD106, CD166, Stro-1, and HLADR. The relationship between the stem cell biology and the materials and methods forming a cell culturing microenvironment serves as a critical aspect in the successful adhesion and growth within two-dimensional cell culture microenvironments such as polystyrene, laminin, fibronectin, or poly-L-lysine and within three-dimensional cell culture microenvironments such as hydrogel, ceramic, collagen, polymer based nanofibers, agitation, forced floating, and hang drop systems. Further, electrical stimulation of the stem cells may be implemented during the cell culturing process to measure stem cell growth and to determine stem cell viability. In addition, electrical stimulation of implanted stem cells may facilitate tracking by measuring stem cell migration distance and travel area. Although many biochemical and inflammatory biomarkers are expressed based on severity in stroke including, but not limited to, Interluken-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and glutamate (Glu), current methodologies of stem cell directing lack localization and biological effector specificity. Biological effector bound magnetic particle stem cells may serve as a potential treatment method in ischemic stroke. In particular, a stem cell biomarker may be configured to communicate with inflammatory biomarkers, thus, more efficiently delivering the stem cells to site specific areas having the most severely affected <i>in-vivo</i> biochemical microenvironments.</p>

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Mechanical and Chemical Stimulation of Bone-Marrow Stem Cells in a Three-Dimensional Fibrin Matrix: Preliminary Results

ASME 2008 Summer Bioengineering Conference, Parts A and B ◽

10.1115/sbc2008-193117 ◽

2008 ◽

Author(s):

Jessica L. LoSurdo ◽

Douglas W. Chew ◽

Alejandro Nieponice ◽

David A. Vorp

Keyword(s):

Tissue Engineering ◽

Stem Cells ◽

Bone Marrow ◽

Extracellular Matrix ◽

Vascular Graft ◽

Three Dimensional ◽

Chemical Stimulation ◽

Alternative Source ◽

Immunological Rejection ◽

Stimulation Of

The primary goal of tissue engineering is to develop a biological, mechanically-robust, and anti-thrombogenic vascular graft to replace diseased or damaged tissue and organs [1]. For example, researchers have incorporated smooth muscle cells (SMCs) into extracellular matrix to provide a living, functional conduits with the intended purpose of replacing SMC-containing tubes, such as the blood vessel, urethra, esophagus, intestine, etc. Although the preferred source is autologous cells to avoid immunological rejection, adult SMCs are difficult to obtain and expand. An alternative source of autologous cells could be bone marrow derived stem cells (BMSCs), which differentiate toward mesenchymal and hematopoietic lineages [2].

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Aplastic anemia: lack of inhibitory effect of bone marrow lymphocytes on in vitro granulopoiesis

Blood ◽

10.1182/blood.v56.4.625.625 ◽

1980 ◽

Vol 56 (4) ◽

pp. 625-632 ◽

Cited By ~ 18

Author(s):

R Sullivan ◽

PJ Quesenberry ◽

R Parkman ◽

KS Zuckerman ◽

RH Levey ◽

...

Keyword(s):

Stem Cells ◽

Bone Marrow ◽

Aplastic Anemia ◽

Marrow Cell ◽

Inhibitory Effect ◽

Soft Agar ◽

Control Subjects ◽

B And T Lymphocytes ◽

Stimulation Of

Abstract Prompted by previous reports that in certain patients with aplastic anemia, cell-mediated autoimmune suppression of myeloid stem cell proliferation may be demonstrable in vitro, we studied the effects of bone marrow lymphocytes from 18 patients with myeloid aplasia on the proliferation of committed granulocytic-monocytic progenitor cells (CFU- C). When assayed in soft agar cultures, marrow suspensions from 10 patients with aplastic anemia contained significantly fewer viable CFU- C than similar cell preparations from control subjects. To deplete marrow cell suspensions of lymphocytes, we employed rabbit anti-human thymocyte serum (ATS), which after multiple adsorptions exhibited marked cytotoxicity for human B and T lymphocytes but had negligible effect on normal CFU-C proliferation. Preincubation of marrow samples from 12 patients with ATS and complement resulted in no inhibition or enhancement of CFU-C growth. In further experiments, marrow cells from 8 patients were incubated with marrow from control subjects prior to CFU-C culture. No suppression of donor CFU-C proliferation was observed in any of these studies, and in 4 cocultures, mixture of the 2 marrow suspensions resulted in stimulation of CFU-C growth. Using these assays, we detected no evidence of cell-mediated inhibition of CFU-C proliferation in any of the 18 patients that we evaluated. Our data support the conclusion that in the majority of patients with aplastic anemia, an absolute deficiency of hemopoietic stem cells is present within the marrow that does not appear to be effected or sustained by suppressor lymphocytes. Whether the reduction of viable stem cells is the cause or the consequence of the process that leads to marrow failure remains unknown.

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Ex-vivo Tendon Repair Augmented with Bone Marrow Derived Mesenchymal Stem Cells Stimulated with Myostatin for Tenogenesis

The Journal of Hand Surgery (Asian-Pacific Volume) ◽

10.1142/s2424835518500066 ◽

2018 ◽

Vol 23 (01) ◽

pp. 47-57 ◽

Cited By ~ 3

Author(s):

Wei Le ◽

Andre Eu-Jin Cheah ◽

Jeffrey Yao

Keyword(s):

Stem Cells ◽

Bone Marrow ◽

Mesenchymal Stem Cells ◽

Upper Limb ◽

Ex Vivo ◽

Tendon Repair ◽

Tendon Tissue ◽

Flexor Tendons ◽

Stimulation Of

Background: To investigate the effect of myostatin (GDF-8) stimulation of bone marrow derived mesenchymal stem cells (BMSCs) on tenogenesis in the setting of tendon repair. GDF-8 has demonstrated the ability to augment tenogenesis and we sought to identify if this effect could lead to the focused differentiation of pluripotential stem cells down a tenocyte lineage ex vivo.Methods: Cadaveric upper limb flexor tendons were harvested, decellularized and divided into 1 cm segments. Sutures seeded with stem cells were passed through tendon segments to simulate repair. The repaired tendons were then cultured either with or without myostatin for 3, 5, and 7 days. The experiment was also repeated with non-decellularized tendons for a total of 4 groups. The tendons were then evaluated for the expression of scleraxis and tenomodulin, two biomarkers for tendon.Results: Myostatin stimulation led to an increase in expression of tenomodulin and scleraxis at 5 and 7 days in both the decellularized and non-decellularized tendons. Myostatin increased the differentiation of BMSCs into tenocytes and/or led to the upregulation of tenomodulin and scleraxis production by the native tenocytes present within the non-decellularized tendons.Conclusions: The addition of myostatin to BMSCs leads to tenocyte differentiation as evidenced by the expression of tenocyte biomarkers, scleraxis and tenomodulin. This effect is maintained in an ex vivo tendon repair model suggestive that these cells survive the passage through tendon tissue and remain metabolically active.

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