KIF26B silencing prevents osseous transdifferentiation of progenitor/stem cells and attenuates ectopic calcification in a murine model

2021 ◽  
Author(s):  
Mingming Yan ◽  
Xin Duan ◽  
Lei Cai ◽  
Weili Zhang ◽  
Matthew J. Silva ◽  
...  
Keyword(s):  
Stem Cells ◽  
Murine Model ◽  
Ectopic Calcification

scholarly journals Human Oral Mucosal Stem Cells Reduce Anastomotic Leak in an Animal Model of Colonic Surgery

2021 ◽  
pp. 1-8
Author(s):  
Ilan Kent ◽  
Cyrus Jahansouz ◽  
Amandeep Ghuman ◽  
Baruch Shpitz ◽  
Debora Kidron ◽  
...  
Keyword(s):  
Stem Cells ◽  
Anastomotic Leak ◽  
Murine Model ◽  
Colonic Anastomosis ◽  
Colon Surgery ◽  
Leak Rate ◽  
Colonic Surgery ◽  
Colon Wall ◽  
Anastomotic Leak Rate ◽  
Suture Anastomosis

<b><i>Background:</i></b> Anastomotic leak is regarded as one of the most feared complications of bowel surgery; avoiding leaks is a major priority. Attempts to reduce or eliminate leaks have included alternate anastomotic techniques. Human oral mucosa stem cells (hOMSC) are self-renewing and expandable cells derived from buccal mucosa. Studies have shown that hOMSC can accelerate tissue regeneration and wound healing. The objective of this study was to evaluate whether hOMSC can decrease anastomotic leak rates in a murine model of colon surgery. <b><i>Methods:</i></b> Two experiments were performed. In the first study, mice underwent colonic anastomosis using five interrupted sutures. hOMSC (<i>n</i> = 7) or normal saline (NS; <i>n</i> = 17) was injected into the colon wall at the site of the anastomosis. To evaluate whether hOMSC can impact anastomotic healing, the model was stressed by repeating the first experiment, reducing the number of sutures used for the construction of the anastomosis from five to four. Either hOMSC (<i>n</i> = 8) or NS (<i>n</i> = 20) was injected at the anastomosis. All mice that survived were sacrificed on postoperative day 7. Anastomotic leak rate, mortality, daily weight, and daily wellness scores were compared. <b><i>Results:</i></b> In the five-suture anastomosis, there were no differences in anastomotic leak rate, mortality, or daily weight. Mice that received hOMSC had significantly higher wellness scores on postoperative day 2 (<i>p</i> &#x3c; 0.05). In the four-suture anastomosis, there was a significant decrease in leak rate (70% [NS] vs. 25% [hOMSC], <i>p</i> = 0.029) and higher wellness scores in mice that received hOMSC (<i>p</i> &#x3c; 0.05). <b><i>Conclusion:</i></b> Our study suggests that injecting hOMSC at the colonic anastomosis can potentially reduce anastomotic leak and improve postoperative wellness in a murine model of colon surgery.

scholarly journals Human adipose-derived stromal/stem cells demonstrate short-lived persistence after implantation in both an immunocompetent and an immunocompromised murine model

2014 ◽  
Vol 5 (6) ◽  
pp. 142 ◽  
Author(s):  
Hitesh Agrawal ◽  
Hulan Shang ◽  
Anna Sattah ◽  
Ning Yang ◽  
Shayn M Peirce ◽  
...  
Keyword(s):  
Stem Cells ◽  
Murine Model ◽  
Stromal Stem Cells

scholarly journals Immunomodulatory Effects of Mesenchymal Stem Cells in a Murine Model of TNBS-Induced Colitis

2010 ◽  
Vol 79 (5) ◽  
pp. 317 ◽  
Author(s):  
Yong Beom Cho ◽  
Min Shik Kim ◽  
Min Jeong Kang ◽  
Hee Jung Shin ◽  
Seok-Hyung Kim ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Murine Model ◽  
Immunomodulatory Effects

scholarly journals Mouse Muscle‐Derived Stem Cells in a Murine Model of Accelerated Aging

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Mitra Lavasani ◽  
Andria R Robinson ◽  
Aiping Lu ◽  
Joseph M Feduska ◽  
Jeremy S Tilstra ◽  
...  
Keyword(s):  
Stem Cells ◽  
Murine Model ◽  
Accelerated Aging ◽  
Mouse Muscle

scholarly journals Uterine Cells Improved Ovarian Function in a Murine Model of Ovarian Insufficiency

2019 ◽  
Vol 26 (12) ◽  
pp. 1633-1639 ◽  
Author(s):  
Andres Reig ◽  
Ramanaiah Mamillapalli ◽  
Alexis Coolidge ◽  
Joshua Johnson ◽  
Hugh S. Taylor
Keyword(s):  
Stem Cells ◽  
Young Women ◽  
Murine Model ◽  
Ovarian Function ◽  
Fluorescent Protein ◽  
Primary Ovarian Insufficiency ◽  
Age Group ◽  
Ovarian Dysfunction ◽  
Ovarian Insufficiency ◽  
Green Fluorescent

Primary ovarian insufficiency (POI) is defined as ovarian dysfunction in women younger than 40 years. It affects 1% of the women in this age-group and can occur iatrogenically after chemotherapy. Stem cells have been used in attempt to restore ovarian function in POI. In particular, endometrial mesenchymal stem cells (eMSCs) are easily obtainable in humans and have shown great potential for regenerative medicine. Here, we studied the potential for uterine cell (UC) suspensions containing eMSCs to improve ovarian function in a murine model of chemotherapy-induced POI. Green fluorescent protein (GFP)-labeled UC or phosphate-buffered solution (PBS) was delivered intravenously after chemotherapy. There was a significant increase in oocytes production and serum anti-Müllerian hormone concentrations after 6 weeks, as well as a 19% higher body mass in UC-treated mice. Similarly, we observed an increased number of pups in mice treated with UC than in mice treated with PBS. None of the oocytes or pups incorporated GFP, suggesting that there was no contribution of these stem cells to the oocyte pool. We conclude that treatment with UC indirectly improved ovarian function in mice with chemotherapy-induced POI. Furthermore, our study suggests that endometrial stem cell therapy may be beneficial to young women who undergo ovotoxic chemotherapy.

scholarly journals Gpr44 Mediates the Selenium-Dependent Anti-Leukemic Effect in Acute Myeloid Leukemia

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1835-1835
Author(s):  
Fenghua Qian ◽  
Fenghua Qian ◽  
Diwakar Tukaramrao ◽  
Jiayan Zhou ◽  
Nicole Palmiero ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Acute Myeloid Leukemia ◽  
Murine Model ◽  
Myeloid Leukemia ◽  
Hematopoietic Stem ◽  
Cell Counts ◽  
Pparγ Agonist ◽  
Acute Myeloid

Abstract Objectives The relapse of acute myeloid leukemia (AML) remains a significant concern due to persistent leukemia stem cells (LSCs) that are not targeted by existing therapies. LSCs show sensitivity to endogenous cyclopentenone prostaglandin J (CyPG) metabolites that are increased by dietary trace element selenium (Se), which is significantly decreased in AML patients. We investigated the anti-leukemic effect of Se supplementation in AML via mechanisms involving the activation of the membrane-bound G-protein coupled receptor 44 (Gpr44) and the intracellular receptor, peroxisome proliferator-activated receptor gamma (PPARγ), by endogenous CyPGs. Methods A murine model of AML generated by transplantation of hematopoietic stem cells (HSCs- WT or Gpr44−/−) expressing human MLL-AF9 fusion oncoprotein, in the following experiments: To investigate the effect of Se supplementation on the outcome of AML, donor mice were maintained on either Se-adequate (Se-A; 0.08–0.1 ppm Se) or Se-supplemented (Se-S; 0.4 ppm Se) diets. Complete cell counts in peripheral blood were analyzed by hemavet. LSCs in bone marrow and spleen were analyzed by flow cytometry. To determine the role of Gpr44 activation in AML, mice were treated with Gpr44 agonists, CyPGs. LSCs in bone marrow and spleen were analyzed. Mice transplanted with Gpr44−/- AML cells were compared with mice transplanted with wild type AML cells and the progression of the disease was followed as above. To determine the role of PPARγ activation in AML, PPARγ agonist (Rosiglitazone, 6 mg/kg, i.p, 14 d) and antagonist (GW9662, 1 mg/kg, i.p. once every other day, 7 injections) were applied to Se-S mice transplanted with Gpr44−/- AML cells and disease progression was followed. Results Se supplementation at supraphysiological levels alleviated the disease via the elimination of LSCs in a murine model of AML. CyPGs induced by Se supplementation mediate the apoptosis in LSCs via the activation of Gpr44 and PPARγ. Conclusions Endogenous CyPGs produced upon supplementation with Se at supraphysiological levels improved the outcome of AML by targeting LSCs to apoptosis via the activation of two receptors, Gpr44 and PPARg. Funding Sources NIH DK 07,7152; CA 175,576; CA 162,665. Office of Dietary Supplements, USDA Hatch funds PEN04605, Accession # 1,010,021 (KSP, RFP).

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