Expression of glucose transporter 2 during differentiation of human umbilical cord mesenchymal stem cells into islet precursor cells  

QIN Xiao-li TAN Meng-tian HONG Yan

Acta Anatomica Sinica ›› 2017, Vol. 48 ›› Issue (4) : 410-415.

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Acta Anatomica Sinica ›› 2017, Vol. 48 ›› Issue (4) : 410-415. DOI: 10.16098/j.issn.0529-1356.2017.04.007
Cell and Molecules Biology

Expression of glucose transporter 2 during differentiation of human umbilical cord mesenchymal stem cells into islet precursor cells  

  • QIN Xiao-li1 TAN Meng-tian2 HONG Yan 1*
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Abstract

 Objective To detect the expression of glucose transperter 2 (Glut2) when human umbilical cord mesenchymal stem cells (hUMSCs) were transformed into islet precursor cells. Methods hUMSCs were isolated, cultivated, identified and differentiated. The cells and supernatant were collected on the 7th,14th and 21st day of the induction. Immunocytochemistry,immunofluorescence, ELISA, Western blotting and Realtime PCR were used to detect the expression of cell-associated proteins and genes. Results 1.The expression of pancreas duodenum homeobox-1 (PDX-1) was positive; 2.Positive expressions of Ngn3 and insulin were detected by immunofluorescence; 3.The expression of Glut2 protein was measured by Western blotting. The Glut2 protein gradually increased in the induction process, and reached the peak value on the 14th day, compared with the normal group (P<0.01). Glut2 gene increased from the 7th day(P<0.05)in Real-time PCR. Conclusion After induction, hUMSCs turn into pancreatic precursor cells and have functional features of islet B cell initially for expressing Glut2 protein, which can cause insulin secretion.

Key words

Human umbilical cord mesenchymal stem cell / Islet precursor cell / Glucose transporters 2 / Immunohistochemistry / Immunofluorescence / Real-time PCR

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QIN Xiao-li TAN Meng-tian HONG Yan. Expression of glucose transporter 2 during differentiation of human umbilical cord mesenchymal stem cells into islet precursor cells  [J]. Acta Anatomica Sinica. 2017, 48(4): 410-415 https://doi.org/10.16098/j.issn.0529-1356.2017.04.007

References

[1]Kadam SS, Bhonde RR. Islet neogenesis from the constitutively nestin expressing human umbilical cord matrix derived mesenchymal stem cells[J]. Islets, 2010, 2(2):112-120.
[2]Wang GY, Zhao F, Hao YL, et al. Islet-like cells derived from mesenchymal stem cells in Wharton’s Jelly of the human umbilical cord co-cultured with rat pancreatic cells for transplantation to control type Ⅰ diabetes mellitus[J]. Journal of Clinical Rehabilitative Tissue Engineering Research, 2011, 15(40):7467-7473.
[3]Lancaster MA, Knoblich JA. Organogenesis in a dish: modeling development and disease using organoid technologies[J]. Science, 2014, 345(6194):1247125.
[4]Sherwood RI, Hashimoto T, O’Donnell CW, et al. Discovery of directional and nondirectional pioneer transcription factors by modeling DNase profile magnitude and shape[J]. Nat Biotechnol, 2014, 32(2):171-178.
[5]Chai ShH, Bao ChY. To compare the ability of human umbilical cord mesenchymal stem cells and bone marrow mesenchymal stem cells to differentiate into insulin-secreting cells [J]. Journal of Practical Medicine, 2014, 30(1): 52-54. (in Chinese)
柴树宏,鲍春艳. 人脐带间充质干细胞分化为胰岛素分泌细胞的能力比较[J]. 实用医学杂志,2014,30(1):52-54.
[6]Mueckler M, Thorens B. The SLC2 (GLUT) family of membrane transporters[J]. Mol Aspects Med, 2013, 34(2-3):121-138.
[7]Kapoor A, Yao W, Ying H, et al. Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer[J]. Cell, 2014, 158(1):185-197.
[8]Rezania A, Bruin JE, Arora P, et al. Reversal of diabetes with insulin-producing cells derived in vitro from human pluripotent stem cells[J]. Nat Biotechnol, 2014, 32(11):1121-1133.
[9]Zhang FX, Hong Y, Liang WM. Isolation and culture of human umbilical cord mesenchymal stem cells and analysis on their ultrastructural characteristics [J].Guiyang Medical College, 2013, 38 (1): 5-9. (in Chinese)
张芬熙, 洪艳, 梁文妹. 人脐带间充质干细胞的分离培养及超微结构特点研究[J]. 贵阳医学院学报, 2013, 38(1):5-9.
[10]Tian MT,  Hong Y, Han J, et al. Expression of Hes1 during transdifferentiation of hUMSCs into islet progenitor cells [J]. World Chinese Journal of Digestion, 2016 (9): 1357-1365.  (in Chinese)
檀梦天, 洪艳, 韩晶,等. Hes1在hUMSCs向胰岛前体细胞诱导过程中的表达改变[J]. 世界华人消化杂志, 2016(9):1357-1365.
[11]Hang Y, Yamamoto T, Benninger RK, et al. The MafA transcription factor becomes essential to islet β-cells soon after birth[J]. Diabetes, 2014, 63(6):1994-2005.
[12]Richardson CC, Hussain K, Jones PM, et al. Low levels of glucose transporters and K+ ATP channels in human pancreatic beta cells early in development[J]. Diabetologia, 2007, 50(5):1000-1005.
[13]Pasquali L. Pancreatic islet enhancer clusters enriched in type 2 diabetes risk-associated variants[J]. Nat Genet, 2014, 46(2):136-143.
[14]Shih HP, Wang A, Sander M. Pancreas Organogenesis: From Lineage Determination to Morphogenesis[J]. Annu Rev Cell Dev Biol, 2013, 29:81-105.
[15]Benner C, Meulen TVD, Cacéres E, et al. The transcriptional landscape of mouse beta cells compared to human beta cells reveals notable species differences in long non-coding RNA and protein-coding gene expression[J]. BMC Genomics, 2014, 15(1):620.
[16]Ohtsubo K, Chen MZ, Olefsky JM, et al. Pathway to diabetes through attenuation of pancreatic beta cell glycosylation and glucose transport[J]. Nat Med,2011, 17(9):1067-1075.[17]Leturque A, Brotlaroche E, Gall ML. GLUT2 mutations, translocation, and receptor function in diet sugar managing[J]. Ame J Physiol Endocrinol Metab, 2009, 296(5):E985-E992.[18]Thorens B. GLUT2, glucose sensing and glucose homeostasis[J]. Diabetologia, 2015, 58(2):221-232.
[19]Eddouks M, Bidi A, Ei Bouhali B, et al. Antidiabetic plants improving insulin sensitivity[J]. J Pharm Pharmacol, 2014, 66(9):1197-1214.
[20]Shu S, Liu H, Wang M, et al. Subchronic olanzapine treatment decreases the expression of pancreatic glucose transporter 2 in rat pancreatic β cells[J]. J Endocrinol Invest, 2014, 37(7):667-673.
[21]Hagenfeldt-Johansson KA, Herrera PL, Wang H, et al. Beta-cell-targeted expression of a dominant-negative hepatocyte nuclear factor-1 alpha induces a maturity-onset diabetes of the young (MODY)3-like phenotype in transgenic mice[J]. Endocrinology, 2013, 142(12):5311-5320.
[22]Guillam MT, Dupraz P, Thorens B. Glucose uptake, utilization, and signaling in GLUT2-null islets[J]. Diabetes, 2000, 49(9):1485.
[23]Wang ZV, Mu J, Schraw TD, et al. PANIC-ATTAC: a mouse model for inducible and reversible β-cell ablation[J]. Diabetes, 2008, 57(8): 2137-2148.
[24]Guo J, Teng LP, De W. Gene expression of different stages of pancreas development in rats [J]. Advances in Modern Biomedicine, 2010, 10 (15): 2847-2850. (in Chinese)
郭静, 滕丽萍, 德伟,等. 大鼠胰腺发育不同阶段基因表达分析[J]. 现代生物医学进展, 2010, 10(15):2847-2850.
[25]Yuan QX,Teng LP,Xu KF,et al. The functional maturation of insulin secretion during pancreatic development in rat [J].Journal of Nanjing Medical University (Natural Science Edition), 2010, 30 (11): 1568-1574. (in Chinese)
袁庆新, 滕丽萍, 徐宽枫,等. 大鼠胰腺发育过程中胰岛素释放功能完善的研究[J]. 南京医科大学学报(自然科学版), 2010, 30(11):1568-1574.
[26]Zhao L, Li Z, Kullin M, et al. Alterations in net glucose uptake and in the pancreatic B-cell GLUT2 transporter induced by diazoxide and by secretory stimuli[J]. J Endocrinol, 2005, 185(2):291-299.
[27]Lee EY, Kaneko S, Jutabha P, et al. Distinct action of the α-glucosidase inhibitor miglitol on SGLT3, enteroendocrine cells, and GLP1 secretion[J]. J Endocrinol, 2015, 224(3):205-214.
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