PREPARATION OF SULFATED CHITOSAN/POLYLYSINE/TRANSFORM GROWTH FACTOR-β1 NANOPARTICLES AND THEIR ABILITY TO INDUCE CHONDROGENESIS DIFFERENTIATION OF BMSCs

Diabetic nephropathy is a leading cause of chronic renal failure. Recently, Euonymus alatus showed therapeutic potential in the treatment of diabetes and its chronic complications. In this study, effects of Euonymus alatus and its mechanism in the treatment of diabetic nephropathy were investigated. Diabetic nephropathy was induced in Sprague-Dawley rats by uninephrectomy plus streptozotocin (STZ) administration. Euonymus alatus and irbesartan, as a positive control, were lavaged to these rats for 12 weeks. Our data showed that Euonymus alatus was efficient in lowering HbA1c, improving blood lipids, decreasing 24 h urine protein and protecting kidney function. Pathological studies found kidney damage, including extracellular matrix expansion and glomerulosclerosis, were improved by Euonymus alatus treatment. Further investigation found that the herb had a role in downregulating the expression of transform growth factor β1. In conclusion, Euonymus alatus has a protective role in diabetic nephropathy, which may be related to its downregulation of transform growth factor β1 expression.

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Enhanced bioactivity of transform growth factor-β1 from sulfated chitosan microspheres for in vitro chondrogenesis of mesenchymal stem cells

Pure and Applied Chemistry ◽

10.1515/pac-2014-0704 ◽

2014 ◽

Vol 86 (12) ◽

pp. 1885-1895 ◽

Cited By ~ 1

Author(s):

Feifei Li ◽

Lie Ma ◽

Bo Li ◽

Changyou Gao

Keyword(s):

Stem Cells ◽

Mesenchymal Stem Cells ◽

Growth Factor ◽

In Vitro Release ◽

Transform Growth Factor ◽

Blank Group ◽

Chitosan Microspheres ◽

Tgf Β1

Abstract Transform growth factor-β1 (TGF-β1) is an extremely powerful protein to induce the chondrogenesis of mesenchymal stem cells (MSCs) both in vitro and in vivo. However, due to the short-life of TGF-β1, the direct application of TGF-β1 may deteriorate its bioactivity and thereby the repair effect. In this study, uniform sulfated chitosan microspheres (SCMs) with a mean diameter of ∼ 2 μm were fabricated by membrane emulsification as a carrier for TGF-β1. The in vitro release study showed that TGF-β1 could be sustainedly released from the microspheres up to 16 days. Under the protection of SCMs, about 13 % TGF-β1 was preserved even after stored for 14 days. The microspheres cytotoxicity was evaluated by coculture of MSCs with different concentrations SCMs and no obvious deterioration of cell viability was observed when the concentration of SCMs is lower than 2 μg/1.0 × 104 cells. In comparison with the blank group, the addition of TGF-β1 either in free state or loaded in SCMs inhibited the proliferation trend of MSCs. Quantitative analysis of GAGs production and genes expression of COL II and aggrecan by qRT-PCR revealed that enhanced bioactivity of TGF-β1 was obtained in the group of TGF-β1/SCMs, indicating that SCMs could be functioned as a promising carrier of TGF-β1 for the in vitro chondrogenesis of MSCs.

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Hambatan Mesenchymal Stem Cell Terhadap Proliferasi Limfosit T

Jurnal Biosains Pascasarjana ◽

10.20473/jbp.v20i3.2018.212-218 ◽

2018 ◽

Vol 20 (3) ◽

pp. 212

Author(s):

Sofia Fajarwati

Keyword(s):

Nitric Oxide ◽

Stem Cells ◽

Cell Proliferation ◽

Growth Factor ◽

Transform Growth Factor ◽

T Cell Proliferation ◽

Oxide Synthase ◽

Hepatocyte Growth ◽

Inducible Nitric Oxide

AbstractMesenchymal stem cells (MSCs) are a kind of stem cells that can differentiate into several kinds of mesodermal cell decent. MSCs can be cultured in vitro therefore it can serve many purposes. However, MSCs also have immunosuppresion effects, one of the way is by suppresing T cell proliferation. MSCs need cell-to-cell contact with activated T cells in certain rasio to release it’s surppresion properties. Primery help from inflamatory cytokines is also needed. MSCs’s suppresion effect can be mediated by several molecules such as indoleamine 2,3-dioxygenase (IDO), inducible nitric-oxide synthase (iNOS), prostaglandin E2 (PGE2), transform growth factor-β (TGF-β), hepatocyte growth factor (HGF), and HLA-G5 soluble. MSCs’s characteristic and culture conditions can affect clinical applications.Keywords: Mesenchymal stem cells, T cell proliferation, immunosuppresion AbstrakMesenchymal stem cells (MSC) adalah salah satu jenis stem cell yang dapat berdiferensiasi menjadi beberapa macam turunan sel mesodermal. MSC dapat dikembangkan secara in-vitro sehingga memiliki banyak kegunaan. Namun, MSC juga dapat memberikan beberapa efek imunosupresi, salah satunya dengan cara menekan proliferasi sel T. Untuk melakukan supresi, MSC memerlukan kontak cell-to-cell dengan sel T teraktivasi dengan rasio tertentu. MSC juga membutuhkan bantuan awal dari sitokin inflamasi. Efek supresi MSC dapat diperantarai oleh beberapa molekul seperti indoleamine 2,3-dioxygenase (IDO), inducible nitric- oxide synthase (iNOS), prostaglandin E2 (PGE2), transform growth factor-β (TGF-β), hepatocyte growth factor (HGF), dan HLA-G5 terlarut. Sifat dan kondisi biakan MSC dapat mempengaruhi aplikasi klinis.Kata kunci: Mesenchymal stem cells, proliferasi sel T, imunosupresi

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Quantitative Microscopic Comparison of the Organization of the Lung in Transgenic Mice Expressing Transforming Growth Factor-α (TGF-α)

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100162533 ◽

1996 ◽

Vol 54 ◽

pp. 14-15

Author(s):

C. G. Plopper ◽

C. Helton ◽

A. J. Weir ◽

J. A. Whitsett ◽

T. R. Korfhagen

Keyword(s):

Growth Factor ◽

Pulmonary Fibrosis ◽

Transgenic Mice ◽

Blood Vessels ◽

Lung Parenchyma ◽

Lung Maturation ◽

Alveolar Air ◽

Parenchymal Tissue ◽

Air Space ◽

Conducting Airways

A wide variety of growth factors are thought to be involved in the regulation of pre- and postnatal lung maturation, including factors which bind to the epidermal growth factor receptor. Marked pulmonary fibrosis and enlarged alveolar air spaces have been observed in lungs of transgenic mice expressing human TGF-α under control of the 3.7 KB human SP-C promoter. To test whether TGF-α alters lung morphogenesis and cellular differentiation, we examined morphometrically the lungs of adult (6-10 months) mice derived from line 28, which expresses the highest level of human TGF-α transcripts among transgenic lines. Total volume of lungs (LV) fixed by airway infusion at standard pressure was similar in transgenics and aged-matched non-transgenic mice (Fig. 1). Intrapulmonary bronchi and bronchioles made up a smaller percentage of LV in transgenics than in non-transgenics (Fig. 2). Pulmonary arteries and pulmonary veins were a smaller percentage of LV in transgenic mice than in non-transgenics (Fig. 3). Lung parenchyma (lung tissue free of large vessels and conducting airways) occupied a larger percentage of LV in transgenics than in non-transgenics (Fig. 4). The number of generations of branching in conducting airways was significantly reduced in transgenics as compared to non-transgenic mice. Alveolar air space size, as measured by mean linear intercept, was almost twice as large in transgenic mice as in non-transgenics, especially when different zones within the lung were compared (Fig. 5). Alveolar air space occupied a larger percentage of the lung parenchyma in transgenic mice than in non-transgenic mice (Fig. 6). Collagen abundance was estimated in histological sections as picro-Sirius red positive material by previously-published methods. In intrapulmonary conducting airways, collagen was 4.8% of the wall in transgenics and 4.5% of the wall in non-transgenic mice. Since airways represented a smaller percentage of the lung in transgenics, the volume of interstitial collagen associated with airway wall was significantly less. In intrapulmonary blood vessels, collagen was 8.9% of the wall in transgenics and 0.7% of the wall in non-transgenics. Since blood vessels were a smaller percentage of the lungs in transgenics, the volume of collagen associated with the walls of blood vessels was five times greater. In the lung parenchyma, collagen was 51.5% of the tissue volume in transgenics and 21.2% in non-transgenics. Since parenchyma was a larger percentage of lung volume in transgenics, but the parenchymal tissue was a smaller percent of the volume, the volume of collagen associated with parenchymal tissue was only slightly greater. We conclude that overexpression of TGF-α during lung maturation alters many aspects of lung development, including branching morphogenesis of the airways and vessels and alveolarization in the parenchyma. Further, the increases in visible collagen previously associated with pulmonary fibrosis due to the overexpression of TGF-α are a result of actual increases in amounts of collagen and in a redistribution of collagen within compartments which results from morphogenetic changes. These morphogenetic changes vary by lung compartment. Supported by HL20748, ES06700 and the Cystic Fibrosis Foundation.

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