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Trypsin Potentiates Human Fibrocyte Differentiation  [PDF]
Michael J. V. White, Melissa Glenn, Richard H. Gomer
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0070795
Abstract: Trypsin-containing topical treatments can be used to speed wound healing, although the mechanism of action is unknown. To help form granulation tissue and heal wounds, monocytes leave the circulation, enter the wound tissue, and differentiate into fibroblast-like cells called fibrocytes. We find that 20 to 200 ng/ml trypsin (concentrations similar to those used in wound dressings) potentiates the differentiation of human monocytes to fibrocytes in cell culture. Adding trypsin inhibitors increases the amount of trypsin needed to potentiate fibrocyte differentiation, suggesting that the potentiating effect is dependent on trypsin proteolytic activity. Proteases with other site specificities such as pepsin, endoprotease GluC, and chymotrypsin do not potentiate fibrocyte differentiation. This potentiation requires the presence of albumin in the culture medium, and tryptic fragments of human or bovine albumin also potentiate fibrocyte differentiation. These results suggest that topical trypsin speeds wound healing by generating tryptic fragments of albumin, which in turn potentiate fibrocyte differentiation.
High and Low Molecular Weight Hyaluronic Acid Differentially Regulate Human Fibrocyte Differentiation  [PDF]
Anu S. Maharjan, Darrell Pilling, Richard H. Gomer
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0026078
Abstract: Background Following tissue injury, monocytes can enter the tissue and differentiate into fibroblast-like cells called fibrocytes, but little is known about what regulates this differentiation. Extracellular matrix contains high molecular weight hyaluronic acid (HMWHA; ~2×106 Da). During injury, HMWHA breaks down to low molecular weight hyaluronic acid (LMWHA; ~0.8–8×105 Da). Methods and Findings In this report, we show that HMWHA potentiates the differentiation of human monocytes into fibrocytes, while LMWHA inhibits fibrocyte differentiation. Digestion of HMWHA with hyaluronidase produces small hyaluronic acid fragments, and these fragments inhibit fibrocyte differentiation. Monocytes internalize HMWHA and LMWHA equally well, suggesting that the opposing effects on fibrocyte differentiation are not due to differential internalization of HMWHA or LMWHA. Adding HMWHA to PBMC does not appear to affect the levels of the hyaluronic acid receptor CD44, whereas adding LMWHA decreases CD44 levels. The addition of anti-CD44 antibodies potentiates fibrocyte differentiation, suggesting that CD44 mediates at least some of the effect of hyaluronic acid on fibrocyte differentiation. The fibrocyte differentiation-inhibiting factor serum amyloid P (SAP) inhibits HMWHA-induced fibrocyte differentiation and potentiates LMWHA-induced inhibition. Conversely, LMWHA inhibits the ability of HMWHA, interleukin-4 (IL-4), or interleukin-13 (IL-13) to promote fibrocyte differentiation. Conclusions We hypothesize that hyaluronic acid signals at least in part through CD44 to regulate fibrocyte differentiation, with a dominance hierarchy of SAP>LMWHA≥HMWHA>IL-4 or IL-13.
Toll-like receptor 2 agonists inhibit human fibrocyte differentiation
Anu S Maharjan, Darrell Pilling, Richard H Gomer
Fibrogenesis & Tissue Repair , 2010, DOI: 10.1186/1755-1536-3-23
Abstract: When human peripheral blood mononuclear cells (PBMCs) were cultured with TLR3, TLR4, TLR5, TLR7, TLR8 or TLR9 agonists, there was no significant effect on fibrocyte differentiation, even though enhanced extracellular tumor necrosis factor (TNF)-α accumulation and/or increased cell surface CD86 or major histocompatibility complex (MHC) class II levels were observed. However, all TLR2 agonists tested inhibited fibrocyte differentiation without any significant effect on cell survival. Adding TLR2 agonists to purified monocytes had no effect on fibrocyte differentiation. However, some TLR2 agonists caused PBMCs to secrete a factor that inhibits the differentiation of purified monocytes into fibrocytes. This factor is not interferon (IFN)-α, IFN-γ, interleukin (IL)-12, aggregated immunoglobulin G (IgG) or serum amyloid P (SAP), factors known to inhibit fibrocyte differentiation. TLR2 agonist-treated PBMCs secrete low levels of IL-6, TNF-α, IFN-γ, granulocyte colony-stimulating factor and tumor growth factor β1, but combinations of these factors had no effect on fibrocyte differentiation from purified monocytes.Our results indicate that TLR2 agonists indirectly inhibit fibrocyte differentiation and that, for some TLR2 agonists, this inhibition involves other cell types in the PBMC population secreting an unknown factor that inhibits fibrocyte differentiation. Together, these data suggest that the presence of some bacterial signals can inhibit fibrocyte differentiation and may thus slow wound closure.Following injury, circulating peripheral blood cells such as neutrophils, monocytes, dendritic cells and lymphocytes leave the bloodstream and enter the injured site. Once monocytes are in the injured site, they can differentiate into fibroblast-like cells called fibrocytes [1-8]. Fibrocytes have a distinct spindle-shaped appearance. Fibrocytes express hematopoietic markers, including CD45, major histocompatibility complex (MHC) class II, and CD34, along with stromal markers i
HDAC2 Cytoplasmic Sequestration Potentiates Keratinocyte Terminal Differentiation
Robert E. BakinMira O. Jung
The Open Cell Development & Biology Journal , 2008, DOI: 10.2174/1874085500801010001]
Abstract: A balance of histone acetylation and deacetylation governs the regulation of genes that are involved in the differentiation and stratification of the mammalian epidermis. Class II HDACs (HDAC4, 5, 6, 7, 9, 10) frequently undergo nucleocytoplasmic flux resulting in gene derepression. Of the Class I HDACs (HDAC1, 2, 3, 8), HDAC2 has only been described in a nuclear setting. Here we report that a specific in vivo subpopulation of epidermal keratinocytes undergoing apoptotic-like terminal differentiation demonstrate complete cytoplasmic sequestration of HDAC2, robust Keratin-10 expression, and canonical nuclear fragmentation. Paralleling our in vivo findings, proteosomal degradation of total cellular HDAC2 enhanced Keratin-10 expression in undifferentiated HFK cells. Forced HDAC2 nuclear overexpression and retention results in a partial differentiation block as measured by reduced Keratin-10 expression and delayed chromatin fragmentation. We offer a preliminary model whereby cytoplasmic sequestration of the HDAC2 transcriptional corepressor contributes, in part, to the process of mammalian epidermal differentiation. (words 150)
Sox9 Potentiates BMP2-Induced Chondrogenic Differentiation and Inhibits BMP2-Induced Osteogenic Differentiation  [PDF]
Junyi Liao, Ning Hu, Nian Zhou, Liangbo Lin, Chen Zhao, Shixiong Yi, Tingxu Fan, Wei Bao, Xi Liang, Hong Chen, Wei Xu, Cheng Chen, Qiang Cheng, Yongming Zeng, Weike Si, Zhong Yang, Wei Huang
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0089025
Abstract: Bone morphogenetic protein 2 (BMP2) is one of the key chondrogenic growth factors involved in the cartilage regeneration. However, it also exhibits osteogenic abilities and triggers endochondral ossification. Effective chondrogenesis and inhibition of BMP2-induced osteogenesis and endochondral ossification can be achieved by directing the mesenchymal stem cells (MSCs) towards chondrocyte lineage with chodrogenic factors, such as Sox9. Here we investigated the effects of Sox9 on BMP2-induced chondrogenic and osteogenic differentiation of MSCs. We found exogenous overexpression of Sox9 enhanced the BMP2-induced chondrogenic differentiation of MSCs in vitro. Also, it inhibited early and late osteogenic differentiation of MSCs in vitro. Subcutaneous stem cell implantation demonstrated Sox9 potentiated BMP2-induced cartilage formation and inhibited endochondral ossification. Mouse limb cultures indicated that BMP2 and Sox9 acted synergistically to stimulate chondrocytes proliferation, and Sox9 inhibited BMP2-induced chondrocytes hypertrophy and ossification. This study strongly suggests that Sox9 potentiates BMP2-induced MSCs chondrogenic differentiation and cartilage formation, and inhibits BMP2-induced MSCs osteogenic differentiation and endochondral ossification. Thus, exogenous overexpression of Sox9 in BMP2-induced mesenchymal stem cells differentiation may be a new strategy for cartilage tissue engineering.
Heterothallism of the human in the context of contemporary concept of sexual differentiation
Devyatykh S. Y.
Sociosfera , 2010,
Abstract: Sexual differentiation is considered as function of interaction of organism and environment; it was found out that biological factors of sexual differentiation are complemented with social factors in postnatal ontogenesis. Herewith, heterothallism stands as first and global phenomenon of human sexuality.
Sphingosine-1-phosphate promotes the differentiation of human umbilical cord mesenchymal stem cells into cardiomyocytes under the designated culturing conditions
Zhenqiang Zhao, Zhibin Chen, Xiubo Zhao, Fang Pan, Meihua Cai, Tan Wang, Henggui Zhang, Jian R Lu, Ming Lei
Journal of Biomedical Science , 2011, DOI: 10.1186/1423-0127-18-37
Abstract: Cardiomyogenic differentiation of HUMSCs was performed by culturing these cells with either designated cardiomyocytes conditioned medium (CMCM) alone, or with 1 μM S1P; or DMEM with 10% FBS + 1 μM S1P. Cardiomyogenic differentiation was determined by immunocytochemical analysis of expression of cardiomyocyte markers and patch clamping recording of the action potential.A cardiomyocyte-like morphology and the expression of α-actinin and myosin heavy chain (MHC) proteins can be observed in both CMCM culturing or CMCM+S1P culturing groups after 5 days' culturing, however, only the cells in CMCM+S1P culture condition present cardiomyocyte-like action potential and voltage gated currents. A new approach was used to form PIPAAm based temperature-responsive culture surfaces and this successfully produced cell sheets from HUMSCs derived cardiomyocytes.This study for the first time demonstrates that S1P potentiates differentiation of HUMSCs towards functional cardiomyocytes under the designated culture conditions. Our engineered cell sheets may provide a potential for clinically applicable myocardial tissues should promote cardiac tissue engineering research.Mesenchymal Stem cells (MSCs) are pluripotent cells that are able to differentiate into various specific cell types. Because of their plasticity, MSCs have been suggested as potential therapies for numerous diseases and conditions. In vitro differentiation of MSCs into cardiomyocytes offers a new cellular therapy for heart diseases. Therefore, it is of growing interest to develop novel approaches to initiate differentiation of various types of MSCs into cardiomyocytes. Human umbilical cord (UC) has been a tissue of increasing interest for such purpose due to the MSCs potency of stromal cells isolated from the human UC mesenchymal tissue, namely, Wharton's jelly[1]. A number of recent studies have shown that HUMSCs are able to differentiate towards multiple lineages including neuronal and myocardiogenic cells in vitro, thu
HOX gene analysis in the osteogenic differentiation of human mesenchymal stem cells
Chae, Song Wha;Jee, Bo Keun;Lee, Joo Yong;Han, Chang Whan;Jeon, Yang-Whan;Lim, Young;Lee, Kweon-Haeng;Rha, Hyoung Kyun;Chae, Gue-Tae;
Genetics and Molecular Biology , 2008, DOI: 10.1590/S1415-47572008005000019
Abstract: keywords : human mesenchymal stem cells; hox genes; osteogenic differentiation; stem cell differentiation; gene profiling.
Stem cell differentiation and human liver disease  [cached]
Wen-Li Zhou,Claire N Medine,Liang Zhu,David C Hay
World Journal of Gastroenterology , 2012, DOI: 10.3748/wjg.v18.i17.2018
Abstract: Human stem cells are scalable cell populations capable of cellular differentiation. This makes them a very attractive in vitro cellular resource and in theory provides unlimited amounts of primary cells. Such an approach has the potential to improve our understanding of human biology and treating disease. In the future it may be possible to deploy novel stem cell-based approaches to treat human liver diseases. In recent years, efficient hepatic differentiation from human stem cells has been achieved by several research groups including our own. In this review we provide an overview of the field and discuss the future potential and limitations of stem cell technology.
Different level of population differentiation among human genes
Dong-Dong Wu, Ya-Ping Zhang
BMC Evolutionary Biology , 2011, DOI: 10.1186/1471-2148-11-16
Abstract: Here, we study the level of population differentiation among different populations of human genes. Intriguingly, genes involved in osteoblast development were identified as being enriched with higher FST SNPs, a result consistent with the proposed role of the skeletal system in accounting for variation among human populations. Genes involved in the development of hair follicles, where hair is produced, were also found to have higher levels of population differentiation, consistent with hair morphology being a distinctive trait among human populations. Other genes that showed higher levels of population differentiation include those involved in pigmentation, spermatid, nervous system and organ development, and some metabolic pathways, but few involved with the immune system. Disease-related genes demonstrate excessive SNPs with lower levels of population differentiation, probably due to purifying selection. Surprisingly, we find that Mendelian-disease genes appear to have a significant excessive of SNPs with high levels of population differentiation, possibly because the incidence and susceptibility of these diseases show differences among populations. As expected, microRNA regulated genes show lower levels of population differentiation due to purifying selection.Our analysis demonstrates different level of population differentiation among human populations for different gene groups.After dispersal from Africa, humans have evolved to be characterized by substantial phenotypic variation, including variation in skin, hair, and eye color, body mass, height, diet, drug metabolism, susceptibility and resistance to disease, during the colonization of the World. Efforts to reveal the genetic bases of these variations should provide important insight into the history of human evolution, gene function, and the mechanisms of disease [1,2]. Indeed, with the advent of large scale comparative genomic and human polymorphism data, a flood of studies have identified many candidate g
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