共查询到20条相似文献,搜索用时 31 毫秒
1.
Helen E Gruber David Mauerhan Yin Chow Jane A Ingram H James Norton Edward N HanleyJr Yubo Sun 《BMC biotechnology》2008,8(1):54
Background
The meniscus is a complex tissue whose cell biology has only recently begun to be explored. Published models rely upon initial culture in the presence of added growth factors. The aim of this study was to test a three-dimensional (3D) collagen sponge microenvironment (without added growth factors) for its ability to provide a microenvironment supportive for meniscal cell extracellular matrix (ECM) production, and to test the responsiveness of cells cultured in this manner to transforming growth factor-β (TGF-β). 相似文献2.
Balzer Sandrock Karen M. Hudson Douglas E. Williams Michael A. Lieberman 《In vitro cellular & developmental biology. Animal》1996,32(4):225-233
Summary The regulation of megakaryopoeisis by cytokines is not yet well understood. It is possible that autocrine loops are established
during megakaryocyte growth and differentiation, aiding in the maturation of these cells. The CHRF-288-11 human megakaryoblastic
cell line has been examined for cytokine production in growing cells and cells stimulated to differentiate by the addition
of phorbol esters. It has been demonstrated that these cells produce RNA corresponding to the interleukins IL-1α, 1β, 3, 7,
8, and 11, granulocyte-macrophage colony stimulating factor (GM-CSF), stem cell factor (SCF), transforming growth factor-β
(TGF-β), tumor necrosis factor-α (TNF-α), interferon-α (INF-α), and basic fibroblast growth factor (bFGF). Additionaly, RNA
corresponding to the receptors for IL-6, GM-CSF, SCF, INF-α,β, bFGF, and monocyte colony stimulating factor (M-CSF) were also
expressed by the cells. The receptor for TNF-α was detected immunologically. Analysis at the protein level demonstrated that
significant amounts of INF-α, TNF-α, GM-CSF, SCF, IL-1α, and a soluble form of the IL-6 receptor were produced by the cells.
Addition of phorbol esters to CHRF-288-11 cells enhances their megakaryocytic phenotype; such treatment also results in increased
secretion of INF-α, TNF-α, and GM-CSF. These results suggest that potential autocrine loops are established during the differentiation
of CHRF-288-11 cells, which may alter the capability of the cell to differentiate. These findings are similar to those recently
obtained for marrow-derived megakaryocytes (Jiang et al.) suggesting that CHRF-288-11 cells provide a useful model system
for the study of cytokine release during megakaryocyte differentiation. 相似文献
3.
Yeo Dae Yoon Eun Sook Lee Jong Pil Park Mee Ree Kim Jun Won Lee Tae Hoon Kim Min Kyun Na Jin Hee Kim 《Biotechnology and Bioprocess Engineering》2011,16(6):1099-1105
Hizikia fusiforme is a commonly used food that possesses potent anti-bacterial, anti-fungal, and anti-inflammatory activities. The immunostimulatory
activities of aqueous extract of Hizikia fusiforme (HFAE) in RAW 264.7 macrophages and whole spleen cells were investigated. HFAE activated RAW 264.7 macrophages to produce
cytokines such as nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in
a dose-dependent manner. In addition, HFAE induced the mRNA expression of TNF-α, IL-1β, and IL-6 in RAW 264.7 macrophages.
Moreover, HFAE stimulated proliferation of whole spleen cells and reference mitogen. Taken together, the results demonstrate
that HFAE potently activates the immune function by regulating NO, TNF-α, IL-1β, and IL-6 in RAW 264.7 macrophage and promoting
spleen cell proliferation. 相似文献
4.
Katri Lindfors Keijo M Viiri Marjo Niittynen Taisto YK Heinonen Markku M?ki Heikki Kainulainen 《BMC genomics》2003,4(1):53
Background
We have previously set up an in vitro mesenchymal-epithelial cell co-culture model which mimics the intestinal crypt villus axis biology in terms of epithelial cell differentiation. In this model the fibroblast-induced epithelial cell differentiation from secretory crypt cells to absorptive enterocytes is mediated via transforming growth factor-β (TGF-β), the major inhibitory regulator of epithelial cell proliferation known to induce differentiation in intestinal epithelial cells. The aim of this study was to identify novel genes whose products would play a role in this TGF-β-induced differentiation. 相似文献5.
The capacity of cornel iridoid glycoside (CIG) to suppress the manifestations of ischemic stroke was investigated. CIG was
administered to rats by the intragastric route once daily for 7 days. Focal cerebral ischemia was induced by 2 h of middle
cerebral artery occlusion followed by 24 h of reperfusion. In non-treated rats large infarct areas were observed within 24 h
of reperfusion. Examination of the ischemic cerebral cortex revealed microglia and astrocyte activation, increased interleukin-1β
(IL-1 β) and tumor necrosis factor-α (TNF-α) concentrations, increased DNA fragmentation in the ischemia penumbra, elevated
Bax expression, increased caspase-3 cleavage, and decreased Bcl-2 expression. Pretreatment with CIG decreased the infarct
area, DNA fragmentation, IL-1β and TNF-α concentrations, microglia and astrocyte activation, Bax expression, and caspase-3
cleavage while increasing Bcl-2 expression. CIG exerts anti-neuroinflammatory and anti-apoptotic effects which should prove
beneficial for prevention or treatment of stroke. 相似文献
6.
Danielle Burger 《Arthritis research & therapy》2000,2(6):472-5
The intricate interactions that regulate relationships between endogenous tissue cells and infiltrating immune cells in the rheumatic joint, particularly in rheumatoid arthritis (RA), were the subject of the meeting. A better understanding of these interactions might help to define intervention points that could be used to develop specific therapies. The presentations and discussions highlighted the fact that, once chronic inflammation is established, several pro-inflammatory loops involving tumour necrosis factor (TNF)-α and interleukin (IL)-1β can be defined. Direct cellular contact with stimulated T lymphocytes induces TNF-α and IL-1β in monocytes which in turn induce functions in fibroblast-like synoviocytes. The latter include the production of stromal cell-derived factor-1α (SDF-1α) which enhances the expression of CD40L in T cells, which stimulates SDF-1α production in synoviocytes, which in turn protects T and B cells from apoptosis and enhances cell recruitment thus favoring inflammatory processes. IL-1β and TNF-α also induce IL-15 in fibroblast-like synoviocytes, which induces the production of IL-17 which in turn potentiates IL-1β and TNF-α production in monocyte-macrophages. This underlines the importance of TNF-α and IL-1β in RA pathogenesis, and helps explain the efficiency of agents blocking the activity of these cytokines in RA. Factors able to block the induction of cytokine production (such as apolipoprotein A-I [apo A-I] and interferon [IFN]-β) might interfere more distally in the inflammatory process. Furthermore, stimulated T lymphocytes produce osteoclast differentiation factor (ODF), which triggers erosive functions of osteoclasts. Therefore, factors capable of affecting the level of T lymphocyte activation, such as IFN-β, IL-15 antagonist, or SDF-1α antagonist, might be of interest in RA therapy. 相似文献
7.
Xiaoyu Wang Susan V. McLennan Terri J. Allen Stephen M. Twigg 《Journal of cell communication and signaling》2010,4(1):15-23
Connective tissue growth factor (CTGF), also known as CCN2, is implicated in fibrosis through both extracellular matrix (ECM)
induction and inhibition of ECM degradation. The role of CTGF in inflammation in cardiomyocytes is unknown. In some mesenchymal
cell systems, CTGF mediates effects through TGF-β or tyrosine kinase cell surface receptor, TrkA, signalling. In this study,
cellular mechanisms by which CTGF regulates pathways involved in fibrosis and inflammation were explored. Murine H9c2 cardiomyocytes
were treated with recombinant human (rh)CTGF and ECM formation gene expression: fibronectin, collagen type -I and -III and
ECM degradation genes: TIMP-1, TIMP-2 and PAI-1 were found to be induced. CTGF treatment also increased pro-inflammatory cytokines
TNF-α, IL-6, MCP-1 and IL-8. CTGF upregulated TGF-β1 mRNA and rapidly induced phosphorylation of TrkA. The CTGF-induced pro-fibrotic
and pro-inflammatory effects were blocked by anti-TGF-β neutralizing antibody and Alk 5 inhibitor (SB431542). A specific blocker
of TrkA activation, k252a, also abrogated CTGF-induced effects on fibrosis and gene expresison of MCP-1 and IL-8, but not
TNF-α or IL-6. Collectively, this data implicates CTGF in effects on pro-fibrotic genes and pro-inflammatory genes via TGF-β
pathway signalling and partly through TrkA. 相似文献
8.
Lance E Wyatt Chi Y Chung Brian Carlsen Akiko Iida-Klein George H Rudkin Kenji Ishida Dean T Yamaguchi Timothy A Miller 《BMC cell biology》2001,2(1):14-6
Background
Bone morphogenetic proteins (BMPs) and transforming growth factor-βs (TGF-βs) are important regulators of bone repair and regeneration. BMP-2 and TGF-β1 have been shown to inhibit gap junctional intercellular communication (GJIC) in MC3T3-E1 cells. Connexin 43 (Cx43) has been shown to mediate GJIC in osteoblasts and it is the predominant gap junctional protein expressed in these murine osteoblast-like cells. We examined the expression, phosphorylation, and subcellular localization of Cx43 after treatment with BMP-2 or TGF-β1 to investigate a possible mechanism for the inhibition of GJIC. 相似文献9.
Gudrun Valdimarsdottir Marie-José Goumans Fumiko Itoh Susumu Itoh Carl-Henrik Heldin Peter ten Dijke 《BMC cell biology》2006,7(1):16-11
Background
In endothelial cells (EC), transforming growth factor-β (TGF-β) can bind to and transduce signals through ALK1 and ALK5. The TGF-β/ALK5 and TGF-β/ALK1 pathways have opposite effects on EC behaviour. Besides differential receptor binding, the duration of TGF-β signaling is an important specificity determinant for signaling responses. TGF-β/ALK1-induced Smad1/5 phosphorylation in ECs occurs transiently. 相似文献10.
11.
Background
The transforming growth factor-β (TGF-β) family constitutes of dimeric proteins that regulate the growth, differentiation and metabolism of many cell types, including that of skeletal muscle in mammals. The potential role of TGF-βs in fish muscle growth is not known. 相似文献12.
In this study, the levels of TNF-α and its soluble receptors sTNF-Rp55 and sTNF-Rp75 were analyzed in cocultures of human
colon carcinoma cell spheroids prepared from different grades of tumors with normal human colon epithelium, myofibroblast,
and endothelial cell monolayers. Additionally, the influence of exogenously added rhTGF-β1 (2 ng/ml) on the TNF-α and sTNF-Rs
levels was tested. Direct interactions of colon carcinoma spheroids with normal cells caused decreases in TNF-α levels and
normal cell-dependent changes in sTNF-Rs amounts as compared to normal cells cultured alone. The addition of rhTGF-β1 to the
cocultures caused a significant increase in TNF-α levels with a simultaneous decrease in the amounts of both sTNF-Rs. During
direct interactions of colon carcinoma cells with normal tissue, paracrine effects are very important. We showed that TGF-β1
acts synergistically with TNF-α and significantly limits sTNF-Rs shedding. Therefore, TNF-Rs bound to cellular membranes,
but not their soluble forms, play an important role in tumor/normal cell interactions. TGF-β1 and sTNF-Rs, in turn, may be
valuable factors in colon cancer development and metastasis. 相似文献
13.
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15.
Birk Poller Jürgen Drewe Stephan Krähenbühl Jörg Huwyler Heike Gutmann 《Cellular and molecular neurobiology》2010,30(1):63-70
Brain capillary endothelial cells form the blood–brain barrier (BBB), a highly selective permeability membrane between the
blood and the brain. Besides tight junctions that prevent small hydrophilic compounds from passive diffusion into the brain
tissue, the endothelial cells express different families of drug efflux transport proteins that limit the amount of substances
penetrating the brain. Two prominent efflux transporters are the breast cancer resistance protein and P-glycoprotein (P-gp).
During inflammatory reactions, which can be associated with an altered BBB, pro-inflammatory cytokines are present in the
systemic circulation. We, therefore, investigated the effect of the pro-inflammatory cytokines interleukin-1β (IL-1β), interleukin-6
(IL-6) and tumor necrosis factor-α (TNF-α) on the expression and activity of BCRP and P-gp in the human hCMEC/D3 cell line.
BCRP mRNA levels were significantly reduced by IL-1β, IL-6 and TNF-α. The strongest BCRP suppression at the protein level
was observed after IL-1β treatment. IL-1β, IL-6 and TNF-α also significantly reduced the BCRP activity as assessed by mitoxantrone
uptake experiments. P-gp mRNA levels were slightly reduced by IL-6, but significantly increased after TNF-α treatment. TNF-α
also increased protein expression of P-gp but the uptake of the P-gp substrate rhodamine 123 was not affected by any of the
cytokines. This in vitro study indicates that expression levels and activity of BCRP, and P-gp at the BBB may be altered by
acute inflammation, possibly affecting the penetration of their substrates into the brain. 相似文献
16.
Background
The proliferation and final density of Sertoli cells in the testis are regulated by hormones and local factors. Glial cell line-derived neurotrophic factor (GDNF), a distantly related member of the transforming growth factor-β superfamily, and its receptor subunits GDNF family receptor alpha 1 (GFRα1), RET tyrosine kinase, and neural cell adhesion molecule (NCAM) have been reported to be expressed in the testis and involved in the regulation of proliferation of immature Sertoli cells (ISCs). However, the expression patterns of these receptor subunits and the downstream signaling pathways have not been addressed in ISCs. 相似文献17.
In diabetes the endothelium is either chronically or transiently exposed to hyperglycemic conditions. In addition, endothelial
dysfunction in diabetes is related to changes in the inflammatory response and the turnover of extracellular matrix. This
study was undertaken to study the effects of inflammatory stimuli on one particular matrix component, the heparan sulfate
(HS) proteoglycans (PGs) synthesized by primary human umbilical cord vein endothelial cells (HUVEC). Such cells were cultured
in vitro in 5 mM and 25 mM glucose. The latter concentration was used to mimic hyperglycemic conditions in short-term experiments.
HUVEC were also cultured in the presence of the inflammatory agents tumor necrosis factor α (TNF-α), interleukin 1α (IL-1α),
interleukin 1β (IL-1β) and transforming growth factor β (TGF-β). The cells were labeled with 35S-sulfate and 35S-PGs were recovered for further analyses. The major part of the 35S-PGs was secreted to the medium, irrespective of type of stimuli. Secreted 35S-PGs were therefore isolated and subjected to further analyses. TNF-α and IL-1α slightly increased the release of 35S-PGs to the culture medium, whereas IL-1β treatment gave a significant increase. The different treatments neither changed
the ratio of 35S-HS and 35S-chondroitin sulfate (CS) nor the macromolecular properties of the 35S-PGs. However, the 35S-HS chains were slightly increased in size after TNF-α treatment, and slightly decreased after TGF-β treatment, but not affected
by the other treatments. Compositional analysis of labeled disaccharides showed changes in the amount of 6-O-sulfated glucosamine residues after treatment with TNF-α, IL-1α and IL-1β. Western immunoblotting showed that major HSPGs
recovered from these cells were collagen XVIII, perlecan and agrin, and that secretion of these distinct PGs was increased
after IL-1β stimulation. Hence, short term inflammatory stimuli increased the release of HSPGs in HUVEC and affected both
the size and sulfation pattern of HS, depending on type of stimuli. 相似文献
18.
19.
The duality of the inflammatory response to traumatic brain injury 总被引:19,自引:0,他引:19
Lenzlinger PM Morganti-Kossmann MC Laurer HL McIntosh TK 《Molecular neurobiology》2001,24(1-3):169-181
One and a half to two million people sustain a traumatic brain injury (TBI) in the US each year, of which approx 70,000–90,000
will suffer from long-term disability with dramatic impacts on their own and their families’ lives and enormous socio-economic
costs. Brain damage following traumatic injury is a result of direct (immediate mechanical disruption of brain tissue, or
primary injury) and indirect (secondary or delayed) mechanisms. These secondary mechanisms involve the initiation of an acute
inflammatory response, including breakdown of the blood-brain barrier (BBB), edema formation and swelling, infiltration of
peripheral blood cells and activation of resident immunocompetent cells, as well as the intrathecal release of numerous immune
mediators such as interleukins and chemotactic factors. An overview over the inflammatory response to trauma as observed in
clinical and in experimental TBI is presented in this review. The possibly harmful/beneficial sequelae of post-traumatic inflammation
in the central nervous system (CNS) are discussed using three model mediators of inflammation in the brain, tumor necrosis
factor-α (TNF-α), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β). While the former two may act as important
mediators for the initiation and the support of post-traumatic inflammation, thus causing additional cell death and neurologic
dysfunction, they may also pave the way for reparative processes. TGF-β, on the other hand, is a potent anti-inflammatory
agent, which may also have some deleterious long-term effects in the injured brain. The implications of this duality of the
post-traumatic inflammatory response for the treatment of brain-injured patients using anti-inflammatory strategies are discussed. 相似文献
20.
S Jane Millward-Sadler Patrick W Costello Anthony J Freemont Judith A Hoyland 《Arthritis research & therapy》2009,11(3):R65-10