Quantitative monitoring of the mRNA expression pattern of the TGF-β-isoforms (β1, β2, β3) during transdifferentiation of hepatic stellate cells using a newly developed real-time SYBR Green PCR

Wickert, Lucia; Steinkrüger, S; Abiaka, M.; Bolkenius, Ursula; Purps, O; Schnabel, Claudia; Gressner, A. M.

doi:10.1016/s0006-291x(02)00669-1

Cited by 30 publications

(15 citation statements)

References 21 publications

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“…Primer sequences for ALK5: (GI: 416397) were as follows: forward 5Ј-CGTCTGCATTGCACT-TATGC-3Ј, reverse 5Ј-AGCAGTGGTAAACCTGA-TCC-3Ј. Gene-specific standards were produced as previously reported 18 and sequenced on a semiautomated sequencer (310A, Applied Biosystems, Foster City, CA). Serial 10 times logarithmic dilutions of the cRNA and 1 g total RNA from cell culture samples were reverse transcribed.…”

Section: Methodsmentioning

confidence: 99%

Id1 is a critical mediator in TGF-β-induced transdifferentiation of rat hepatic stellate cells

Wickert²,

et al. 2006

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Section: Methodsmentioning

confidence: 99%

Id1 is a critical mediator in TGF-β-induced transdifferentiation of rat hepatic stellate cells

Wickert²,

et al. 2006

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“…The action of TGFb in hepatic stellate cells (HSC) can be modulated by TGFbRIII [34]. In these cells, it is additionally important because the expression of TGFb2 here is low [35]. TGFbRIII may also be an inhibitor of the signal transduction by prevention of TGFb connections to TGFbRII and TGFbRI in the mechanism independent from ligand binding.…”

Section: Prace Poglądowementioning

confidence: 99%

Transforming growth factor beta1 (TGFbeta1) in physiology and pathology

Kajdaniuk¹,

Marek²,

Borgiel−Marek³

et al. 2013

Endokrynologia Polska

150

117

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This review describes precisely the consequence of TGFb1 prevalence in the organism, and its significant influence on physiological and pathophysiological processes. Organ and tissue distinctiveness hinder unambiguous characterisation of the cytokine. However, there are constant functions of TGFb1 inducing no controversy: it participates in foetal development, control of cell growth and differentiation, induces fibrosis and scar formation (the process of 'wound healing'), causes the suppression of immune response, is involved in angiogenesis, the development of tumours, and inflammatory processes. Thus, TGFb1 is a multifunctional cytokine. There are three fundamental directions of its activities: I. TGFb1 regulates cell proliferation, growth, differentiation and cells movement. II. TGFb1 has immunomodulatory effects. III. TGFb1 has profibrogenic effects. TGFb1 action can be local and systemic. This review describes TGFb1 in pathology: colitis ulcerosa, Crohn's disease, coeliac disease, diabetic nephropathy, diabetic retinopathy and diabetic foot, pulmonary hypertension, and Alzheimer's disease. TGFb1 and its receptors are also of interest to endocrinologists. Lack of TGFb1-dependent growth control may result in oncogenesis: papillary, follicular and anaplastic thyroid cancers, prostate, breast and uterine cervical cancer, oesophagus, gastric, colorectal and liver cancers, NSCLC, and malignant melanoma. Excessive TGFb1 activity is an integral part of the fibrotic processes occurring in the response to injury. An increased TGFb1 expression has been observed in patients with pulmonary, kidney, and liver fibrosis. In chronic hepatitis, the prolonged stimulation of hepatic stellate cells being the result of chronic damage to hepatocytes results in the release of profibrogenic abundant factors such as TGFb1 and leads to the development of liver cirrhosis. The results of experimental procedures and treatment known as anti-TGFb1 strategy acting against the fibrosis in various tissues leads to hope regarding the use of anti-TGFb1 strategy in clinical practice. StreszczenieW artykule poglądowym szczegółowo opisano konsekwencje rozpowszechnienia TGFb1 w organizmie oraz jego wpływ na szereg procesów fizjologicznych i patofizjologicznych. Istotne odrębności narządowe i tkankowe utrudniają jednoznaczną charakterystykę tej cytokiny. Istnieją jednak stałe funkcje TGFb1 nie wzbudzające kontrowersji: uczestniczy w rozwoju płodu, regulacji wzrostu i różnicowa-nia komórek, indukuje proces włóknienia i bliznowacenia (proces "gojenia rany"), powoduje hamowanie odpowiedzi immunologicznej, uczestniczy w angiogenezie, w rozwoju nowotworów, w procesach zapalnych -jest więc cytokiną wieloczynnościową. Można wyróżnić trzy fundamentalne kierunki jego działania: I -TGFb1 reguluje proliferację, wzrost, różnicowanie i przemieszczanie komórek; II -TGFb1 wykazuje działanie immunomodulujące; III -TGFb1 wykazuje działanie profibrogenne. Działanie TGFb1 może mieć charakter miejscowy i systemowy. Opisano udział TGFb1 w stanach patologicznyc...

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“…TGF-β has been used in numerous studies with HSC and has been shown to promote differentiation into the myofibroblast phenotype [3,46] and also within the LX-2 cell line [43]. The substrate that HSC are cultured on has, additionally, been observed to regulate their phenotype.…”

Section: The Hsc As a Fibrogenesis Modelmentioning

confidence: 99%

Hepatic stellate cells and parasite-induced liver fibrosis

Anthony

Allen

et al. 2010

Parasites Vectors

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Fibrogenesis is a common feature of many diseases where there is severe insult to the liver. The hepatic stellate cell trans-differentiation into a myofibroblast has been identified as an important event in liver fibrogenesis and has been well investigated over the last few years in a number of liver diseases. The trans-differentiation process can be monitored in vitro by evaluation of biomarkers that are characteristic of normal quiescent hepatic stellate cells or activated myofibroblasts. Two major parasitic diseases associated with liver injury and fibrosis are schistosomiasis and echinococcosis. Recent studies have highlighted a role for activated hepatic stellate cells in both murine and human schistosomiasis as well as demonstrating that schistosome antigens are able to regulate this trans-differentiation process. Study of the hepatic stellate cell and its interaction with parasite-derived antigens may be pivotal in our understanding of the pathology associated with schistosomiasis and other parasitic diseases, including echinococcosis, as well as revealing new information on the trans-differentiation process in this cell type.

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Quantitative monitoring of the mRNA expression pattern of the TGF-β-isoforms (β1, β2, β3) during transdifferentiation of hepatic stellate cells using a newly developed real-time SYBR Green PCR

Cited by 30 publications

References 21 publications

Id1 is a critical mediator in TGF-β-induced transdifferentiation of rat hepatic stellate cells

Id1 is a critical mediator in TGF-β-induced transdifferentiation of rat hepatic stellate cells

Transforming growth factor beta1 (TGFbeta1) in physiology and pathology

Hepatic stellate cells and parasite-induced liver fibrosis

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