Detection of mRNA for the transforming growth factor β family in human articular chondrocytes by the polymerase chain reaction

Frazer, A. C.; Seid, J. M.; Hart, K.A.; Bentley, H. R.; Bunning, R.A.D.; Russell, R. G. G.

doi:10.1016/s0006-291x(05)81108-8

Cited by 21 publications

(13 citation statements)

References 28 publications

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“…Even when cDNA PCR studies indicated the presence in chondrocytes and in SaOS-2 cells of the specific transcript for TGF-P, it could not be detected in the culture supernatants using a specific enzyme immunoassay for TGF-P2. One explanation may be that the cells produced TGF-Ps other than TGF-P2; this hypothesis is not sustained by previous data showing the presence of the specific mRNA for TGF-P2 in articular chondrocytes and in developing bone (17,18). Thus, the most likely explanation is that in the present culture conditions, TGF-6s are released in a latent form (19), not recognizable by the antibody against the mature TGF-P2.…”

Section: Discussionmentioning

confidence: 83%

In vitro effects of growth hormone and other hormones on chondrocytes and osteoblast‐like cells

1993

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The influence of growth hormone (GH), insulin-like growth factor I (IGF-I), parathyroid hormone(1-34) (PTH(1-34)), 1,25-dihydroxycholecalciferol (1,25(OH)2D3) and 17 beta-oestradiol on proliferation and on production of cytokines, such as interleukin-1 beta (IL-1 beta), IL-6, IL-8 and transforming growth factor-beta (TGF-beta), was studied in chondrocytes obtained from the growing cartilage of the iliac crest and in the osteoblast-like cell clone SaOS-2. GH and IGF-I were mitogenic for chondrocytes and SaOS-2 cells, as indicated by the dose-related increase in uptake of [3H]thymidine. PTH(1-34) was also mitogenic, while 1,25(OH)2D3 inhibited the proliferation of both chondrocytes and SaOS-2 cells in a dose-dependent manner. 17 beta-oestradiol was stimulatory in SaOS-2 cells, but gave a biphasic pattern in chondrocytes; it was stimulatory at low concentrations (0.1 nmol/l) and inhibitory at supraphysiological doses (10 nmol/l). Using the cDNA polymerase chain reaction, specific mRNAs for IL-1 beta, IL-6, IL-8 and TGF-beta were found in chondrocytes, while SaOS-2 cells had a positive signal only for TGF-beta. Specific enzyme immunoassays revealed detectable levels of IL-1 beta, IL-6 and IL-8 only in chondrocytes. IL-6 was increased by GH and IGF-I, and lowered by 1,25(OH)2D3 and supraphysiological doses of 17 beta-oestradiol, while PTH(1-34) had no effects. IL-8 was not influenced by GH or IGF-I, was slightly but not significantly increased by PTH(1-34) and was reduced by 1,25(OH)2D3 and 17 beta-oestradiol at supraphysiological doses.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 83%

In vitro effects of growth hormone and other hormones on chondrocytes and osteoblast‐like cells

1993

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“…The surgical biopsy samples were used to establish baseline mRNA expression. 18 and those for glyceraldehyde 3-phosphate dehydrogenase (GAPDH) to the sequences reported by Narayanan et al 19 and are shown in Table 3. The amplification was carried out in a DNA Thermal Cycler (Perkin Elmer) as follows: an initial denaturing step at 94°C for 7 min, then 1 min at 94°C, 2 min at 58°C and 3 min at 72°C for 35 cycles, and a final extension step of 7 min at 72°C.…”

Section: Patientsmentioning

confidence: 95%

TGF-β isoforms in alcoholic liver disease

Santos

Norton

Esposti

et al. 1998

Journal of Gastroenterology

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The increased deposition of extracellular matrix proteins in the liver is a key factor in the morbidity and mortality of alcoholic liver disease (ALD). This increased fibrosis may be due to a superabundance of profibrogenic factors such as transforming growth factor-beta (TGF-beta). The original peptide is now called TGF-beta 1, and two other isoforms have been recognized in humans (TGF-beta 2 and TGF-beta 3). It was the aim of the present study to determine the expression of the TGF-beta isoforms in different stages of ALD. Thirty patients with ALD had percutaneous liver biopsies performed for diagnostic purposes. They were grouped by clinical findings and by liver histology into four groups: I, steatosis; II, fibrosis; III, hepatitis; and IV, cirrhosis. An unused portion of each biopsy sample was used to evaluate the gene expression of TGF-beta 1, TGF-beta 2, and TGF-beta 3 by reverse transcription polymerase chain reaction (RT-PCR). The expression of all isoforms from patients was significantly greater than their expression in controls. No significant correlation was determined between TGF-beta isoform expression and liver function test results. When the different isoforms were grouped by histology, increased expression with more severe disease was found; however, differences existed among the isoforms. In ALD, all TGF-beta isoforms were increased and their expression was significantly greater in patients with more active and advanced disease. RT-PCR is an effective method for evaluating gene expression in clinical samples which often provide a limited amount of tissue.

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“…Beside IGF-I, the members of the transforming growth factor (TGF)-b family and the related bone morphogenetic protein (BMP) family are the most potent stimulators of chondrocyte biosynthesis. Three isoforms of TGF-b are known to exist in mammals, all of which are expressed in articular chondrocytes [15]. TGF-b induces undifferentiated mesenchymal cells to express a chondrocyte phenotype [16].…”

Section: Growth Factors -Insulin-like Growth-factor-i and The Transfomentioning

confidence: 99%

Molecular aspects of pathogenesis in osteoarthritis: the role of inflammation

Hedbom¹,

Häuselmann²

2002

Cellular and Molecular Life Sciences (CMLS)

191

137

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Arthritic diseases cause enormous burdens in terms of pain, crippling, and disability. Osteoarthritis (OA), the most common form of arthritis, is characterized by a slow progressive degeneration of articular cartilage. The exact etiology of OA is not known, but the degradation of cartilage matrix components is generally agreed to be due to an increased synthesis and activation of extracellular proteinases, mainly matrix metalloproteinases. Insufficient synthesis of new matrix macromolecules is also thought to be involved, possibly as a consequence of deficient stimulation by growth factors. Although OA is defined as a noninflammatory arthropathy, proinflammatory cytokines such as interleukin-1 have been implicated as important mediators in the disease. In response to interleukin-1, chondrocytes upregulate the production of nitric oxide and prostaglandin E2, two factors that have been shown to induce a number of the cellular changes associated with OA. The generation of these key signal molecules depends on inducible enzymes and can be suppressed by pharmacological inhibitors.

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Detection of mRNA for the transforming growth factor β family in human articular chondrocytes by the polymerase chain reaction

Cited by 21 publications

References 28 publications

In vitro effects of growth hormone and other hormones on chondrocytes and osteoblast‐like cells

In vitro effects of growth hormone and other hormones on chondrocytes and osteoblast‐like cells

TGF-β isoforms in alcoholic liver disease

Molecular aspects of pathogenesis in osteoarthritis: the role of inflammation

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