scholarly journals In vivo protection against interleukin-1-induced articular cartilage damage by transforming growth factor-beta 1: age-related differences.

1994 ◽  
Vol 53 (9) ◽  
pp. 593-600 ◽  
Author(s):  
H M van Beuningen ◽  
P M van der Kraan ◽  
O J Arntz ◽  
W B van den Berg
Keyword(s):  
Articular Cartilage ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Interleukin 1 ◽  
Cartilage Damage ◽  
Articular Cartilage Damage ◽  
Age Related ◽  
Growth Factor Beta

The Expression of IL-1, IL-6, and TGF-β in the Synovial Fluid of Horses with Surgically-Induced Transient Synovitis

1998 ◽  
Vol 11 (03) ◽  
pp. 141-145 ◽  
Author(s):  
S. M. Barber ◽  
J. R. Gordon ◽  
Christine Theoret
Keyword(s):  
Articular Cartilage ◽  
Growth Factor ◽  
Synovial Fluid ◽  
Transforming Growth Factor Beta ◽  
Interleukin 6 ◽  
Transforming Growth Factor ◽  
Interleukin 1 ◽  
Transient Synovitis ◽  
Growth Factor Beta ◽  
Surgically Induced

SummaryThis study investigates the presence of various cytokines in the synovial fluid of three horses with surgicallyinduced synovitis in one antebrachiocarpal joint. Synovial fluids were sampled from experimental and control joints, preoperatively and at two and 30 days post-operatively. Samples were analyzed for interleukin-1 and interleukin- 6 bioactivities with a bioassay, and for transforming growth factor-beta protein by ELISA. Peak cytokine levels were detected on day two post-synovectomy, and returned to pre-operative levels by 30 days post-synovectomy (Interleukin-6 in treated joints: day #0; 0.53 ±0.2, day #2; 9.8 ± 0.7, day #30; 0.4 ± 0.2. Transforming growth factorbeta in treated joints: day #0; 314 ± 69, day #2; 1101 ± 325, day #30; 321 ± 101). Arthrocentesis alone (i.e. control joints) caused no increase in interleukin- 1, interleukin-6 and transforming growth factor-beta levels. Interleukin-1 and interleukin-6 are thought to both prevent anabolic and enhance catabolic effects within articular cartilage matrices, whereas it has been proposed that transforming growth factor-beta may have a protective effect on the articular cartilage. This study is the first to document elevated transforming growth factor-beta levels in equine joints.This study documents elevated levels of transforming growth factor-beta, interleukin-1 and interleukin-6 in the joints of horses with surgically-induced transient synovitis.

In vitro modulation of endothelial fenestrae: opposing effects of retinoic acid and transforming growth factor beta

1988 ◽  
Vol 91 (2) ◽  
pp. 313-318
Author(s):  
T. Lombardi ◽  
R. Montesano ◽  
M.B. Furie ◽  
S.C. Silverstein ◽  
L. Orci
Keyword(s):  
Endothelial Cells ◽  
Retinoic Acid ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Surface Density ◽  
Transforming Growth Factor ◽  
Control Cell ◽  
Tgf Beta ◽  
Growth Factor Beta

Cultured endothelial cells isolated from fenestrated capillaries express many properties characteristic of their in vivo differentiated phenotype, including the formation of a limited number of fenestrae. In this study, we have investigated whether physiological factors that control cell differentiation might regulate the surface density of fenestrae in capillary endothelial cells. We have found that treatment of the cultures with retinoic acid (10 microM) induces a more than threefold increase in the surface density of endothelial fenestrae, whereas transforming growth factor beta (TGF beta) (2 ng ml-1) causes a sevenfold decrease in the surface density of these structures. These results show that the expression of endothelial fenestrae is susceptible to bidirectional modulation by physiological signals, and suggest that retinoids and TGF beta may participate in the regulation of fenestral density of capillary endothelium in vivo.

scholarly journals Transforming growth factor beta 1 (TGF-beta 1) induced neutrophil recruitment to synovial tissues: implications for TGF-beta-driven synovial inflammation and hyperplasia.

1991 ◽  
Vol 173 (5) ◽  
pp. 1121-1132 ◽  
Author(s):  
R A Fava ◽  
N J Olsen ◽  
A E Postlethwaite ◽  
K N Broadley ◽  
J M Davidson ◽  
...  
Keyword(s):  
Growth Factor ◽  
Synovial Tissue ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Biologically Active ◽  
Tgf Beta ◽  
Histological Techniques ◽  
Growth Factor Beta

We have studied the consequences of introducing human recombinant transforming growth factor beta 1 (hrTGF-beta 1) into synovial tissue of the rat, to begin to better understand the significance of the fact that biologically active TGF-beta is found in human arthritic synovial effusions. Within 4-6 h after the intra-articular injection of 1 microgram of hrTGF-beta 1 into rat knee joints, extensive recruitment of polymorphonuclear leukocytes (PMNs) was observed. Cytochemistry and high resolution histological techniques were used to quantitate the influx of PMNs, which peaked 6 h post-injection. In a Boyden chamber assay, hrTGF-beta 1 at 1-10 fg/ml elicited a chemotactic response from PMNs greater in magnitude than that evoked by FMLP, establishing that TGF-beta 1 is an effective chemotactic agent for PMNs in vitro as well as in vivo. That PMNs may represent an important source of TGF-beta in inflammatory infiltrates was strongly suggested by a demonstration that stored TGF-beta 1 was secreted during phorbol myristate acetate-stimulated degranulation in vitro. Acid/ethanol extracts of human PMNs assayed by ELISA contained an average of 355 ng of TGF/beta 1 per 10(9) cells potentially available for secretion during degranulation of PMNs. [3H]Thymidine incorporation in vivo and autoradiography of tissue sections revealed that widespread cell proliferation was triggered by TGF-beta 1 injection. Synovial lining cells and cells located deep within the subsynovial connective tissue were identified as sources of at least some of the new cells that contribute to TGF-beta 1-induced hyperplasia. Our results demonstrate that TGF-beta is capable of exerting pathogenic effects on synovial tissue and that PMNs may represent a significant source of the TGF-beta present in synovial effusions.

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