scholarly journals Early metabolic effects of platelet-derived growth factor and transforming growth factor-beta in rat liver in vivo.

1987 ◽  
Vol 262 (18) ◽  
pp. 8712-8715
Author(s):  
B Y Reed ◽  
M T King ◽  
W L Gitomer ◽  
R L Veech
Keyword(s):  
Growth Factor ◽  
Rat Liver ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Platelet Derived Growth Factor ◽  
Metabolic Effects ◽  
Growth Factor Beta

scholarly journals Platelet-derived growth factor and transforming growth factor-beta enhance tissue repair activities by unique mechanisms.

1989 ◽  
Vol 109 (1) ◽  
pp. 429-440 ◽  
Author(s):  
G F Pierce ◽  
T A Mustoe ◽  
J Lingelbach ◽  
V R Masakowski ◽  
G L Griffin ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Tissue Repair ◽  
Transforming Growth Factor ◽  
Breaking Strength ◽  
Platelet Derived Growth Factor ◽  
Tgf Beta ◽  
Growth Factor Beta

Platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta) markedly potentiate tissue repair in vivo. In the present experiments, both in vitro and in vivo responses to PDGF and TGF-beta were tested to identify mechanisms whereby these growth factors might each enhance the wound-healing response. Recombinant human PDGF B-chain homodimers (PDGF-BB) and TGF-beta 1 had identical dose-response curves in chemotactic assays with monocytes and fibroblasts as the natural proteins from platelets. Single applications of PDGF-BB (2 micrograms, 80 pmol) and TGF-beta 1 (20 micrograms, 600 pmol) were next applied to linear incisions in rats and each enhanced the strength required to disrupt the wounds at 5 d up to 212% of paired control wounds. Histological analysis of treated wounds demonstrated an in vivo chemotactic response of macrophages and fibroblasts to both PDGF-BB and to TGF-beta 1 but the response to TGF-beta 1 was significantly less than that observed with PDGF-BB. Marked increases of procollagen type I were observed by immunohistochemical staining in fibroblasts in treated wounds during the first week. The augmented breaking strength of TGF-beta 1 was not observed 2 and 3 wk after wounding. However, the positive influence of PDGF-BB on wound breaking strength persisted through the 7 wk of testing. Furthermore, PDGF-BB-treated wounds had persistently increased numbers of fibroblasts and granulation tissue through day 21, whereas the enhanced cellular influx in TGF-beta 1-treated wounds was not detectable beyond day 7. Wound macrophages and fibroblasts from PDGF-BB-treated wounds contained sharply increased levels of immunohistochemically detectable intracellular TGF-beta. Furthermore, PDGF-BB in vitro induced a marked, time-dependent stimulation of TGF-beta mRNA levels in cultured normal rat kidney fibroblasts. The results suggest that TGF-beta transiently attracts fibroblasts into the wound and may stimulate collagen synthesis directly. In contrast, PDGF is a more potent chemoattractant for wound macrophages and fibroblasts and may stimulate these cells to express endogenous growth factors, including TGF-beta, which, in turn, directly stimulate new collagen synthesis and sustained enhancement of wound healing over a more prolonged period of time.

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.

scholarly journals Pengaruh pemberian plasma kaya trombosit dan karbonat hidroksiapatit pada proses penutupan defek tulang kepala hewan coba tikus

2016 ◽  
Vol 8 (3) ◽  
Author(s):  
Lucia Nirmalasari ◽  
Maximillian Ch. Oley ◽  
Eko Prasetyo ◽  
Mendy Hatibie ◽  
Lily L. Loho
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Rattus Norvegicus ◽  
Transforming Growth Factor ◽  
Platelet Rich Plasma ◽  
Platelet Derived Growth Factor ◽  
Vascular Endothelial ◽  
Angiogenesis Factor ◽  
Growth Factor Beta ◽  
Endothelial Growth Factor

Abstract: Recently, platelet rich plasma has been popular and its use has begin on human in developed countries. Platelet rich plasma is defined as autologus blood with concentration of platelets three to five times above baseline level, which contains at least seven growth factors like Platelet Derived Growth Factor (PDGF), Platelet Derived Angiogenesis Factor (PDAF), Platelet Derived Endothelial Growth Factor (PDEGF), Transforming Growth Factor Beta (TGF- β), Insulin like Growth Factor (IGF), Fibroblast Growth Factor (FGF), and Vascular Endothelial Growth Factor (VEGF). The golden standard for reconstruction of cranial bone defects demonstrates osteoconduction scaffold, osteoinduction like growth factors, and osteogenesis. Alloplastic biomaterials have revolutionalized craniofacial reconstruction. Carbonated hydroxyapatite (CHA) has been studied for years as implant material due to its similarity with the mineral component of bone. In this study we investigated and compare the effects of PRP and CHA on bone regeneration in rat cranial defects. This was an experimental study with a true experimental design on white male rats (Rattus norvegicus). Cranial deffects of 3 mm diameter were created in rat cranium and grafted with CHA and PRP combination, CHA alone, and control. The relationships among them were analyzed by using Mann Whitney and SPSS Statistics Program Package Version 22.0. The results showed that the experimental group of 2 weeks had no different between inflammatory reaction (P = 0.119), woven bone (P = 0.094) and lamellar bone (P = 0.130). At 4 weeks,a combination of PRP and CHA showed a superior growth of lamellar bone compared to CHA (P = 0.009). Conclusion: A combination of PRP and CHA in bone regeneration showed a histological tendency toward increased bone formation. However, future investigations should be conducted in different period times.Keywords: platelet rich plasma, carbonated hydroxyapatite, cranial defectAbstrak: Plasma kaya trombosit makin banyak digunakan dalam dunia kedokteran. Di negara maju pengunaannya sudah mulai diteliti pada manusia. Plasma kaya trombosit adalah fraksi plasma darah dengan konsentrasi platelet 3-5 kali diatas nilai normal yang mengandung sekurang-kurangnya 7 faktor pertumbuhan, diantaranya Platelet Derived Growth Factor (PDGF), Platelet Derived Angiogenesis Factor (PDAF), Platelet Derived Endothelial Growth Factor (PDEGF), Transforming Growth Factor Beta (TGF- β), Insulin like Growth Factor (IGF), Fibroblast Growth Factor (FGF), dan Vascular Endothelial Growth Factor (VEGF) yang dapat meningkatkan proses osteogenesis. Karbonat hidroksiapatit adalah material pengganti tulang yang dapat mempercepat regenerasi jaringan tulang serta memiliki kandungan kalsium,fosfat dan karbonat yang mirip dengan tulang manusia. Tulang yang tumbuh pada awal berupa tulang muda yang memiliki serat kolagen yang tidak teratur dan banyak osteosit disebut tulang imatur. Tulang imatur kemudian akan diganti oleh tulang matur yang memiliki serabut kolagen yang teratur. Jenis penelitian ini ialah eksperimental pada 36 hewan coba tikus putih wistar (Rattus norvegicus). Defek kalvaria pada tikus dengan diameter 3 mm diisi sesuai perlakuan: plasma kaya trombosit dengan karbonat hidroksiapatit, karbonat apatit tunggal, dan kontrol. Plasma kaya trombosit dibuat dari autologus darah tikus yang diberi perlakuan plasma kaya trombosit serta karbonat hidroksiapatit dan karbonat apatit tunggal. Data dianalisis dengan uji Mann Whitney dan diolah dengan SPSS. Hasil penelitian memperlihatkan pada minggu ke-2, tidak terdapat perbedaan bermakna reaksi inflamasi (P = 0,119), tulang imatur (P = 0,094), dan tulang matur (P = 0,130) diantara ketiga perlakuan. Pada minggu ke-4, tulang matur yang terbentuk lebih banyak pada perlakuan plasma kaya trombosit dan karbonat hidroksiapatit (P = 0,009). Simpulan: Pemberian plasma kaya trombosit dan karbonat hidroksiapatit dapat meningkatkan proses penutupan defek tulang kepala hewan percobaan tikus.Kata kunci : plasma kaya trombosit, karbonat hidroksiapatit, defek tulang kepala.

scholarly journals Regulation of Trypanosoma cruzi infections in vitro and in vivo by transforming growth factor beta (TGF-beta).

1991 ◽  
Vol 174 (3) ◽  
pp. 539-545 ◽  
Author(s):  
J S Silva ◽  
D R Twardzik ◽  
S G Reed
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Tgf Beta ◽  
Ifn Gamma ◽  
Human Macrophages ◽  
Growth Factor Beta ◽  
Cruzi Infection

The effects of transforming growth factor beta (TGF-beta) on interferon gamma-mediated killing of the intracellular protozoan parasite Trypanosoma cruzi and on the course of T. cruzi infection in mice were investigated. Spleen cells from mice with acute T. cruzi infections were found to produce elevated levels of biologically active TGF-beta in vitro, and the possibility that TGF-beta may mediate certain aspects of T. cruzi infection was then addressed. When mouse peritoneal macrophages were treated with TGF-beta in vitro, the ability of IFN-gamma to activate intracellular inhibition of the parasite was blocked. This occurred whether cells were treated with TGF-beta either before or after IFN-gamma treatment. TGF-beta treatment also blocked the T. cruzi-inhibiting effects of IGN-gamma on human macrophages. Additionally, treatment of human macrophages with TGF-beta alone led to increased parasite replication in these cells. The effects of TGF-beta on T. cruzi infection in vivo were then investigated. Susceptible C57BL/6 mice developed higher parasitemias and died earlier when treated with TGF-beta during the course of infection. Resistant C57BL/6 x DBA/2 F1 mice treated with TGF-beta also had increased parasitemias, and 50% mortality, compared with no mortality in infected, saline-treated controls. A single dose of TGF-beta, given at the time of infection, was sufficient to significantly decrease resistance to infection in F1 mice and to exacerbate infection in susceptible C57BL/6 mice. Furthermore, a single injection of TGF-beta was sufficient to counter the in vivo protective effects of IFN-gamma. We conclude that TGF-beta, produced during acute T. cruzi infection in mice, is a potent inhibitor of the effects of macrophage activating cytokines in vivo and in vitro and may play a role in regulating infection.

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