Journal articles: 'Transforming growth factor-P'

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Tremollieres, Florence A., Donna D. Strong, David J. Baylink, and Subburaman Mohan. "Insulin-like growth factor II and transforming growth factor β1 regulate insulin-like growth factor I secretion in mouse bone cells." Acta Endocrinologica 125, no. 5 (November 1991): 538–46. http://dx.doi.org/10.1530/acta.0.1250538.

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Abstract. Bone cells in culture produce and respond to growth factors, suggesting that local as well as systemic factors regulate bone volume. Previous studies have shown that IGF-I is the major mitogen produced by mouse bone cells and that its production is regulated by systemic agents such as PTH and estrogen. Because IGF-II and transforming growth factor β1 have been shown, respectively, to increase and decrease MC3T3-E1 cell proliferation, we tested the hypothesis that these two growth factors modulate the production of IGF-I in this cell line. In order to eliminate artifacts owing to IGF binding proteins, conditioned media samples were pretreated with IGF-II before measurement of IGF-I by RIA. After 24 h treatment at a density of 2.5× 104 cells/cm2, IGF-II (10 μg/l) induced a 2.2-fold increase compared with untreated control (9.5±1.5 vs 4.2±0.44 pg/μg protein, p<0.001), whereas transforming growth factor β1 (1 μg/l) caused a 66% decrease in IGF-I production (1.5±0.3 vs 4.2±0.44 pg/μg protein, p<0.001). Both IGF-II and transforming growth factor β1 regulated IGF-I production in a dose-, time- and cell density-dependent manner. The lowest effective doses for IGF-II and transforming growth factor β1 were 1 and 0.01 μg/l, respectively. These results support a role for IGF-II and transforming growth factor β1 as potent modulators of IGF-I secretion in mouse bone cells. Furthermore, regulation of IGF-I production in bone cells by IGF-II and transforming growth factor β1 in an autocrine/paracrine manner could represent a component part of the mechanism whereby the skeleton locally adapts in reponse to external stimuli.

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Peña-Ortiz, Miguel Ángel, Liliana Germán-Castelán, and Aliesha González-Arenas. "Growth factors and kinases in glioblastoma growth." Advances in Modern Oncology Research 2, no. 5 (October 19, 2016): 248. http://dx.doi.org/10.18282/amor.v2.i5.100.

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<p>Glioblastoma multiforme (GBM) is the most aggressive type of brain cancer, having the highest invasion, migration, proliferation, and angiogenesis rates. Several signaling pathways are involved in the regulation of these processes including growth factors and their tyrosine kinase receptors, such as vascular endothelial growth factor (VEGF), transforming growth factor beta (TGFβ), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), and insulin-like growth factor–I (IGF–I). Different kinases and regulators also participate in signaling pathways initiated by growth factors, such as mitogen-activated kinases (MAPK), protein kinases C (PKC), phosphatidylinositol-3 kinases (PI3K), protein kinase B (PKB or Akt), glycogen synthase kinase 3β (GSK3β), the mTOR complex, and Bcl-2. In this review, we will focus on the role of these proteins as possible therapeutic targets in GBM.</p>

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KIRA, S. "P-481 Expression of transforming growth factor alpha and epidermal growth factor receptor in human hepatocellular carcinoma." International Hepatology Communications 3 (July 1995): S157. http://dx.doi.org/10.1016/0928-4346(95)90778-6.

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Zhang, Nan, Tingting Zhao, Meirong Bi, Xuejia He, Yamin Zhang, and Weiwei Zhu. "Hyperin Ameliorates Proliferation, Migration, and Extracellular Matrix Formation in Airway Smooth Muscle Cells by Inhibiting Transforming Growth Factor-β1-Induced Nuclear Factor-κB Activation." Current Topics in Nutraceutical Research 19, no. 2 (September 28, 2020): 222–27. http://dx.doi.org/10.37290/ctnr2641-452x.19:222-227.

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We have explored the role of hyperin remodeling of airway smooth muscle cells during asthma. To this end, airway smooth muscle cells were isolated from tracheae and bronchi of mice, treated with transforming growth factor-β1 and increasing concentrations of hyperin followed by analysis of cell viability, proliferation, and migration. The levels of extracellular matrix formation were evaluated by analysis of fibronectin and type I collagen. Western blot analysis was used to assess the function of the downstream pathway of nuclear factor-kappa B. Transforming growth factor-β1 treatment led to a dose-dependent increase in type I collagen and fibronectin that was reversed by hyperin. Transforming growth factor-β1 promoted activation of nuclear factor-kappa B pathway with reduced IκBα and enhanced phospho (p)-p65 and p-IκBα. However, hyperin treatment upregulated IκBα and downregulated p-p65/p-IκBα to inactivate NF-κB pathway. In conclusion, hyperin ameliorates proliferation, migration, and extracellular matrix formation in airway smooth muscle cells by inhibiting transforming growth factor-β1-induced nuclear factor-kappa B activation suggesting potential prevention of airway remodeling during asthma.

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Looney, Micheal, Peter Doran, and Donal J. Buggy. "Effect of Anesthetic Technique on Serum Vascular Endothelial Growth Factor C and Transforming Growth Factor β in Women Undergoing Anesthesia and Surgery for Breast Cancer." Anesthesiology 113, no. 5 (November 1, 2010): 1118–25. http://dx.doi.org/10.1097/aln.0b013e3181f79a69.

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Background In breast cancer, vascular endothelial growth factor C, transforming growth factor β, placental growth factor, and fibroblast growth factor (acidic and basic) promote angiogenesis and metastases. We tested the hypothesis that a propofol-paravertebral anesthetic (PPA) technique would attenuate postoperative changes in these angiogenic factors to a greater extent than balanced general anesthesia (GA) and morphine analgesia in women undergoing surgery for primary breast cancer. Method Forty women with primary breast cancer undergoing surgical excision were randomized to receive either standard GA or PPA technique. Venous blood was sampled before and at 24 h after surgery and serum analyzed. The primary endpoint was a preoperative versus postoperative change in vascular endothelial growth factor C and transforming growth factor β concentrations. Results Using a visual analog scale (median [25-75% interquartile range]), PPA patients (1 [0-2]) had less pain at 2 h (P = 0.02) than did GA patients (3 [2-5]). The mean postoperative change in vascular endothelial growth factor C concentrations among GA patients was 733 versus 27 pg/ml for PPA patients (difference, 706 [97.5% CI, 280-1,130] pg/ml, P = 0.001). In contrast, the mean postoperative change in transforming growth factor β concentration among GA patients was -163 versus 146 pg/ml for PPA patients (difference, 309 [97.5% CI, -474 to -143] pg/ml, P = 0.005). Concentrations of placental growth factor and fibroblast growth factor, both acidic and basic, were undetectable in serum. Conclusion Anesthetic technique influences serum concentrations of factors associated with angiogenesis in primary breast cancer surgery.

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Barcellos-Hoff, M. "SP-0269 THERAPEUTIC BENEFIT FROM TRANSFORMING GROWTH FACTOR p INHIBITION DURING RADIOTHERAPY." Radiotherapy and Oncology 103 (May 2012): S105—S106. http://dx.doi.org/10.1016/s0167-8140(12)70608-4.

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Choi, I. G., H. W. Kim, Y. C. Kim, C. H. Han, B. C. Lee, B. J. Ham, and B. H. Yang. "P.6.b.001 Increased transforming growth factor-beta1 in alcohol dependence." European Neuropsychopharmacology 17 (October 2007): S547. http://dx.doi.org/10.1016/s0924-977x(07)70848-9.

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Korah, J., N. Falah, and J. J. Lebrun. "1023 POSTER Role of the E2F1 Transcription Factor in Transforming Growth Factor-p-mediated Apoptosis." European Journal of Cancer 47 (September 2011): S103. http://dx.doi.org/10.1016/s0959-8049(11)70666-9.

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Blanco, F. F., S. Sanduja, N. G. Deane, P. J. Blackshear, and D. A. Dixon. "Transforming Growth Factor Regulates P-Body Formation through Induction of the mRNA Decay Factor Tristetraprolin." Molecular and Cellular Biology 34, no. 2 (November 4, 2013): 180–95. http://dx.doi.org/10.1128/mcb.01020-13.

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Brahmatewari, Just, Anton Serafini, Victoria Serralta, Patricia M. Mertz, and William H. Eaglstein. "The Effects of Topical Transforming Growth Factor-β2 and Anti-Transforming Growth Factor-β2,3 on Scarring in Pigs." Journal of Cutaneous Medicine and Surgery 4, no. 3 (July 2000): 126–31. http://dx.doi.org/10.1177/120347540000400303.

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Background: Transforming growth factor-β2 (TGF-β2) has been implicated in the inflammatory response and subsequent scarring during wound healing. Objective: The experiment was designed to study the effects of a topical application of TGF-β2 and mouse monoclonal anti-TGF-β2,3 neutralizing antibody (and TGF-β2,3) on the development of fibrosis during healing. Methods: Sixteen full-thickness excision wounds were made in the paravertebral and thoracic area of four domestic pigs. On day 0, three wounds each were treated with: a) 5 μg of TGF-β2, b) 5 μg of 2% methylcellulose (mc), or c) 1.2 mg of anti-TGF-β2,3. As a vehicle for treatment of each wound methylcellulose 2% was used. Four wounds served as the untreated air-exposed control. Wounds were biopsied and the tissue sectioned and stained with hematoxylin and eosin on days 7, 14, and 45. Three blinded observers evaluated the wound specimens. Results: Using computer-aided point count stereology on days 7, 14, and 45, we found a statistically significant increase (p < .05) in the number of nucleated cells in the TGF-β2-treated wounds as compared to the other control wounds. Wounds treated with anti-TGF-β2,3 had significantly (p < .05) fewer nucleated cells on days 7,14, and 45. Microscopically, the TGF-β2-treated wounds had a larger scar area as compared to anti-TGF-β2,3 and controls. Conclusion: Treating wounds with an antibody directed against TGF-β2 might be a useful clinical approach to reduce fibrosis.

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Warstat, K., T. Pap, G. Klein, S. Gay, and W. K. Aicher. "Co-activation of synovial fibroblasts by laminin-111 and transforming growth factor-β induces expression of matrix metalloproteinases 3 and 10 independently of nuclear factor-κB." Annals of the Rheumatic Diseases 67, no. 4 (August 24, 2007): 559–62. http://dx.doi.org/10.1136/ard.2007.073809.

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We showed previously that the attachment of synovial fibroblasts to laminin (LM)-111 in the presence of transforming growth factor-β induces significant expression of the matrix metalloproteinase (MMP)-3. Here we go on to investigate the regulation of additional MMPs and their specific tissue inhibitors of matrix proteases (TIMPs). Changes in steady-state mRNA levels encoding TIMPs and MMPs were investigated by quantitative reverse transcription–polymerase chain reaction. Production of MMPs was monitored by a multiplexed immunoarray. Signal transduction pathways were studied by immunoblotting. Attachment of synovial fibroblasts to LM-111 in the presence of transforming growth factor-β induced significant increases in MMP-3 mRNA (12.35-fold, p<0.001) and protein (mean 62 ng/ml, sixfold, p<0.008) and in expression of MMP-10 mRNA (11.68-fold, p<0.05) and protein (54 ng/ml, 20-fold, p⩾0.02). All other TIMPs and MMPs investigated failed to show this LM-111-facilitated transforming growth factor-β response. No phosphorylation of nuclear factor-κB was observed. We conclude that co-stimulation of synovial fibroblasts by LM-111 together with transforming growth factor-β suffices to induce significant expression of MMP-3 and MMP-10 by synovial fibroblasts and that this induction is independent of nuclear factor-κB phosphorylation.

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van Zoelen, E. J., W. J. van de Ven, H. J. Franssen, T. M. van Oostwaard, P. T. van der Saag, C. H. Heldin, and S. W. de Laat. "Neuroblastoma cells express c-sis and produce a transforming growth factor antigenically related to the platelet-derived growth factor." Molecular and Cellular Biology 5, no. 9 (September 1985): 2289–97. http://dx.doi.org/10.1128/mcb.5.9.2289-2297.1985.

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Mouse neuroblastoma Neuro-2A cells produce transforming growth factors during exponential growth in a defined hormone-free medium, which, on Bio-Gel columns in 1 M HAc, elute at a molecular size of 15 to 20 kilodaltons (kDa). These neuroblastoma-derived transforming growth factors have strong mitogenic activity, but they do not compete with epidermal growth factor for receptor binding (E. J. J. van Zoelen, D. R. Twardzik, T. M. J. van Oostwaard, P. T. van der Saag, S. W. de Laat, and G. J. Todaro, Proc. Natl. Acad. Sci. U.S.A. 81:4085-4089, 1984). In this study approximately 80% of the mitogenic activity was immunoprecipitated by antibodies raised against platelet-derived growth factor (PDGF). Immunoblotting indicated a true molecular size of 32 kDa for this PDGF-like growth factor. Analysis of poly(A)+ RNA from Neuro-2A cells demonstrated the expression of the c-sis oncogene in this cell line, whereas in vitro translation of the RNA yielded a 20-kDa protein recognized by anti-PDGF antibodies. Separation by reverse-phase high-pressure liquid chromatography demonstrated the presence of two distinct mitogenic activities in neuroblastoma-derived transforming growth factor preparations, one of which is antigenically related to PDGF. Both activities had the ability to induce anchorage-independent growth in normal rat kidney cells, both in the presence and in the absence of epidermal growth factor. It is concluded that Neuro-2A cells express c-sis with concomitant production and secretion of a PDGF-like growth factor, which plays a role in the induction of phenotypic transformation on normal rat kidney cells.

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van Zoelen, E. J., W. J. van de Ven, H. J. Franssen, T. M. van Oostwaard, P. T. van der Saag, C. H. Heldin, and S. W. de Laat. "Neuroblastoma cells express c-sis and produce a transforming growth factor antigenically related to the platelet-derived growth factor." Molecular and Cellular Biology 5, no. 9 (September 1985): 2289–97. http://dx.doi.org/10.1128/mcb.5.9.2289.

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Mouse neuroblastoma Neuro-2A cells produce transforming growth factors during exponential growth in a defined hormone-free medium, which, on Bio-Gel columns in 1 M HAc, elute at a molecular size of 15 to 20 kilodaltons (kDa). These neuroblastoma-derived transforming growth factors have strong mitogenic activity, but they do not compete with epidermal growth factor for receptor binding (E. J. J. van Zoelen, D. R. Twardzik, T. M. J. van Oostwaard, P. T. van der Saag, S. W. de Laat, and G. J. Todaro, Proc. Natl. Acad. Sci. U.S.A. 81:4085-4089, 1984). In this study approximately 80% of the mitogenic activity was immunoprecipitated by antibodies raised against platelet-derived growth factor (PDGF). Immunoblotting indicated a true molecular size of 32 kDa for this PDGF-like growth factor. Analysis of poly(A)+ RNA from Neuro-2A cells demonstrated the expression of the c-sis oncogene in this cell line, whereas in vitro translation of the RNA yielded a 20-kDa protein recognized by anti-PDGF antibodies. Separation by reverse-phase high-pressure liquid chromatography demonstrated the presence of two distinct mitogenic activities in neuroblastoma-derived transforming growth factor preparations, one of which is antigenically related to PDGF. Both activities had the ability to induce anchorage-independent growth in normal rat kidney cells, both in the presence and in the absence of epidermal growth factor. It is concluded that Neuro-2A cells express c-sis with concomitant production and secretion of a PDGF-like growth factor, which plays a role in the induction of phenotypic transformation on normal rat kidney cells.

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Khalifa, Ali, Samar K. Kassim, Maha I. Ahmed, and Salah T. Fayed. "Transforming Growth Factor-βand Nitrates in Epithelial Ovarian Cancer." Disease Markers 15, no. 4 (1999): 249–58. http://dx.doi.org/10.1155/1999/956707.

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The role of transforming growth factor-β(TGF-β) and nitric oxide (NO) in ovarian neoplasia is still not clear. We studied the expression of TGF-βby enzyme immunoassay, and nitrates (as a stable end product of NO) in 127 ovarian tissues (36 normal, 37 benign, and 54 malignant). Ploidy status and synthetic phase fraction (SPF) were also assessed by flow cytometry. Mean ranks of TGF-β, nitrate, and SPF were significant among different groups (X2= 12.01, P = 0.0025, X2= 67.42, P = 0.000, X2= 9.06, P = 0.011 respectively). Nitrate mean ranks were significant among different FIGO stages of the disease (X2= 17.6, P = 0.000). A significant correlation was shown between TGF-â, and nitrate levels in all tissues (r = 0.24, P = 0.01), as well as in malignant tissues (r = 0.3, P = 0.026). Cutoff values were determined for both TGF-β(290 pg/mg protein), and nitrates (310 nmole/mg non protein nitrogenous substances). At these cut-offs, nitrates showed a sensitivity of 93% and 84% specificity for malignant versus normal cases, while TGF-βhad 76% sensitivity, and 82.4% specificity for poor versus good outcome. Patients with epithelial ovarian cancer were followed up for a total of 40 months. Survival analysis showed that patients with TGF-βabove the cut-off had worse prognosis (X2= 12.69, P = 0.004). The present results suggest that malignant transformation of ovarian tissues is associated with increased TGF-βand NO production. NO level is related to the development and progression of epithelial ovarian cancer, while high levels of TGF-βcould be of prognostic significance.

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Mostert, Volker, Ingeborg Dreher, Josef Köhrle, and Josef Abel. "Transforming growth factor-β1inhibits expression of selenoprotein P in cultured human liver cells." FEBS Letters 460, no. 1 (October 22, 1999): 23–26. http://dx.doi.org/10.1016/s0014-5793(99)01298-3.

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Saha, Debabrata, Neil A. Bhowmick, Carolyn Cao, Jaechul Kim, Konjeti R. Sekhar, Michael L. Freeman, and Hak Choy. "P-349 Flavopiridol prevented transforming growth factor-beta-mediated epithelial to mesenchymal transdifferentiation." Lung Cancer 41 (August 2003): S180. http://dx.doi.org/10.1016/s0169-5002(03)92317-8.

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Song, Young-Min, Kyung-Hwan Na, Hyun-Jin Lee, and Jun-Beom Park. "The Effects of Transforming Growth Factor-β1 on the Differentiation of Cell Organoids Composed of Gingiva-Derived Stem Cells." BioMed Research International 2022 (July 14, 2022): 1–9. http://dx.doi.org/10.1155/2022/9818299.

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This study was aimed at evaluating the effects of transforming growth factor-β on the differentiation and mRNA expression of organoids made out of human mesenchymal stem cells. Cell organoids composed of gingiva-derived stem cells were cultured in the presence of transforming growth factor-β1 at concentrations ranging from 0, 1, 10, to 20 ng/ml. Evaluations of the cell morphology of the organoids were performed on days 7, 9, 11, and 14. Quantitative cellular viability was completed on day 14. Alkaline phosphatase activity assays were performed to evaluate the differentiation of stem cells on day 14. Real-time polymerase chain reactions were used to determine the expression levels of TGF-β1, RUNX2, OCN, SOX9, and COL1A1 mRNA on day 14. The stem cells produced well-formed organoids on day 7, and the addition of transforming growth factor-β1 did not result in relevant changes in their shape. The organoids grew in size and became more intact with longer incubation times. On day 14, the diameters were 222.2 ± 9.6 , 186.1 ± 4.8 , 197.2 ± 9.6 , and 211.1 ± 19.2 m for transforming growth factor-β1 at final concentrations of 0, 1, 10, and 20 ng/ml, respectively. Quantitative cell viability results from day 14 exhibited no significant difference between the groups ( P > 0.05 ). There was significantly higher alkaline phosphatase activity with the addition of transforming growth factor-β1 with the highest value for the 1 ng/ml group ( P < 0.05 ). Real-time polymerase chain reaction results demonstrated that the mRNA expression levels of RUNX2, OCN, and SOX were higher in 1 ng/ml but did not reach statistical significance. Treatment with 1 ng/ml of transforming growth factor-β1 significantly increased COL1A1 mRNA expression at day 14. The application of transforming growth factor-β1 increased differentiation, which was confirmed by alkaline phosphatase activity and mRNA expression while maintaining cell viability.

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Qi, W., S. Twigg, X. Chen, T. S. Polhill, P. Poronnik, R. E. Gilbert, and C. A. Pollock. "Integrated actions of transforming growth factor-β1 and connective tissue growth factor in renal fibrosis." American Journal of Physiology-Renal Physiology 288, no. 4 (April 2005): F800—F809. http://dx.doi.org/10.1152/ajprenal.00179.2004.

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Matrix accumulation in the renal tubulointerstitium is predictive of a progressive decline in renal function. Transforming growth factor-β1 (TGF-β1) and, more recently, connective tissue growth factor (CTGF) are recognized to play key roles in mediating the fibrogenic response, independently of the primary renal insult. Further definition of the independent and interrelated effects of CTGF and TGF-β1 is critical for the development of effective antifibrotic strategies. CTGF (20 ng/ml) induced fibronectin and collagen IV secretion in primary cultures of human proximal tubule cells (PTC) and cortical fibroblasts (CF) compared with control values ( P < 0.005 in all cases). This effect was inhibited by neutralizing antibodies to either TGF-β or to the TGF-β type II receptor (TβRII). TGF-β1 induced a greater increase in fibronectin and collagen IV secretion in both PTC ( P < 0.01) and CF ( P < 0.01) compared with that observed with CTGF alone. The combination of TGF-β1 and CTGF was additive in their effects on both PTC and CF fibronectin and collagen IV secretion. TGF-β1 (2 ng/ml) stimulated CTGF mRNA expression within 30 min, which was sustained for up to 24 h, with a consequent increase in CTGF protein ( P < 0.05), whereas CTGF had no effect on TGF-β1 mRNA or protein expression. TGF-β1 (2 ng/ml) induced phosphorylated (p)Smad-2 within 15 min, which was sustained for up to 24 h. CTGF had a delayed effect on increasing pSmad-2 expression, which was evident at 24 h. In conclusion, this study has demonstrated the key dependence of the fibrogenic actions of CTGF on TGF-β. It has further uniquely demonstrated that CTGF requires TGF-β, signaling through the TβRII in both PTCs and CFs, to exert its fibrogenic response in this in vitro model.

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Jankowski, J., H. J. Al-Rawi, D. A. Johnston, D. Hopwood, M. I. Filipe, G. Coghill, and K. G. Wormsley. "Growth regulatory peptides in gastric mucosa." Clinical Science 82, no. 5 (May 1, 1992): 581–87. http://dx.doi.org/10.1042/cs0820581.

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1. Epidermal growth factor and the related peptide transforming growth factor α have been implicated in the stimulation of gastric mucosal proliferation. We assessed the immunohistochemical distribution of these peptides and their receptor, epidermal growth factor receptor, in mucosa from the antrum and body of the stomach from 28 patients. Twenty-three of the 56 biopsies were histologically normal (12 antrum and 11 body), whereas the other 33 showed varying degrees of inflammation. 2. Epidermal growth factor, transforming growth factor α and epidermal growth factor receptor had maximal density of distribution on the apical surfaces of the superficial epithelial cells, but were also expressed to a lesser extent on neck and body cells of the glandular tissue (P < 0.05). We also demonstrated that epidermal growth factor expression was greater in the epithelial cells of inflamed mucosa than in those of normal mucosa (P < 0.05). 3. We assessed mucosal proliferation by the Ki-67 labelling index. Ki-67-positive cells were found predominantly in the neck area of the glands and were more frequent in glandular antral tissue than in body glandular tissue (P < 0.05). Expression of epidermal growth factor receptor in the neck and isthmus cells had a significant correlation with the Ki-67 labelling index (P < 0.05). 4. We conclude that epidermal growth factor and epidermal growth factor receptor may be important in the adaptation of gastric mucosa to inflammation.

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Miettinen, P. J., T. Otonkoski, and R. Voutilainen. "Insulin-like growth factor-II and transforming growth factor-α in developing human fetal pancreatic islets." Journal of Endocrinology 138, no. 1 (July 1993): 127—NP. http://dx.doi.org/10.1677/joe.0.1380127.

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ABSTRACT To understand the development of the human pancreas better, we studied the expression and regulation of insulin, insulin-like growth factor-II (IGF-II) and transforming growth factor-α (TGF-α) genes in the human fetal pancreas and islet-like cell clusters (ICC) from the second trimester human fetuses. Northern blot analysis revealed an abundant expression of IGF-II, insulin and TGF-α mRNAs in the intact pancreas and the cultured ICCs. Furthermore, transcripts for insulin receptor, type-1 and -2 IGF receptors, and GH receptor could be amplified by polymerase chain reaction analysis from the pancreas and the ICCs. With in-situ hybridization, IGF-II mRNA was found in abundance in both the exocrine and endocrine pancreas, exceeding the amount of insulin mRNA. In ICCs, insulin mRNA-containing cells were present as small clusters in the periphery and in the centre of the clusters corresponding to the immunolocation of insulin. The ICCs also contained many epidermal growth factor-, insulin- and type-1 IGF receptor- and TGF-α-positive cells. When the ICCs were cultured in the presence of various secretagogues, only dibutyryl cyclic AMP was found to up-regulate insulin mRNA (39%; P < 0·05). IGF-II mRNA was also under cyclic AMP-dependent regulation (threefold increase; P = 0·025). Furthermore, blocking the type-1 IGF receptor with a monoclonal receptor antibody drastically reduced insulin expression (87%; P = 0·005) and additionally down-regulated IGF-II mRNA (49%; P = 0·005). IGF-1, IGF-II, TGF-α or epidermal growth factor-receptor antibody had no significant effect on either insulin or IGF-II mRNA. Exogenous TGF-α inhibited the release of insulin by the ICCs. It was concluded that IGF-II and TGF-α may be involved in the regulation of islet growth and differentiation. Journal of Endocrinology (1993) 138, 127–136

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Stoika, R. S., S. I. Sushelnitsky, and S. I. Kusen'. "The influence of the transforming growth factor-p, epidermal growth factor and insulin on cellular proliferation in semisolid agar medium." Biopolymers and Cell 5, no. 1 (January 20, 1989): 96–99. http://dx.doi.org/10.7124/bc.00009c.

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An, Ji-long, Wei Zhang, Jian Zhang, Li-chao Lian, Yong Shen, and Wen-yuan Ding. "Vitamin D improves the content of TGF-β and IGF-1 in intervertebral disc of diabetic rats." Experimental Biology and Medicine 242, no. 12 (May 24, 2017): 1254–61. http://dx.doi.org/10.1177/1535370217707744.

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Objective: The contents of transforming growth factor-β and insulin-like growth factor-1 in disc of diabetic rats were measured at three different periods after injected with 1,25-Dihydroxyvitamin D3, and compared with that in normal rats. The significance of content changes was also discussed. Methods: Fourty-five Sprague-Dawley (SD) rats were divided into three groups, namely the experimental group (STZ+calcitriol), control group (STZ+citrate buffer), and normal group (citrate buffer). Complete lumbar discs in these groups were obtained at the second, fourth, sixth week, respectively. After paraffin-embedded sections and HE staining, the structure and morphology changes of disc were observed. The content of transforming growth factor-β and insulin-like growth factor-1 was measured by immunohistochemical method, and the expression of transforming growth factor-β and insulin-like growth factor-1 was detected by Western Blot. Results: In hematoxylin–eosin staining, degenerative changes were observed in disc of experimental and control group at three different periods, and there were no changes in disc in normal group. Immunohistochemical method indicated the content of transforming growth factor-β and insulin-like growth factor-1 in experimental and control group was significantly lower than normal group at three different periods ( P < 0.05). And there were significant differences between experimental and control group at three different periods ( P < 0.05). Conclusion: Vitamin D can protect the degeneration of intervertebral disc and improve the content of transforming growth factor-β and insulin-like growth factor-1 in the intervertebral disc, which provides a new idea for the prevention and treatment of degenerative changes of the intervertebral disc in diabetic patients. Impact statement No researchers reported Vitamin D could protect degeneration of intervertebral disc. That is to say, we found a new method to prevent and treat degenerative changes of the intervertebral disc in diabetic patients. And Vitamin D prevented the discs by improving the content of TGF-β and IGF-1.

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Ye, XF, N. Yorioka, H. Oda, Y. Taniguchi, and M. Yamakido. "Role of Transforming Growth Factor-β and -β in ddY Mous Nephropathy." Journal of International Medical Research 25, no. 3 (May 1997): 141–54. http://dx.doi.org/10.1177/030006059702500304.

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We investigated the glomerular distribution of transforming growth factor −β (TGF −β1, and TGF −β2) protein and the expression of its mRNA, and related factors, in ddY mice, aged 5 — 60 weeks, before and after the onset of nephropathy. TGF −β1 protein expression was observed from the age of 20 weeks onwards, peaking at 50 weeks, and then declining. Expression of TGF −β2 protein gradually increased from 5 to 60 weeks. TGF −β1 and TGF −β2 mRNA were both detected from 5 to 60 weeks. The mesangial matrix expansion index (MMEI) was significantly higher in mice with nephropathy than in those without nephropathy, as was the expression of TGF −β1 and TGF −β2 proteins ( P < 0.05). TGF −β2 was significantly positively correlated with the MMEI ( P < 0.05). Infiltration of CD68-positive monocytes/macrophages gradually increased until 60 weeks, and was significantly correlated with the expression of TGF −β1 ( P < 0.05) and TGF −β2 ( P < 0.01). These findings indicate that TGF −β1 and TGF −β2 were overexpressed in ddY mice with overt nephropathy compared with pre-nephropathic mice. TGF −β2 may be an important mediator of mesangial matrix expansion in ddY mouse nephropathy.

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Kimura, Mitsutoshi, and Masahiko Ogihara. "Transforming growth factor-p, inhibits the growth of primary adult rat hepatocyte cultures by increasing cAMP levels." Japanese Journal of Pharmacology 82 (2000): 146. http://dx.doi.org/10.1016/s0021-5198(19)48045-1.

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Samuelov, Liat, Eli Sprecher, Daisuke Tsuruta, Tamás Bíró, Jennifer E. Kloepper, and Ralf Paus. "P-Cadherin Regulates Human Hair Growth and Cycling via Canonical Wnt Signaling and Transforming Growth Factor-β2." Journal of Investigative Dermatology 132, no. 10 (October 2012): 2332–41. http://dx.doi.org/10.1038/jid.2012.171.

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Ständer, Marko, Ulrike Naumann, Wolfgang Wick, and M. Weller. "Transforming growth factor-β and p-21: multiple molecular targets of decorin-mediated suppression of neoplastic growth." Cell and Tissue Research 296, no. 2 (April 21, 1999): 221–27. http://dx.doi.org/10.1007/s004410051283.

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Fabia, Benedict-Uy, Joshua Bingwa, Jiyeon Park, Nguyen-Mihn Hieu, and Jung-Hoon Ahn. "Utilizing the ABC Transporter for Growth Factor Production by fleQ Deletion Mutant of Pseudomonas fluorescens." Biomedicines 9, no. 6 (June 16, 2021): 679. http://dx.doi.org/10.3390/biomedicines9060679.

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Pseudomonas fluorescens, a gram-negative bacterium, has been proven to be a capable protein manufacturing factory (PMF). Utilizing its ATP-binding cassette (ABC) transporter, a type I secretion system, P. fluorescens has successfully produced recombinant proteins. However, besides the target proteins, P. fluorescens also secretes unnecessary background proteins that complicate protein purification and other downstream processes. One of the background proteins produced in large amounts is FliC, a flagellin protein. In this study, the master regulator of flagella gene expression, fleQ, was deleted from P. fluorescens Δtp, a lipase and protease double-deletion mutant, via targeted gene knockout. FleQ directs flagella synthesis, so the new strain, P. fluorescens ΔfleQ, does not produce flagella-related proteins. This not only simplifies purification but also makes P. fluorescens ΔfleQ an eco-friendly expression host because it will not survive outside a controlled environment. Six recombinant growth factors, namely, insulin-like growth factors I and II, beta-nerve growth factor, fibroblast growth factor 1, transforming growth factor beta, and tumor necrosis factor beta, prepared using our supercharging method, were successfully secreted by P. fluorescens ΔfleQ. Our findings demonstrate the potential of P. fluorescens ΔfleQ, combined with our supercharging process, as a PMF.

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Stief, M., J. Gottschalk, J. C. Ionita, A. Einspanier, G. Oechtering, and P. Böttcher. "Concentration of platelets and growth factors in canine autologous conditioned plasma." Veterinary and Comparative Orthopaedics and Traumatology 24, no. 02 (2011): 122–25. http://dx.doi.org/10.3415/vcot-10-04-0064.

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Summary Objectives: To report the concentration of blood cells and selected growth factors in canine autologous conditioned plasma (ACP). Methods: The density of blood cells in whole blood (WB), ACP and standard plasma preparation (SP) of 10 healthy mature dogs was determined. In both ACP and SP, the concentration of insulin-like growth factor-1 (IGF-1), epidermal growth factor, vascular endothelial growth factor, platelet-derived growth factor-AA, platelet-derived growth factor-AB, platelet-derived growth factor-BB, transforming growth factor-β1 (TGF-β1), and transforming growth factor-β2 was measured using the ELISA technique. In another ten dogs, ACP was prepared using an ultra-soft spinning protocol, and again blood cell density was compared to that obtained in WB. Results: The density of platelets in ACP was significantly higher than that in SP (p = 0.0002), but there was not any significant difference between ACP and WB, nor between WB and ACP prepared using softer centrifugations. Interestingly, only for IGF-1, PDGFBB, and TGF-β1 could reliable measurements be obtained, showing a significant increase in PDGF-BB and TGF-β1 concentrations in ACP compared to SP (p = 0.001, p = 0.0028). Regarding IGF-1 content, there was not any significant difference between ACP and SP. Clinical significance: Canine ACP prepared according to the manufacturer’s recommendations, or by using a softer spin does not show the same specifications as human ACP, which shows a doubling in platelet count compared to WB. Even though canine ACP has a similar number of platelets per injected volume and consequently, probably the same amount of injected growth factors than WB, application of canine ACP would not be associated with the proinflammatory potential reported for WB, as it is almost free of erythrocytes and nucleated cells.

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Saadeh, Pierre B., Babak J. Mehrara, Douglas S. Steinbrech, Matthew E. Dudziak, Joshua A. Greenwald, Jonathan S. Luchs, Jason A. Spector, Hikaru Ueno, George K. Gittes, and Michael T. Longaker. "Transforming growth factor-β1 modulates the expression of vascular endothelial growth factor by osteoblasts." American Journal of Physiology-Cell Physiology 277, no. 4 (October 1, 1999): C628—C637. http://dx.doi.org/10.1152/ajpcell.1999.277.4.c628.

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Angiogenesis is essential to both normal and pathological bone physiology. Vascular endothelial growth factor (VEGF) has been implicated in angiogenesis, whereas transforming growth factor-β1 (TGF-β1) modulates bone differentiation, matrix formation, and cytokine expression. The purpose of this study was to investigate the relationship between TGF-β1 and VEGF expression in osteoblasts and osteoblast-like cells. Northern blot analysis revealed an early peak of VEGF mRNA (6-fold at 3 h) in fetal rat calvarial cells and MC3T3-E1 osteoblast-like cells after stimulation with TGF-β1 (2.5 ng/ml). The stability of VEGF mRNA in MC3T3-E1 cells was not increased after TGF-β1 treatment. Actinomycin D inhibited the TGF-β1-induced peak in VEGF mRNA, whereas cycloheximide did not. Blockade of TGF-β1 signal transduction via a dominant-negative receptor II adenovirus significantly decreased TGF-β1 induction of VEGF mRNA. Additionally, TGF-β1 induced a dose-dependent increase in VEGF protein expression by MC3T3-E1 cells ( P < 0.01). Dexamethasone similarly inhibited VEGF protein expression. Both TGF-β1 mRNA and VEGF mRNA were concurrently present in rat membranous bone, and both followed similar patterns of expression during rat mandibular fracture healing (mRNA and protein). In summary, TGF-β1-induced VEGF expression by osteoblasts and osteoblast-like cells is a dose-dependent event that may be intimately related to bone development and fracture healing.

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SÖNMEZER, M., M. GÜNGÖR, A. Ensari, and F. Ortaç. "Prognostic significance of tumor angiogenesis in epithelial ovarian cancer: in association with transforming growth factor β and vascular endothelial growth factor." International Journal of Gynecologic Cancer 14, no. 1 (January 2004): 82–88. http://dx.doi.org/10.1136/ijgc-00009577-200401000-00010.

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We aimed to evaluate the prognostic significance of microvessel density (MVD), vascular endothelial growth factor (VEGF), and transforming growth factor β (TGFβ), as well as to find out the relationship between MVD, and VEGF and TGFβ in epithelial ovarian cancer (EOC). Surgical specimens of 47 patients with stage I–IV primary EOC, who underwent extended surgical staging according to FIGO, were investigated. Five-μm thick tissue sections were immunostained with antibody to factor VIII-related antigen, and MVD was assessed at three separate areas of ×200 magnification. Expressions for VEGF and TGFβ were evaluated by immunohistochemical staining using related monoclonal antibodies. Results were correlated with clinicopathologic factors and survival. We did not find any correlation between MVD and clinicopathologic factors, or patient survival. Similarly, there was no association between the degree of VEGF staining and survival or clinicopathologic factors, except preoperative ascites volume, which was higher in patients showing moderate and intense VEGF staining than those with weak VEGF staining (P = 0.052). The expression of TGFβ was inversely correlated with preoperative CA-125 levels (P < 0.05). Furthermore, there was no correlation between MVD and the staining intensity of VEGF or TGFβ. In conclusion, angiogenesis does not appear as a prognostic factor in EOC. We suggest that VEGF is an important mediator of ascites formation, and that TGFβ, which is supposed to have tissue-specific actions in tumorigenesis, may have growth-inhibitory functions in EOC.

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Thomae, Tami L., Emily A. Stevens, and Christopher A. Bradfield. "Transforming Growth Factor-β3 Restores Fusion in Palatal Shelves Exposed to 2,3,7,8-Tetrachlorodibenzo-p-dioxin." Journal of Biological Chemistry 280, no. 13 (January 24, 2005): 12742–46. http://dx.doi.org/10.1074/jbc.m410780200.

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Kapelski, P., M. Skibinska, and J. Hauser. "P.3.b.011 Association study of transforming growth factor-beta gene polymorphisms in schizophrenia." European Neuropsychopharmacology 23 (October 2013): S435—S436. http://dx.doi.org/10.1016/s0924-977x(13)70689-8.

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Wallace, Megan J., Alison M. Thiel, Andrea M. Lines, Graeme R. Polglase, Foula Sozo, and Stuart B. Hooper. "Role of platelet-derived growth factor-B, vascular endothelial growth factor, insulin-like growth factor-II, mitogen-activated protein kinase and transforming growth factor-β1 in expansion-induced lung growth in fetal sheep." Reproduction, Fertility and Development 18, no. 6 (2006): 655. http://dx.doi.org/10.1071/rd05163.

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Increased fetal lung expansion induces lung growth, cell differentiation and extracellular matrix remodelling, although the mechanisms involved are unknown. Platelet-derived growth factor (PDGF)-B, vascular endothelial growth factor (VEGF) and insulin-like growth factor (IGF)-II are mitogens activating the mitogen-activated protein kinase (MAPK) pathway, whereas transforming growth factor (TGF)-β1 induces differentiation and extracellular matrix remodelling. In the present study, we investigated the mRNA levels of PDGF-B, VEGF, IGF-II and TGF-β1, as well as active MAPK levels, during increased fetal lung expansion induced by tracheal obstruction (TO) in sheep for 0 (controls), 36 h or 2, 4, or 10 days (n = 5 in each group). The 3.7-kb VEGF transcript increased by 30% (P < 0.05) at 36 h TO. The expression of PDGF-B decreased by approximately 25% (P < 0.01) at 2–10 days TO. In contrast, TGF-β1 mRNA increased by 96% (P < 0.05) at 10 days TO, when bioactive TGF-β1 decreased by 55% (P < 0.05). Insulin-like growth factor-II mRNA tended to increase at 10 days TO (37% above controls; P = 0.07), whereas mRNA for its receptor, IGF1R, was reduced by TO. There was no change in active MAPK levels preceding or at the time of a TO-induced 800% increase in cell proliferation. We conclude that VEGF is likely to promote expansion-induced endothelial cell proliferation, but the mechanisms underlying expansion-induced proliferation of fibroblasts and alveolar epithelial cells are unlikely to be mediated by increases in PDGF-B or IGF-II expression or activation of the MAPK pathway.

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Tonello, Raquel, Wenrui Xie, Sang Hoon Lee, Min Wang, Xiaojuan Liu, Judith A. Strong, Jun-Ming Zhang, and Temugin Berta. "Local Sympathectomy Promotes Anti-inflammatory Responses and Relief of Paclitaxel-induced Mechanical and Cold Allodynia in Mice." Anesthesiology 132, no. 6 (June 1, 2020): 1540–53. http://dx.doi.org/10.1097/aln.0000000000003241.

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Abstract Background Patients undergoing cancer treatment often experience chemotherapy-induced neuropathic pain at their extremities, for which there is no U.S. Food and Drug Administration–approved drug. The authors hypothesized that local sympathetic blockade, which is used in the clinic to treat various pain conditions, can also be effective to treat chemotherapy-induced neuropathic pain. Methods A local sympathectomy (i.e., cutting the ipsilateral gray rami entering the spinal nerves near the L3 and L4 dorsal root ganglia) was performed in mice receiving intraperitoneal injections every other day of the chemotherapeutic drug paclitaxel. Sympathectomy effects were then assessed in chemotherapy-induced pain-like behaviors (i.e., mechanical and cold allodynia) and neuroimmune and electrophysiologic responses. Results Local microsympathectomy produced a fast recovery from mechanical allodynia (mean ± SD: sympathectomy vs. sham at day 5, 1.07 ± 0.34 g vs. 0.51 ± 0.17g, n = 5, P = 0.030 in male mice, and 1.08 ± 0.28 g vs. 0.62 ± 0.16 g, n = 5, P = 0.036 in female mice) and prevented the development of cold allodynia in both male and female mice after paclitaxel. Mechanistically, microsympathectomy induced transcriptional increases in dorsal root ganglia of macrophage markers and anti-inflammatory cytokines, such as the transforming growth factor-β. Accordingly, depletion of monocytes/macrophages and blockade of transforming growth factor-β signaling reversed the relief of mechanical allodynia by microsympathectomy. In particular, exogenous transforming growth factor-β was sufficient to relieve mechanical allodynia after paclitaxel (transforming growth factor-β 100 ng/site vs. vehicle at 3 h, 1.21 ± 0.34g vs. 0.53 ± 0.14 g, n = 5, P = 0.001 in male mice), and transforming growth factor-β signaling regulated neuronal activity in dorsal root ganglia. Conclusions Local sympathetic nerves control the progression of immune responses in dorsal root ganglia and pain-like behaviors in mice after paclitaxel, raising the possibility that clinical strategies already in use for local sympathetic blockade may also offer an effective treatment for patients experiencing chemotherapy-induced neuropathic pain. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

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Balcan, Eray, Fuat Demirkiran, Yavuz Aydin, Cevdet Sanioglu, Tugan Bese, Macit Arvas, Tulay Akçay, and Tayfur Cift. "Serum Levels of Epidermal Growth Factor, Transforming Growth Factor, and c-erbB2 in Ovarian Cancer." International Journal of Gynecologic Cancer 22, no. 7 (September 2012): 1138–42. http://dx.doi.org/10.1097/igc.0b013e31825b7dcc.

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ObjectiveThis study aimed to investigate serum levels of epidermal growth factor (EGF), transforming growth factor α (TGF-α), and c-erbB2 in patients with ovarian cancer.Materials and MethodsIn this retrospective cohort study, the study and control groups were composed of 43 women with a prediagnosis of ovarian cancer and 43 healthy women, respectively. Blood samples from all women were obtained and studied by enzyme-linked immunosorbent assay kits for EGF, TGF-α, and c-erbB2. After surgery of the study group, ovarian cancer was confirmed and compared with control group. Stage, grade, and histological types were defined after histopathologic examination, and subgroups were constructed and compared.ResultsSerum EGF, TGF-α, and c-erbB2 levels were significantly increased in study group compared with those in the control group (P < 0.001). There were no differences in serum levels of EGF, TGF-α, and c-erbB2 among all stages, grades, and histological types of ovarian cancer. If 47.90 pg/mL was selected as the cutoff value, EGF has an 80% sensitivity and a 65% specificity for detecting ovarian cancer. The cutoff value of 41,095.00 pg/mL for TGF-α has a 90% sensitivity and a 72% specificity for detecting ovarian cancer. The c-erbB2 level of 4.63 pg/mL as the cutoff value has an 83% sensitivity and a 76% specificity for predicting ovarian cancer.ConclusionsSerum levels of EGF, TGF-α, and c-erbB2 may be used for diagnosing ovarian cancer.

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Gabrilove, JL, G. Wong, E. Bollenbacher, K. White, S. Kojima, and EL Wilson. "Basic fibroblast growth factor counteracts the suppressive effect of transforming growth factor-beta 1 on human myeloid progenitor cells." Blood 81, no. 4 (February 15, 1993): 909–15. http://dx.doi.org/10.1182/blood.v81.4.909.909.

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Abstract We have previously shown that basic fibroblast growth factor (bFGF) is mitogenic for human bone marrow stromal cells and enhances myelopoiesis in human long-term bone marrow culture. In the present study, we examined the mechanism by which bFGF enhances granulopoiesis. We observed that bFGF significantly abrogated the inhibitory effect of transforming growth factor-beta 1 (TGF-beta 1) on granulocyte- macrophage colony-stimulating factor (GM-CSF)-supported progenitor cell growth (P = .009). The partial reversal of TGF-beta 1-mediated suppression was dependent on the dose of bFGF used. In addition, we noted that the inclusion of neutralizing antibody to TGF-beta 1 significantly augmented the clonogenic response to GM-CSF. We have also shown that 10 ng/mL or 100 ng/mL of bFGF resulted in a 30% to 100% increase in GM-CSF-mediated progenitor cell growth (P = .0001). These data suggest that bFGF may enhance myelopoiesis by modulating the inhibitory response to TGF-beta 1.

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Gabrilove, JL, G. Wong, E. Bollenbacher, K. White, S. Kojima, and EL Wilson. "Basic fibroblast growth factor counteracts the suppressive effect of transforming growth factor-beta 1 on human myeloid progenitor cells." Blood 81, no. 4 (February 15, 1993): 909–15. http://dx.doi.org/10.1182/blood.v81.4.909.bloodjournal814909.

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We have previously shown that basic fibroblast growth factor (bFGF) is mitogenic for human bone marrow stromal cells and enhances myelopoiesis in human long-term bone marrow culture. In the present study, we examined the mechanism by which bFGF enhances granulopoiesis. We observed that bFGF significantly abrogated the inhibitory effect of transforming growth factor-beta 1 (TGF-beta 1) on granulocyte- macrophage colony-stimulating factor (GM-CSF)-supported progenitor cell growth (P = .009). The partial reversal of TGF-beta 1-mediated suppression was dependent on the dose of bFGF used. In addition, we noted that the inclusion of neutralizing antibody to TGF-beta 1 significantly augmented the clonogenic response to GM-CSF. We have also shown that 10 ng/mL or 100 ng/mL of bFGF resulted in a 30% to 100% increase in GM-CSF-mediated progenitor cell growth (P = .0001). These data suggest that bFGF may enhance myelopoiesis by modulating the inhibitory response to TGF-beta 1.

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Aubrecht, Jiri, Karen I. Hirsch-ernst, Volker Becker-Rabbenstein, Georg Friedrich Kahl, Hisaaki Taniguchi, and Martin W. Höhne. "Induction of cytochrome P-4502B1-related mouse cytochrome P-450 and regulation of its expression by epidermal growth factor/transforming growth factor α in primary hepatocyte culture." Biochemical Pharmacology 50, no. 6 (September 1995): 781–85. http://dx.doi.org/10.1016/0006-2952(95)00200-j.

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Kallmes, D. F., G. R. Hankins, M. K. Borland, H. J. Cloft, M. E. Jensen, J. E. Dion, and G. A. Helm. "Transforming Growth Factor-Beta Binds Reversibly in Vitro to Guglielmi Detachable Coils." Interventional Neuroradiology 4, no. 1 (March 1998): 21–26. http://dx.doi.org/10.1177/159101999800400102.

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We determined the propensity for and reversibility of transforming growth factor-ß (TGFß) binding to uncoated Guglielmi Detachable Coils (GDC) and to GDC coated with extracellular matrix (ECM) proteins. Three 1.0 centimetre samples each of uncoated GDC-18 and of GDC-18 coated with either poly-L-lysine, laminin, type I collagen, type IV collagen, fibronectin, or poly-L-lysine and laminin were prepared. These samples were immersed briefly in a solution containing I125-labelled TGFß at a concentration of 0.225 μg/ml with initial specific activity of 123.3 mCi/mg (DuPont-NEN, Billerica, MA), and were counted using a scintillation counter. Each sample was then placed in a vial containing saline, shaken for 60 seconds, and counted again. Selected samples were immersed for varying periods within the TGFß solution and counted before and after saline rinse. Samples were rinsed one week after initial rinsing and counted again. The amount of binding between coil types was compared using the Student t test. For all samples initial binding of TGFß was in the order of 60–120 pg/cm. For the pre-rinse data there were no statistically significant differences between the amount bound to any single coil coating type relative to other coatings. Compared to the initial accumulations, the amount remaining after rinsing ranged from 40% (poly-L-lysine) to 63% (poly-L-lysine with laminin), with a mean of 55% among the seven coil types. After rinsing there was more growth factor remaining on uncoated coils than on poly-L-lysine-coated coils (p=0.05), fibronectin-coated coils (p=0.01), and type IV collagen-coated coils (p=0.04). There was a trend toward greater residual growth factor on coils coated with poly-L-lysine and laminin compared to coils coated with poly-L-lysine alone (p=0.10). Delayed, second rinsing of the samples one week after initial testing demonstrated only minor incremental loss of TGFß from the coil surfaces. After five minutes of immersion, accumulation was approximately 200% greater than that noted with brief submersion, but immersions lasting over five minutes did not yield increasing levels of TGFß binding. TGFß binds to GDC coils. Binding is not improved with ECM protein-coated coils compared to uncoated coils. The absolute amount of TGFß bound to the coil will likely result in local concentrations of growth factor in the order of those required for biological activity in vivo.

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Wulandari, Pratidina, Magda Hutagalung, and David Perdanakusuma. "Deteksi Kadar Transforming Growth Factor (Tgf-Β) Pada Luka Akut." Jurnal Rekonstruksi dan Estetik 6, no. 1 (July 12, 2021): 1. http://dx.doi.org/10.20473/jre.v6i1.28225.

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Latar Belakang. TGF-β merupakan growth factor yang paling dominan dalam peningkatan sintesis kolagen, memiliki peran utama pada penyembuhan luka dengan menstimulasi fibroblas sehingga menimbulkan penyembuhan dan berperan serta dalam pembentukan parut, baik itu parut normal maupun abnormal seperti parut hipertrofik dan keloid. Penelitian ini bertujuan untuk mengukur kadar TGF-β pada fase penyembuhan luka.Metode. Penelitian eksperimental ini menggunakan randomized post test only control group design. Dua belas luka akut kulit tikus dirandomisasi menjadi dua kelompok, dimana kelompok 1 diambil spesimen pada hari ke-5 dan kelompok 2 pada hari ke-21 dan dilakukan pemeriksaan ELISA untuk mengukur kadar TGF-.Hasil. Pengukuran kadar TGF-β pada luka akut kulit tikus didapatkan jumlah yang meningkat secara signifikan dari hari ke-5 (fase inflamasi) ke hari ke-21 (fase proliferasi) dengan nilai p = 0,003. Kesimpulan. Terjadi peningkatan kadar TGF- pada akhir fase proliferasi atau awal fase remodelling. Hal ini menyebabkan peningkatan proliferasi fibroblas untuk mensintesis kolagen yang nantinya dapat menjadi parut hipertrofik dan keloid.

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Mamta, Sajwan Khatri. "Implicating transforming growth factor-β and sex steroids in the regulation of brain-gonadal functions." Journal of Reproductive Healthcare and Medicine 3 (December 9, 2022): 9. http://dx.doi.org/10.25259/jrhm_12_2022.

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Transforming growth factor-beta (Tgf-β) significantly mediates TGF signals in the brain and gonadal development. The present study insights into the implication of novel factor Tgf-β and sex steroids in coordination with catecholaminergic activity; moreover, the influence on catecholamines, gonadotropin-releasing hormone (GnRH1), and related transcripts/genes by implanting osmotic pump-mediated mismatches sex steroids in the teleost. The outcome collectively showed the severe effect of estrogenic compounds at the nominal dose over androgenic to alter reproductive conditions. In addition, the differential pattern of key transcription factors/genes revealed significantly higher expression in the brain and gonads than in other organs, which seem to have a role in the hypothalamic-pituitary-gonadal (H-P-G) axis to regulate brain-gonadal functions in catfish. Furthermore, the abundance of crucial factors mRNA and protein expression in the brain suggests a significant role in this correlation. Collectively, the study provides an understanding of the growth factors and sex steroids through dopaminergic system, where upregulated expression levels of GnRH1 vis-a-vis certain brain-related genes, that is, GnRH1, Tgf-β, Gfrα-1, cyp19a1b, tph, and th in teleost revealed their regulatory influence more importantly on the H-P-G axis.

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Hölting, Thomas, Allan E. Siperstein, Orlo H. Clark, and Quan-Yang Duh. "Epidermal growth factor (EGF)- and transforming growth factor alpha-stimulated invasion and growth of follicular thyroid cancer cells can be blocked by antagonism to the EGF receptor and tyrosine kinase in vitro." European Journal of Endocrinology 132, no. 2 (February 1995): 229–35. http://dx.doi.org/10.1530/eje.0.1320229.

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Hölting T, Siperstein AE, Clark OH, Duh Q-Y. Epidermal growth factor (EGF)- and transforming growth factor alpha-stimulated invasion and growth of follicular thyroid cancer cells can be blocked by antagonism to the EGF receptor and tyrosine kinase in vitro. Eur J Endocrinol 1995;132:229–35. ISSN 0804–4643 We have shown recently that epidermal growth factor (EGF) enhanced invasion and growth of differentiated thyroid cancer cells in vitro and in vivo. The present study analyzed the effects of transforming growth factor alpha (TGF-α) on invasion and growth of a follicular thyroid cancer cell line (FTC133) and whether blocking the EGF receptor by a monoclonal antibody (Mab528) or blocking the tyrosine kinase of the receptor by genistein abolished the EGF- and TFG-α-mediated effects. Growth and invasion (penetration of 8-μm pore polycarbonate membranes coated with Matrigel) were determined by the dimethylthiazol-diphenyltetrazolium bromide assay. Epidermal growth factor (10 ng/l) stimulated invasion of FTC133 by 42% and TGF-α (10 ng/l) stimulated invasion of FTC133 by 27% (p < 0.02). Both growth factors also enhanced growth by 62% (EGF) and 30% (TGF-α) (p < 0.003). Epidermal growth factor receptor antibodies (1 μg/ml) abolished EGF-mediated stimulation of invasion and growth completely and that of TGF-α by 93%. At 100 ng/ml genistein reversed EGF and TGF-α stimulation, and at 1 μg/ml it inhibited invasion (27%) and growth (40%) of unstimulated FTC133 (p < 0.02). We conclude that TGF-α stimulates invasion and growth of follicular thyroid cancer by binding to the EGF receptors, that EGF- and TGF-α-mediated effects can be blocked by antagonism to the EGF receptor and to tyrosine kinase, and that genistein not only neutralized EGF and TGF-α effects but also inhibited invasion and growth of unstimulated FTC133. Therefore, tyrosine kinase activity via other signalling systems must be crucial for basal invasion and growth of follicular thyroid cancer cells in culture. Thomas Hölting, Department of Surgery, University of Heidelberg, Im Neuenheimer Feld 110, 69120 Heidelberg, Germany

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DOUTHWAITE, JULIE A., TIMOTHY S. JOHNSON, JOHN L. HAYLOR, PHIL WATSON, and A. MEGUID EL NAHAS. "Effects of Transforming Growth Factor-β1 on Renal Extracellular Matrix Components and Their Regulating Proteins." Journal of the American Society of Nephrology 10, no. 10 (October 1999): 2109–19. http://dx.doi.org/10.1681/asn.v10102109.

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Abstract. Transforming growth factor-β1 (TGF-β1) is widely regarded as a potent fibrogenic renal growth factor. In cell culture, TGF-β1 has been shown to increase various extracellular matrix (ECM) proteins and tissue inhibitors of metalloproteinases (TIMP), while decreasing matrix metalloproteinases (MMP), providing the optimum environment for progressive ECM accumulation. This study, which uses the isolated perfused rat kidney (IPRK), describes for the first time in a whole kidney preparation the action of TGF-β1 on factors associated with ECM processing. This model allows the study of the intact rat kidney with physiologic cell-cell interactions in the absence of confounding systemic influences. Left kidneys were removed from male Wistar rats by a nonischemic technique and perfused with a sterile, apyrogenic, endotoxin-free perfusate, based on the plasma volume expander Hemaccel (polygeline), at constant pressure in a recirculating IPRK system. Kidneys were perfused for 1 h either with (n = 3) or without (n = 3) recombinant human TGF-β1 (20 ng/ml). The effects of perfusion were controlled by comparison with the nonperfused contralateral kidney (n = 6). TGF-β1 was measured in the perfusate and urine, at the start and end of the experiment using an enzyme-linked immunosorbent assay to its biologically active form. After perfusion, sections of the kidneys were analyzed for changes in mRNA by Northern blotting. Significant increases in mRNA for fibronectin (7.5-fold, P < 0.01), heparan sulfate proteoglycan core protein (53-fold, P < 0.001), laminin β1 (12-fold, P < 0.001), collagen α1(IV) (17-fold, P < 0.001), collagen α1(III) (fourfold, P < 0.001), and MMP9 (twofold, P < 0.05) were observed after perfusion with TGF-β1. Measurement of TIMP1, TIMP2, TIMP3, MMP1, and MMP2 mRNA demonstrated no detectable change, whereas determination of mRNA for tissue transglutaminase, an enzyme capable of cross-linking many ECM components, showed an eightfold increase (P < 0.01). This study suggests that in the IPRK and in the absence of other exogenous growth factors, TGF-β1 selectively increases the synthesis of ECM and tissue transglutaminase without changes that would result in the reduction of ECM degradation.

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RAINEY, W. E., D. NAVILLE, J. M. SAEZ, B. R. CARR, W. BYRD, R. R. MAGNESS, and J. I. MASON. "Transforming Growth Factor-β Inhibits Steroid 17α-Hydroxylase Cytochrome P-450 Expression in Ovine Adrenocortical Cells*." Endocrinology 127, no. 4 (October 1990): 1910–15. http://dx.doi.org/10.1210/endo-127-4-1910.

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Kumar, R., and I. Lorimer. "P.106 Thrombospondin 1 mediates transforming growth factor beta induced premature senescence in primary glioblastoma cells." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 43, S2 (June 2016): S45. http://dx.doi.org/10.1017/cjn.2016.207.

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Background: Glioblastoma is the most common primary malignant brain tumor. Primary Glioblastoma (PriGO) cells are key drivers of glioblastoma. Senescence is the irreversible growth arrest of cells with continued metabolic activity. Recently, I discovered PriGO cells undergo premature senescence in response to Fetal Bovine Serum (FBS). Determining the underlying molecular mechanisms may allow development of novel therapeutic strategies to decrease the malignant potential of glioblastoma. Methods: Global gene expression changes in PriGO cells treated with serum were analyzed and compared to untreated cells. Senescence was determined by the Senescence-Associated-Beta-Galactosidase (SA-B-Gal) assay. Results: PriGO cells treated with serum demonstrated increased expression of genes in the Transforming Growth Factor Beta (TGF-B) pathway, such as Thrombospondin 1 (TSP1), compared to untreated cells. TGF-B treatment of PriGO cells significantly increased senescence compared to untreated cells. Treatment of PriGO cells with serum and the TGF-B inhibitor SB431542 led to a decrease in senescence compared to serum only treated cells. Treatment of PriGO cells with serum and the TSP1 inhibitor LSKL led to a reduction in senescence compared to serum only treated cells. Conclusions: Our data identifies TGF-B as an important component of serum responsible for inducing senescence in PriGO cells. Furthermore, TGF-B induced senescence in PriGO cells is in part mediated by TSP1.

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Dohgu, Shinya, Atsushi Yamauchi, Fuyuko Takata, Mikihiko Naito, Takashi Tsuruo, Shun Higuchi, Yasufumi Sawada, and Yasufumi Kataoka. "Transforming Growth Factor- 1 Upregulates the Tight Junction and P-glycoprotein of Brain Microvascular Endothelial Cells." Cellular and Molecular Neurobiology 24, no. 3 (June 2004): 491–97. http://dx.doi.org/10.1023/b:cemn.0000022776.47302.ce.

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Deng, Liang, Ying Li, Jin ming Huang, Guan yu Zhou, Wei Qian, and Ke shu Xu. "Effects of p-CREB-1 on transforming growth factor-β3 auto-regulation in hepatic stellate cells." Journal of Cellular Biochemistry 112, no. 4 (March 11, 2011): 1046–54. http://dx.doi.org/10.1002/jcb.23017.

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Scott, P. G., C. M. Dodd, A. Ghahary, Y. J. Shen, and E. E. Tredget. "Fibroblasts from Post-Burn Hypertrophic Scar Tissue Synthesize Less Decorin than Normal Dermal Fibroblasts." Clinical Science 94, no. 5 (May 1, 1998): 541–47. http://dx.doi.org/10.1042/cs0940541.

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1. Fibroblast cultures were established from biopsies of hypertrophic scar and normal dermis taken from nine patients recovering from second- and third-degree burns. The capacity of these fibroblasts to synthesize the small proteoglycan decorin was assessed by quantitative Western blot analysis of conditioned medium collected from confluent cultures. Levels of mRNA for decorin were assessed by quantitative Northern analysis. Since transforming growth factor-β1 is implicated in various fibrotic conditions, including post-burn hypertrophic scar, its effect on decorin synthesis by these paired fibroblast cell strains was assessed. 2. Production of decorin was lower in all cell strains of hypertrophic scar fibroblasts tested, compared with normal dermal fibroblasts cultured from the same patients (mean 49 ± 23%; P < 0.001, n = 9). Levels of mRNA for decorin were also lower (mean 59 ± 28%; P < 0.02, n = 7) but those for biglycan and versican were not significantly different. Four pairs of cell strains were examined at more than one passage and the differences in decorin protein were found to be phenotypically persistent. Treatment of confluent cultures with transforming growth factor-β1 for 3 days caused a reduction in both decorin protein and mRNA in all six strains of hypertrophic scar fibroblasts tested and in five of six strains of normal dermal fibroblasts. An increase in the length of the dermatan sulphate chain on decorin, a previously reported characteristic of this glycosaminoglycan in hypertrophic scar, was seen in all but two of the strains treated with transforming growth factor-β1. The depression of decorin synthesis by transforming growth factor-β1 was reversed on removal of the agent and passaging the fibroblasts. 3. The reduced capacity of fibroblasts in hypertrophic scar tissue to synthesize decorin may have implications for the development of the condition since this small proteoglycan is involved in tissue organization and may also play a role in modulating the activity in vivo of fibrogenic cytokines such as transforming growth factor-β1.

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Sorokman, T. V., P. M. Moldovan, D. І. Kolіesnik, I. S. Sokolnyk, and O. V. Makarova. "Endogenous polypeptide growth factors in children with duodenal ulcer." Modern pediatrics. Ukraine, no. 2(122) (March 30, 2022): 27–31. http://dx.doi.org/10.15574/sp.2022.122.27.

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Currently, the attention of many researchers is drawn to determine the features of the regeneration of the mucous membrane of the gastrointestinal tract in ulcers, as one of the most important protective factors in this pathology. Purpose - to investigate the indicators of endogenous polypeptides (epidermal growth factor - EGF and transforming growth factor α-TGF-α) in the serum of children with duodenal ulcers. Materials and methods. The study included 56 children aged 7-18 years (36 children with duodenal ulcer - the main group and 20 healthy children (comparison group). The content of endogenous polypeptides in serum was determined by enzyme-linked immunosorbent assay (ELISA) using the Human EGF ELISA Kit (Invitrogen, USA) for EGF and R&D system (USA) for TGF-α according to the manufacturer’s instructions. Statistical processing of the obtained results was carried out using parametric and non-parametric methods of evaluation of the obtained results. Results. Slightly higher levels of EGF and TGF-α were found in boys of both subgroups of the main group (EGF: 561.45 [391.81-699.34] pg/ml and 544.67 [411.23-569.77] pg/ml, p>0.05; TGF-α: 47.91 [21.41-29.69] and 42.56 [35.45-49.21] pg/ml, p>0.05). Concentrations of endogenous factors in exacerbation of ulcerative process are higher than in remission (p<0.001) and in remission does not reach that in healthy children, p<0.01). In patients with severe duodenal ulcers, EGF and TGF-α concentrations are higher (p<0.01), which may be due to the maximum degree of inflammatory-destructive process. Conclusions. The course of duodenal ulcer leads to disorders in the regulation of proliferative processes in the mucous membrane, which is manifested by increased levels of EGF and TGF-α in the serum of sick children, the more severe the course, the higher process. The research was carried out in accordance with the principles of the Helsinki declaration. The study protocol was approved by the Local ethics committee of the participating institution. The informed consent of the patient was obtained for conducting the studies. No conflict of interest was declared by the authors. Key words: children, duodenal ulcer, epidermal growth factor (EGF), transforming growth factor α (TGF-α).

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Nam, Sang Min, Yong-Sun Maeng, Eung Kweon Kim, Kyoung Yul Seo, and Helen Lew. "Ex Vivo Expansion of Human Limbal Epithelial Cells Using Human Placenta-Derived and Umbilical Cord-Derived Mesenchymal Stem Cells." Stem Cells International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/4206187.

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Ex vivo culture of human limbal epithelial cells (LECs) is used to treat limbal stem cell (LSC) deficiency, a vision loss condition, and suitable culture systems using feeder cells or serum without animal elements have been developed. This study evaluated the use of human umbilical cord or placenta mesenchymal stem cells (C-MSCs or P-MSCs, resp.) as feeder cells in an animal/serum-free coculture system with human LECs. C-/P-MSCs stimulated LEC colony formation of the stem cell markers (p63, ABCG2) and secreted known LEC clonal growth factors (keratinocyte growth factor, β-nerve growth factor). Transforming growth factor-β-induced protein (TGFBIp), an extracellular matrix (ECM) protein, was produced by C-/P-MSCs and resulted in an increase in p63+ ABCG2+ LEC colonies. TGFBIp-activated integrin signaling molecules (FAK, Src, and ERK) were expressed in LECs, and TGFBIp-induced LEC proliferation was effectively blocked by a FAK inhibitor. In conclusion, C-/P-MSCs enhanced LEC culture by increasing growth of the LSC population by secreting growth factors and the ECM protein TGFBIp, which is suggested to be a novel factor for promoting the growth of LECs in culture. C-/P-MSCs may be useful for the generation of animal-free culture systems for the treatment of LSC deficiency.

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Journal articles on the topic 'Transforming growth factor-P'

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