229. Identification of transforming growth factor beta2 (TGF-β2) and its receptors TGF-βRI and TGF-βRII in the possum (Trichosurus vulpecula) prostate: evidence of seasonal changes

2008 ◽  
Vol 20 (9) ◽  
pp. 29
Author(s):  
H. Martyn ◽  
K. Pugazhenthi ◽  
B. McLeod ◽  
H. D. Nicholson
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Stromal Cells ◽  
Seasonal Changes ◽  
Transforming Growth Factor ◽  
Brushtail Possum ◽  
Trichosurus Vulpecula ◽  
Western Blots ◽  
Prostate Growth

Benign Prostatic Hyperplasia is an enlargement of the prostate affecting the ageing male population. The common Brushtail possum (Trichosurus vulpecula) has been identified as a possible model to study factors regulating prostate growth because its prostate grows and regresses seasonally. Transforming growth factor Beta 2 (TGF-β2) is present in human prostatic tissue. In vitro, TGF-β inhibits epithelial cell, but stimulates stromal cell proliferation (Mori et al. 1990). TGF-β2 binds to TGF-β receptor II (TGF-βRII), which then recruits the type 1 receptor (TGF-βRI) (Saez et al. 1998) The aim of this study was to identify any seasonal changes in expression of TGF-β2 and its receptors in the possum prostate. Six wild-caught possums were sacrificed in each of the months of January, March, May, July, September and November. The prostates were divided into a cranial and caudal region and immunohistochemistry and Western Blot analysis performed. In each animal the glandular and periurethral areas of the caudal and cranial prostates were examined separately. Immunohistochemistry identified the presence of TGF-β2 in both the stromal and epithelial cells of the glandular and periurethral areas of the cranial and caudal regions. In the cranial tissue, more immuno-positive stromal cells than epithelial cells were present, whereas in the caudal tissue immuno-reactivity was predominantly localised to the epithelial cells. Analysis of the western blots suggested that TGF-β2 expression was lowest immediately before and during the breeding season (March, May). Both TGF-βRI and TGF-βRII were identified in all regions of the prostate. Furthermore, immunohistochemistry revealed that the receptors were co-localised in the epithelial and stromal cells in all areas. TGF-β2 and its receptors are present in the possum prostate. TGF-β2 localisation varies between the caudal and cranial regions and as predicted from in vitro experiments TGF-β2 expression decreases during prostate growth. (1) Mori H. et al. (1990). The Prostate, 16, 71 - 80. (2) Saez C. et al. (1998). The Prostate, 37, 84 - 90.

Transforming growth factor-β3 protection of epithelial cells from cycle-selective chemotherapy in vitro

1997 ◽  
Vol 53 (8) ◽  
pp. 1149-1159 ◽  
Author(s):  
E.Siobhan McCormack ◽  
Gary V. Borzillo ◽  
Claire Ambrosino ◽  
Gilda Mak ◽  
Laurie Hamablet ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Transforming Growth Factor ◽  
Selective Chemotherapy

Insulin modulation of bronchial epithelial cell fibronectin in vitro

1995 ◽  
Vol 268 (2) ◽  
pp. L230-L238 ◽  
Author(s):  
D. J. Romberger ◽  
P. Pladsen ◽  
L. Claassen ◽  
M. Yoshida ◽  
J. D. Beckmann ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Bronchial Epithelial Cell ◽  
Chemotactic Factor ◽  
Tgf Beta ◽  
Bronchial Epithelial

Fibronectin (Fn) is involved in the migration of epithelial cells in re-epithelialization of wounds. Epithelial cell-derived Fn is particularly potent as a chemotactic factor for bronchial epithelial cells (BECs) in vitro. Thus modulation of airway epithelial cell Fn may be a key aspect of airway repair. Insulin is both an important growth factor and known chemotactic factor for cultured BECs. We postulated that insulin may modulate Fn production of cultured BECs. We examined this hypothesis utilizing bovine BECs in culture with serum-free media with and without insulin. BECs grown in media without insulin released more Fn into culture supernatants and contained more Fn in cell layers than cells grown with insulin. Labeling of cells with [35S]methionine demonstrated an increase in new protein production and Fn mRNA expression was increased. Increased Fn in BEC cultures without insulin was associated with an increase in active transforming growth factor-beta (TGF-beta) release as measured by a standard bioassay. Increased BEC Fn in cultures without insulin was partially inhibited by exposure of cultures to TGF-beta antibody. Thus insulin appears to modulate BEC Fn production in vitro in part through a TGF-beta-dependent mechanism. Insulin may be involved in airway repair mechanisms through modulation of epithelial cell Fn production.

scholarly journals PM2.5 Induced the Expression of Fibrogenic Mediators via HMGB1-RAGE Signaling in Human Airway Epithelial Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Weifeng Zou ◽  
Fang He ◽  
Sha Liu ◽  
Jinding Pu ◽  
Jinxing Hu ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Transforming Growth Factor ◽  
Motor Vehicle ◽  
Airway Remodeling ◽  
High Mobility ◽  
Airway Epithelial Cells ◽  
Sprague Dawley ◽  
Vehicle Exhaust

Background. The aim of the present study was to test whether fine particulate matter (PM2.5) induces the expression of platelet-derived growth factor-AB (PDGF-AB), PDGF-BB, and transforming growth factor-β1 (TGF-β1) in human bronchial epithelial cells (HBECs) in vitro via high-mobility group box 1 (HMGB1) receptor for advanced glycation end products (RAGE) signaling.Methods. Sprague-Dawley rats were exposed to motor vehicle exhaust (MVE) or clean air. HBECs were either transfected with a small interfering RNA (siRNA) targeting HMGB1 or incubated with anti-RAGE antibodies and subsequently stimulated with PM2.5.Results. The expression of HMGB1 and RAGE was elevated in MVE-treated rats compared with untreated rats, and PM2.5 increased the secretion of HMGB1 and upregulated RAGE expression and the translocation of nuclear factor κB (NF-κB) into the nucleus of HBECs. This activation was accompanied by an increase in the expression of PDGF-AB, PDGF-BB, and TGF-β1. The HMGB1 siRNA prevented these effects. Anti-RAGE antibodies attenuated the activation of NF-κB and decreased the secretion of TGF-β1, PDGF-AB, and PDGF-BB from HBECs.Conclusion. PM2.5 induces the expression of TGF-β1, PDGF-AB, and PDGF-BB in vitro via HMGB1-RAGE signaling, suggesting that this pathway may contribute to the airway remodeling observed in patients with COPD.

Effects of epidermal growth factor and transforming growth factor alpha on the mouse trophoblast outgrowth in vitro

1995 ◽  
Vol 133 (6) ◽  
pp. 741-746 ◽  
Author(s):  
Toshifumi Machida ◽  
Michiyoshi Taga ◽  
Hiroshi Minaguchi
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Conditioned Medium ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Alpha ◽  
Epidermal Growth ◽  
Factor Alpha ◽  
Endometrial Epithelial Cells

Machida T, Taga M, Minaguchi H. Effects of epidermal growth factor and transforming growth factor alpha on the mouse trophoblast outgrowth in vitro. Eur J Endocrinol 1995;133:741–6. ISSN 0804–4643 In order to analyze the involvement of growth factors in the implantation mechanism, we examined the direct effects of epidermal growth factor (EGF) and transforming growth factor alpha (TGF-α) on trophoblast outgrowth of the mouse blastocyst in vitro. ICR mouse blastocysts were cultured for 4 days on a culture plate in medium containing EGF or TGF-α or conditioned medium obtained from cultured endometrial epithelial cells. Blastocysts were also co-cultured with endometrial epithelial cells. The trophoblast outgrowth of these cultured blastocysts was observed daily and the percentage of outgrowing embryos was calculated and analyzed statistically by the chi-squared test. Analysis for the specific binding of 125I-EGF in outgrown trophoblasts was carried out by autoradiography. The coculture (days 3 and 4) and the presence of EGF (10 ng/ml, day 4), TGF-α (1 ng/ml, day 3; 10 ng/ml, days 2 and 3; 50 ng/ml, days 2–4) or conditioned medium (days 3 and 4) significantly stimulated the rate of trophoblast outgrowth. Preincubation of the conditioned medium with monoclonal anti-EGF or anti-TGF-α antibody suppressed the stimulatory effect of the conditioned medium on trophoblast outgrowth. The specific 125I-EGF binding in outgrown trophoblasts was demonstrated by autoradiography. These results suggest that EGF and TGF-α play an important role in the implantation process by directly stimulating trophoblast development. Michiyoshi Taga, Department of Obstetrics and Gynecology, Yokohama City University School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236, Japan

scholarly journals Diabetic Kidney Disease Alters the Transcriptome and Function of Human Adipose-Derived Mesenchymal Stromal Cells but Maintains Immunomodulatory and Paracrine Activities Important for Renal Repair

2021 ◽  
Author(s):  
LaTonya J. Hickson ◽  
Alfonso Eirin ◽  
Sabena M. Conley ◽  
Timucin Taner ◽  
Xiaohui Bian ◽  
...  
Keyword(s):  
Growth Factor ◽  
Kidney Disease ◽  
Stromal Cells ◽  
Diabetic Kidney Disease ◽  
Transforming Growth Factor ◽  
Inflammatory Marker ◽  
Patient Characteristics ◽  
Rna Seq ◽  
Diabetic Kidney

<a>Mesenchymal stem/stromal cells (MSC) facilitate repair in experimental diabetic kidney disease (DKD). However, the hyperglycemic and uremic milieu may diminish regenerative capacity of patient-derived therapy. We hypothesized that DKD reduces human MSC paracrine function. Adipose-derived MSC from 38 DKD participants and 16 controls were assessed for cell surface markers, tri-lineage differentiation, RNA-sequencing (RNA-seq), <i>in vitro</i> function (co-culture or conditioned medium experiments with T cells and human kidney cells [HK-2]), secretome profile, and cellular senescence abundance. The direction of association between MSC function and patient characteristics were also tested. RNA-seq analysis identified 353 differentially expressed genes and downregulation of several immunomodulatory genes/pathways in DKD- <i>vs</i>. Control-MSC. DKD-MSC phenotype, differentiation, and tube formation capacity were preserved but migration was reduced. DKD-MSC with and without interferon-γ priming inhibited T-cell proliferation greater than Control-MSC. DKD-MSC-medium contained higher levels of anti-inflammatory cytokines (indoleamine 2,3-deoxygenase-1 and prostaglandin-E2) and pro-repair factors (hepatocyte growth factor and stromal cell-derived factor-1) but lower Interleukin-6 vs. Control-MSC-medium. DKD-MSC-medium protected high glucose plus transforming growth factor-β-exposed HK-2 cells by reducing apoptotic, fibrotic and inflammatory marker expression. Few DKD-MSC functions were affected by patient characteristics including age, gender, body mass index, hemoglobin A1c, kidney function or urine albumin excretion. However, senescence-associated-β-galactosidase activity was lower in DKD-MSC from participants on metformin therapy. Therefore, while </a><a>DKD altered the transcriptome and migratory function of culture-expanded MSC, DKD-MSC functionality, trophic factor secretion and immunomodulatory activities contributing to repair remained intact. </a>These observations support testing patient-derived MSC therapy and may inform preconditioning regimens in DKD clinical trials.

scholarly journals Diabetic Kidney Disease Alters the Transcriptome and Function of Human Adipose-Derived Mesenchymal Stromal Cells but Maintains Immunomodulatory and Paracrine Activities Important for Renal Repair

2021 ◽  
Author(s):  
LaTonya J. Hickson ◽  
Alfonso Eirin ◽  
Sabena M. Conley ◽  
Timucin Taner ◽  
Xiaohui Bian ◽  
...  
Keyword(s):  
Growth Factor ◽  
Kidney Disease ◽  
Stromal Cells ◽  
Diabetic Kidney Disease ◽  
Transforming Growth Factor ◽  
Inflammatory Marker ◽  
Patient Characteristics ◽  
Rna Seq ◽  
Diabetic Kidney

<a>Mesenchymal stem/stromal cells (MSC) facilitate repair in experimental diabetic kidney disease (DKD). However, the hyperglycemic and uremic milieu may diminish regenerative capacity of patient-derived therapy. We hypothesized that DKD reduces human MSC paracrine function. Adipose-derived MSC from 38 DKD participants and 16 controls were assessed for cell surface markers, tri-lineage differentiation, RNA-sequencing (RNA-seq), <i>in vitro</i> function (co-culture or conditioned medium experiments with T cells and human kidney cells [HK-2]), secretome profile, and cellular senescence abundance. The direction of association between MSC function and patient characteristics were also tested. RNA-seq analysis identified 353 differentially expressed genes and downregulation of several immunomodulatory genes/pathways in DKD- <i>vs</i>. Control-MSC. DKD-MSC phenotype, differentiation, and tube formation capacity were preserved but migration was reduced. DKD-MSC with and without interferon-γ priming inhibited T-cell proliferation greater than Control-MSC. DKD-MSC-medium contained higher levels of anti-inflammatory cytokines (indoleamine 2,3-deoxygenase-1 and prostaglandin-E2) and pro-repair factors (hepatocyte growth factor and stromal cell-derived factor-1) but lower Interleukin-6 vs. Control-MSC-medium. DKD-MSC-medium protected high glucose plus transforming growth factor-β-exposed HK-2 cells by reducing apoptotic, fibrotic and inflammatory marker expression. Few DKD-MSC functions were affected by patient characteristics including age, gender, body mass index, hemoglobin A1c, kidney function or urine albumin excretion. However, senescence-associated-β-galactosidase activity was lower in DKD-MSC from participants on metformin therapy. Therefore, while </a><a>DKD altered the transcriptome and migratory function of culture-expanded MSC, DKD-MSC functionality, trophic factor secretion and immunomodulatory activities contributing to repair remained intact. </a>These observations support testing patient-derived MSC therapy and may inform preconditioning regimens in DKD clinical trials.

scholarly journals Transforming Growth Factor-β Mediates Intestinal Healing and Susceptibility to Injury in Vitro and in Vivo Through Epithelial Cells

2003 ◽  
Vol 162 (2) ◽  
pp. 597-608 ◽  
Author(s):  
Paul L. Beck ◽  
Ian M. Rosenberg ◽  
Ramnik J. Xavier ◽  
Theodore Koh ◽  
Josée F. Wong ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β
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