Anti-transforming growth factor-β1 antibody transiently enhances DNA synthesis during liver regeneration after partial hepatectomy in rats

2001 ◽  
Vol 8 (3) ◽  
pp. 250-258 ◽  
Author(s):  
Yuta Enami ◽  
Hirohisa Kato ◽  
Masahiko Murakami ◽  
Toshihiro Fujioka ◽  
Takeshi Aoki ◽  
...  
Keyword(s):  
Growth Factor ◽  
Dna Synthesis ◽  
Liver Regeneration ◽  
Partial Hepatectomy ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1

scholarly journals Platelet-induced cell signaling during liver regeneration

2021 ◽  
Vol 108 (Supplement_4) ◽  
Author(s):  
A Balaphas ◽  
J Meyer ◽  
R Perozzo ◽  
M Zeisser Labouebe ◽  
S Berndt ◽  
...  
Keyword(s):  
Growth Factor ◽  
Liver Regeneration ◽  
Partial Hepatectomy ◽  
Transforming Growth Factor ◽  
Fold Increase ◽  
Transforming Growth Factor Β1 ◽  
Remnant Liver ◽  
Liver Sinusoidal Endothelial Cells

Abstract Objective To investigate the mechanisms driving the interaction of platelets with liver sinusoidal endothelial cells (LSEC) during liver regeneration. Methods Platelets were tracked in vivo in mice by intravital confocal microscopy after partial hepatectomy. In vitro, we isolated highly pure mouse LSEC and analyzed their interactions with platelets, hepatic stellate cells (HSC), Kupffer cells and hepatocytes. Results Recruited platelets adhered to LSEC in vivo within the remnant liver segments following partial hepatectomy and were necessary for the interleukin 6 (IL-6) burst that occurred afterwards. In vitro, platelets were activated after incubation with LSEC and released transforming growth factor β1 (TGF-β1), which stimulated LSEC to secrete IL-6 (fold increase of 9.8±0.73 relative to baseline). Antibody-mediated neutralization of TGF-B1 or its downstream SMAD signalling pathway prevented the effects of activated platelets on LSEC. We also demonstrated that IL-6 released by LSEC stimulates HSC to produce hepatocyte growth factor (HGF) a main mitogen for hepatocytes. Conclusion Our results suggest that after hepatectomy, platelets initiate liver regeneration by interacting with LSEC and stimulate IL-6 release, which in turn stimulates HSC to produce HGF.

Influence of epidermal growth factor on liver regeneration after partial hepatectomy in mice

1991 ◽  
Vol 128 (3) ◽  
pp. 425-431 ◽  
Author(s):  
S. Noguchi ◽  
Y. Ohba ◽  
T. Oka
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Dna Synthesis ◽  
Liver Regeneration ◽  
Partial Hepatectomy ◽  
Dna Content ◽  
Sharp Peak ◽  
Submandibular Glands ◽  
Total Liver ◽  
Epidermal Growth

ABSTRACT The role of epidermal growth factor (EGF) in liver regeneration was studied in mice after partial hepatectomy. Two weeks before partial hepatectomy, mice were sham-operated (control) or sialoadenectomized (removal of submandibular glands) to reduce plasma EGF levels. Sialoadenectomized mice showed low plasma EGF levels (29·7 ±6·6 pmol/l; mean ± s.e.m.) compared with controls (66·0±8·3 pmol/l). After partial hepatectomy, sialoadenectomized mice were treated with or without a daily s.c. injection of 5 μg EGF and the rate of DNA synthesis in the regenerating liver was monitored by [125I]iododeoxyuridine uptake. Control mice showed a sharp peak of DNA synthesis at 48 h after partial hepatectomy while sialoadenectomized mice showed a delayed and broad peak at 84 h. Treatment of sialoadenectomized mice with EGF (5 μg/mouse per day) completely restored the pattern of DNA synthesis so that a sharp peak appeared at 48 h. The total liver DNA content of the control mice (79·1±2·5% of the preoperative level; mean ± s.e.m.) was significantly (P < 0·01) higher than that of the sialoadenectomized mice (65·2±3·0%) 3 days after partial hepatectomy, but this difference disappeared on day 7 when liver regeneration was almost completed in both groups. Treatment of sialoadenectomized mice with EGF increased total liver DNA content (78·2±2·9%) to that of control mice on day 3 after partial hepatectomy. In addition, normal mice showed a rapid increase in plasma EGF levels at 1–8 h after partial hepatectomy, whereas sialoadenectomized mice showed low plasma EGF levels throughout the course of the experiment. These results suggest that EGF derived from the submandibular glands plays a role in promoting the early stage of liver regeneration. Journal of Endocrinology (1991) 128, 425–431

Epidermal growth factor secreted from the salivary gland is necessary for liver regeneration

1995 ◽  
Vol 268 (5) ◽  
pp. G872-G878 ◽  
Author(s):  
D. E. Jones ◽  
R. Tran-Patterson ◽  
D. M. Cui ◽  
D. Davin ◽  
K. P. Estell ◽  
...  
Keyword(s):  
Salivary Gland ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Dna Synthesis ◽  
Liver Regeneration ◽  
Salivary Glands ◽  
Partial Hepatectomy ◽  
Cellular Proliferation ◽  
Remnant Liver ◽  
Epidermal Growth

Partial hepatectomy (PH) in rats induces a synchronized burst of DNA replication in the remnant liver that peaks at 24 h post-PH. We report here that removal of the major salivary glands before one-third and two-thirds PH prevents the proliferative response in the remaining liver. Twelve days after one-third PH, the remnant liver is 89% of the normal liver weight in nonsalivectomized rats but only 55% in salivectomized animals. This indicates that salivectomy does not merely delay the first round of cell division but that it prevents actual regeneration. Salivectomy alters the early protooncogene response to partial hepatectomy. In salivectomized rats, the characteristic peak of c-myc mRNA synthesis at 2-4 h after PH is significantly decreased compared with nonsalivectomized rats. The peak of DNA synthesis at 24 h after PH in salivectomized rats is also dramatically decreased. DNA synthesis as measured by [3H]thymidine incorporation into DNA of hepatic cells is decreased approximately 90% in salivectomized rats vs. nonsalivectomized rats 22-26 h after PH. Ligation of the venous drainage of the salivary gland results in the same inhibitory effect on DNA synthesis, indicating 1) that the salivary gland must release circulating factor(s), and 2) that the early increase in c-myc expression and the subsequent DNA synthesis, both of which reflect the stimulation of cellular proliferation in the regenerating liver, are induced by humoral factor(s) released from the salivary glands. Injection of exogenous epidermal growth factor (EGF) in salivectomized rats results in restoration of both the DNA synthetic and c-myc responses at levels characteristic of those of liver regeneration.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Redox regulation of renal DNA synthesis, transforming growth factor-β1 and collagen gene expression

1998 ◽  
Vol 53 (2) ◽  
pp. 367-381 ◽  
Author(s):  
Karl A. Nath ◽  
Joseph Grande ◽  
Anthony Croatt ◽  
James Haugen ◽  
Youngki Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Dna Synthesis ◽  
Redox Regulation ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Collagen Gene ◽  
Collagen Gene Expression

scholarly journals Augmenter of liver regeneration ameliorates renal fibrosis in rats with obstructive nephropathy

2014 ◽  
Vol 34 (5) ◽  
Author(s):  
Guo-tao Chen ◽  
Ling Zhang ◽  
Xiao-hui Liao ◽  
Ru-yu Yan ◽  
Ying Li ◽  
...  
Keyword(s):  
Growth Factor ◽  
Liver Regeneration ◽  
Renal Fibrosis ◽  
Transforming Growth Factor ◽  
Interstitial Fibrosis ◽  
Transforming Growth Factor Β1 ◽  
Obstructive Nephropathy ◽  
Tubular Atrophy ◽  
Augmenter Of Liver Regeneration ◽  
Smad3 Phosphorylation

Renal fibrosis is a hallmark in CKD (chronic kidney disease) and is strongly correlated to the deterioration of renal function that is characterized by tubulointerstitial fibrosis, tubular atrophy, glomerulosclerosis and disruption of the normal architecture of the kidney. ALR (augmenter of liver regeneration) is a growth factor with biological functions similar to those of HGF (hepatocyte growth factor). In this study, our results indicate that endogenous ALR is involved in the pathological progression of renal fibrosis in UUO (unilateral ureteral obstruction) rat model. Moreover, we find that administration of rhALR (recombinant human ALR) significantly alleviates renal interstitial fibrosis and reduces renal-fibrosis-related proteins in UUO rats. Further investigation reveals that rhALR suppresses the up-regulated expression of TGF-β1 (transforming growth factor β1) induced by UUO operation in the obstructed kidney, and inhibits Smad2 and Smad3 phosphorylation activated by the UUO-induced injury in the animal model. Therefore we suggest that ALR is involved in the progression of renal fibrosis and administration of rhALR protects the kidney against renal fibrosis by inhibition of TGF-β/Smad activity.

Transforming growth factor-β1 (TGF-β1) inhibits DNA synthesis of PWM-stimulated PBMC via suppression of IL-2 and IL-6 production

Cytokine ◽  
1994 ◽  
Vol 6 (4) ◽  
pp. 382-388 ◽  
Author(s):  
D. Reinhold ◽  
U. Bank ◽  
F. Bühling ◽  
U. Lendeckel ◽  
A.J. Ulmer ◽  
...  
Keyword(s):  
Growth Factor ◽  
Dna Synthesis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Tgf Β1
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