Increased ΤGF-β3 in primary biliary cirrhosis: An abnormality related to pathogenesis?

Voumvouraki, Argyro; Koulentaki, Mairi; Tzardi, Maria; Sfakianaki, Ourania; Manousou, Pinelopi; Notas, George

doi:10.3748/wjg.v16.i40.5057

Cited by 9 publications

(11 citation statements)

References 49 publications

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“…Cirrhotic liver tissue samples from human patients showed increased expressions of Tgfb1, Tgfb2 and Tgfb3 mRNAs, of which Tgfb3 showed the highest level of expression in human liver cirrhosis (23). The up-regulation of Tgfb3 mRNA was also observed in livers of patients with primary biliary cirrhosis but not in livers of patients with viral cirrhosis (24). These earlier reports as well as our recent report (25) pointed out the possibility of the involvement of biliary epithelial cells in liver cirrhosis.…”

Section: Discussionsupporting

confidence: 59%

“…For example, retinoid signaling up-regulates TGF-β signaling by inducing the plasminogen activator, which proteolytically converts the latent form of TGF-β to an active form (22). Several former reports stated the importance of TGF-β3 in the pathogenesis of liver cirrhosis (23,24). Cirrhotic liver tissue samples from human patients showed increased expressions of Tgfb1, Tgfb2 and Tgfb3 mRNAs, of which Tgfb3 showed the highest level of expression in human liver cirrhosis (23).…”

Section: Discussionmentioning

confidence: 99%

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Elevated expression of transforming growth factor β3 in carbon tetrachloride-treated rat liver and involvement of retinoid signaling

Mezaki

Morii²,

Yoshikawa³

et al. 2011

Int J Mol Med

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Abstract. Transforming growth factor (TGF) β is a pro-fibrotic cytokine. While three isoforms (TGF-β1, 2 and 3) are known, the functional differences between them are obscure. To investigate the roles of TGF-β isoforms during liver fibrogenesis, male Wistar rats were administrated carbon tetrachloride (CCl 4 ) subcutaneously twice a week for two months. Livers were excised and sectioned for histochemical examinations. These livers were also used to quantitate the expression of genes associated with fibrogenesis, including TGF-β isoforms, as well as those associated with retinoid metabolism. Expression levels of Tgfb1 and Tgfb3 were up-regulated in CCl 4 -treated rat livers while that of Tgfb2 was not changed. The mRNAs for lecithin-retinol acyltransferase (Lrat) and retinoic acid hydroxylase, Cyp26a1, were also elevated. By immunohistochemical staining, TGF-β3 protein was found to be localized mainly in liver parenchymal cells (hepatocytes). These results indicate that retinoid mobilization likely takes place within the rat's liver following CCl 4 treatment, and suggest the possibility that the expression of Tgfb mRNA is regulated by retinoic acid receptors. Reporter analyses of a region of the Tgfb3 gene were performed using the rat liver parenchymal cell line, RLC-16, and a positively responsive region was identified within its intron.

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Elevated expression of transforming growth factor β3 in carbon tetrachloride-treated rat liver and involvement of retinoid signaling

Mezaki

Morii²,

Yoshikawa³

et al. 2011

Int J Mol Med

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“…IIF analysis was performed as previously described [24] . Briefly, antigen retrieval was achieved by incubation with citrate buffer (1.8 mmol/L citric acid and 8.2 mmol/L sodium citrate) for 2 h at 37 ℃.…”

Section: Indirect Immunofluorescence Analysis Of Paraffin-embedded Sementioning

confidence: 99%

Presence of disease specific autoantibodies against liver sinusoidal cells in primary biliary cirrhosis

Sfakianaki¹,

Tzardi²,

Voumvouraki³

et al. 2013

WJH

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“…An increase in TGF-β3 is a characteristic of PBC irrespective of stage and therefore it may be pathogenetically important. Results from the hepatic vein samples indicate that the liver seems to be the source of the TGF-β abnormalities [119] . Plasma levels of IL-6 are decreased in PBC [120] but monocytes from PBC patients secrete more IL-1 and IL-6 after in vitro challenge with TLR ligands [109] and increased liver expression of IL-6 was described in PBC [117] .…”

Section: Cytokines In Pbcmentioning

confidence: 99%

Primary biliary cirrhosis: From bench to bedside

Notas

2015

WJGPT

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Primary biliary cirrhosis (PBC) is a chronic nonsuppurative destructive intrahepatic cholangitis leading to cirrhosis after a protractive non cirrhotic stage. The etiology and pathogenesis are largely unknown and autoimmne mechanisms have been implicated to explain the pathological lesions. Many epitopes and autoantigens have been reported as crucial in the pathophysiology of the disease and T and B cells abnormalities have been described, the exact pathways leading to the destruction of small intrahepatic ductules are mostly speculative. In this review we examined the various epidemiologal and geoepidemiological data as well as the complex pathogenetic aspects of this disease, focusing on recent in vivo and in vitro studies in this field. Initiation and progression of PBC is believed to be a multifactorial process with strong infuences from the patient's genetic background and by various environmental factors. The role of innate and adaptive immunity, including cytokines, chemokines, macrophages and the involvement of apoptosis and reactive oxygen species are outlined in detailed. The current pathogenetic aspects are presented and a novel pathogenetic theory unifying the accumulated clinical information with in vitro and in vivo data is formulated.A review of clinical manifestations and immunological and pathological diagnosis was presented. Treatment modalities, including the multiple mechanisms of action of ursodeoxycholate were finally discussed. Core tip: Primary biliary cirrhosis (PBC) is a chronic nonsuppurative destructive intrahepatic cholangitis leading to cirrhosis of largely unknown pathophysiology. We examined the epidemiological and geoepidemiological data as well as the pathogenetic aspects of PBC. A novel pathogenetic theory unifying the accumulated clinical information with in vitro and in vivo data is formulated.

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Increased ΤGF-β3 in primary biliary cirrhosis: An abnormality related to pathogenesis?

Abstract: The serum profile of TGF-β isoforms is different in cirrhotics. Increased TGF-β3 is characteristic of PBC. These findings may be related to the immunological abnormalities of PBC.

Cited by 9 publications

References 49 publications

Elevated expression of transforming growth factor β3 in carbon tetrachloride-treated rat liver and involvement of retinoid signaling

Elevated expression of transforming growth factor β3 in carbon tetrachloride-treated rat liver and involvement of retinoid signaling

Presence of disease specific autoantibodies against liver sinusoidal cells in primary biliary cirrhosis

Primary biliary cirrhosis: From bench to bedside

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