Up‐regulation of endoglin, a TGF‐β‐binding protein, in rats with experimental renal fibrosis induced by renal mass reduction

Rodríguez-Peña, Ana B.; Prieto, Marta; Düwel, Annette; Rivas, Juan V.; Eleno, Nélida; Pérez‐Barriocanal, Fernando; Arévalo, Miguel; Smith, Joshua D.; Vary, Calvin P.H.; Bernabéu, Carmelo; López‐Novoa, José M.

doi:10.1093/ndt/16.suppl_1.34

Cited by 57 publications

(55 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This study also detected a marked increase in hepatic endoglin expression after BDL. These results agree with previous studies reporting endoglin overexpression in animal models of organ fibrosis [27,28]. After BDL, endoglin is clearly expressed in non-parenchymal cells.…”

Section: Discussionsupporting

confidence: 93%

“…In other experimental model of organ fibrosis such as unilateral ureteral obstruction [27] results shown that the absolute level of endoglin is not critical for the renal fibrosis process. This negative result might be explained by the fact that endoglin and TGF-1 protein and receptors are not coexpressed in the same cell type.…”

Section: Mock-so Mock-bdl End-so End-bdlmentioning

confidence: 95%

“…Endoglin binds TGF-1 and TGF-3 with high affinity in human endothelial cells [25], in association with the type II receptor [26]. We have reported that endoglin is upregulated in several models of renal fibrosis in rats and mice [27,28]. Endoglin has been also shown to be upregulated in other fibrotic tissues [29,30].…”

mentioning

confidence: 99%

See 2 more Smart Citations

Endoglin Upregulation in the Liver after Bile Duct Ligation in Rats

Pérez‐Barriocanal¹

2011

TOGASJ

View full text Add to dashboard Cite

Abstract:Background: Transforming growth factor beta 1 (TGF-1) has been implicated in the stimulation of extracellular matrix synthesis in acute and chronic liver disease. Endoglin (CD-105) is a membrane glycoprotein that binds TGF-1 with high affinity. Endoglin is overexpressed in several model of fibrosis. The goal of the present study was to evaluate the effect of bile duct ligation (BDL) on endoglin expression and the effect of endoglin overexpression on liver fibrosis in rats.Methods: Rat livers were transfected with a vector containing full length human endoglin (h-end) or an empty vector (mock) and 48 hours after were subjected to either BDL or sham operation (SO). Eighteen days after, a blood sample was obtained and bilirubin and serum enzyme activities were measured to assess liver damage. Liver fibrosis was quantified by a computer-assisted image analysis of Sirius red stained livers and by liver hydroxyproline content. Endoglin expression in the liver tissue was assessed by Western blot and immunohystochemistry.Results: Both immunohistochemistry and Western blot reveals endoglin upregulation after BDL in rats. In addition, these techniques also reveal effective human endoglin transfection in the rat's liver. After BDL, liver fibrosis and plasma levels of enzymes were similar in h-end transfected and mock-transfected rats. Western blots showed higher endoglin expression after BDL in h-end transfected and mock-transfected rats. Conclusions:The present study provides clear evidence that endoglin is upregulated in the liver of rats with BDL. h-end overexpression did not improve liver fibrosis after BDL in rats.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Mock-so Mock-bdl End-so End-bdlmentioning

confidence: 95%

See 1 more Smart Citation

Endoglin Upregulation in the Liver after Bile Duct Ligation in Rats

Pérez‐Barriocanal¹

2011

TOGASJ

View full text Add to dashboard Cite

show abstract

“…Progression of CKD is evidenced by the loss of renal cells and their replacement by extracellular matrix (ECM) (5, 7) in glomeruli and interstitium. Chronic glomerulonephritis, tubulointerstitial disease, hypertension, or diabetic nephropathy (8), occurring independently of the associated disease, arise as a consequence of increased synthesis/reduced degradation of ECM (5,7,9). The pathogenesis of glomerulosclerosis has strong similarities to the pathogenesis of tubulointerstitial fibrosis.…”

Section: Renal Fibrosis: Aetiology and Pathophysiologymentioning

confidence: 99%

“…TGFβ1 is extensively expressed in all cells of the kidney, particularly in glomeruli, where the levels are several times those in the kidney as a whole (20), or expressed by macrophages that invade the kidney (15). TGFβ plays a pivotal role in renal fibrogenesis (7,11,20,35), indeed the kidney is particularly susceptible to the overexpression of TGFβ (32).…”

Section: Transforming Growth Factor βmentioning

confidence: 99%

Pathophysiological Mechanisms of Renal Fibrosis: A Review of Animal Models and Therapeutic Strategies

2017

View full text Add to dashboard Cite

Abstract. Chronic kidney disease (CKD) is a long-term condition in which theChronic kidney disease (CKD) represents a serious hazard to human health, and has a high prevalence. In developed countries, it is estimated that more than 10% of adults present some degree of CKD (1). Despite a varied initial evolution, which is related to the diversity of its aetiologies -namely genetics, autoimmune-related infections, environmental factors, diet, and drugs -progressive renal disease frequently results in renal fibrosis and finally in renal failure. The mechanisms implicated in renal fibrosis are still poorly understood, and existing therapies are ineffective or only slightly successful, hence it is essential to understand the pathophysiological mechanisms underlying the usual development of CKD, and to discover and better understand new strategies for treating this disease. In order to study the biopathology of this disease and to evaluate new treatments, animal models are required. The perfect animal model for renal disease research should have human-like renal anatomy, haemodynamics and physiology, as well as enabling the determination of relevant renal, biochemical and haemodynamic parameters. In all probability, no species can consistently meet all these requirements, and the experimental plan and other constraints often determine the choice of animal models for particular research applications. With this in mind, this review aims to describe and analyze animal models of renal fibrosis and suggest new areas of research. Renal Fibrosis: Aetiology and PathophysiologyDiabetes and hypertension are currently the two principal causes of CKD (2), among other causes such as infectious glomerulonephritis, renal vasculitis, ureteral obstruction, genetic alterations, autoimmune diseases (1) and drugs (3, 4). In general, diabetes causes glomerular hypertension by reducing the afferent arteriolar resistance while stimulating the efferent arterioles (2). Thus, elevated glomerular capillary pressure is one of the major factors in progressive renal sclerosis (5). Diabetes and hypertension gradually lead to glomerular expansion, which causes endothelial dysfunction and haemodynamic changes: loss of the glomerular basement membrane electric charge and its thickening, a decreased number of podocytes, foot-process effacement and mesangial distension have been shown to 1

show abstract

TGF-β receptors: Assembly, signalling, and disease relevance

Krishnaveni¹,

Eickelberg²

2006

Signal Transduction

View full text Add to dashboard Cite

TGF‐β superfamily members exert their biological effects by binding to type I, type II and type III cell surface receptors. While the type I and type II receptors entail serine/threonine kinase domains and form signalling entities upon ligand binding, the type III receptors represent accessory receptors with no discernible kinase function identified to date. In TGF‐β signalling, a heterotetrameric complex of the type I and II receptors is induced upon ligand binding, which promotes signal transduction through intracellular Smad proteins. Recent studies have indicated that type I and type II oligomerisation dynamics, which mainly serve to promote signalling purposes of TGF‐β ligands, can also exert functional antagonism and negative regulation of ligand‐induced signalling. The purpose of this review is to supply a detailed description of the TGF‐β ligand‐receptor network and oligomerisation patterns induced thereby, with special emphasis on the emerging and non‐redundant roles of the accessory receptors of the TGF‐β ligands in modulating receptor assembly and biological effects.

show abstract

Up‐regulation of endoglin, a TGF‐β‐binding protein, in rats with experimental renal fibrosis induced by renal mass reduction

Abstract: The present study demonstrates increased endoglin expression in rats with severe hypertension and renal damage. This increased endoglin expression coincides with the period of higher renal damage and renal dysfunction.

Cited by 57 publications

References 0 publications

Endoglin Upregulation in the Liver after Bile Duct Ligation in Rats

Endoglin Upregulation in the Liver after Bile Duct Ligation in Rats

Pathophysiological Mechanisms of Renal Fibrosis: A Review of Animal Models and Therapeutic Strategies

TGF-β receptors: Assembly, signalling, and disease relevance

Contact Info

Product

Resources

About