Endoglin Expression in Human and Rat Mesangial Cells and Its Upregulation by TGF-β1

Rodríguez-Barbero, Alicia; Obreo, Juana; Eleno, Nélida; Rodríguez-Peña, Ana B.; Düwel, Annette; Jerkić, Mirjana; Sánchez‐Rodríguez, Ángel; Bernabéu, Carmelo; López‐Novoa, José M.

doi:10.1006/bbrc.2001.4526

Cited by 47 publications

(51 citation statements)

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“…Moreover, it has been shown in both cell types that BMP-7 directly interferes with profibrogenic TGF-␤1 signaling (57,64). Because endoglin is also expressed by mesangial and hepatic stellate cells (43,65), it is tempting to speculate that endoglin is a critical modifier of fibrogenic responses. The cells were then stimulated with indicated concentrations of TGF-␤1, and the luciferase activities were measured.…”

Section: Discussionmentioning

confidence: 99%

Endoglin Differentially Modulates Antagonistic Transforming Growth Factor-β1 and BMP-7 Signaling

Scherner

Meurer

Tihaa

et al. 2007

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Endoglin Differentially Modulates Antagonistic Transforming Growth Factor-β1 and BMP-7 Signaling

Scherner

Meurer

Tihaa

et al. 2007

Journal of Biological Chemistry

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“…Animal models of experimental liver fibrosis, such as carbon tetrachloride-induced fibrosis [46], bile duct ligation [31] or schistosomiasis infection [11] have reported increased concentrations of TGF-1 very early in the course of fibrogenesis in these animal models. TGF-1-induced endoglin expression has been shown in cultured human monocytes and in the U-937 monocyte line [47], and in cultured mesangial cells [24]. Whereas mesangial cell is major profibrogenic cell in the kidney, hepatic stellate cells is the most profibrogenic cell type in the liver, and endoglin has been reported to be present in hepatic stellate cells, which are a target for TGF-1 [48].…”

Section: Discussionmentioning

confidence: 99%

“…Endoglin, also known as CD105, is a 180-kD homodimeric membrane glycoprotein expressed by human endothelial cells [20,21], macrophages [22], vascular smooth muscle cells [23], mesangial cells [24] and fibroblasts [21]. Endoglin binds TGF-1 and TGF-3 with high affinity in human endothelial cells [25], in association with the type II receptor [26].…”

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confidence: 99%

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Endoglin Upregulation in the Liver after Bile Duct Ligation in Rats

Pérez‐Barriocanal¹

2011

TOGASJ

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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.

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“…Entre las células residentes en el riñón, las CMG constituyen dianas bien definidas para el TGF-β y podrían desempeñar un papel central en la aparición de la fibrosis glomerular. En apoyo de esta idea, se vio que la endoglina se expresa en las CMG y que esta expresión estaba inducida al alza por el TGF-β1 (51,52). Además, se ha observado que la expresión de endoglina reduce la acumulación de colágeno tanto basal como estimulado por el TGF-β1 en las CMG humanas y en los mioblastos de rata transfectados con endoglina (52)(53)(54), lo que indica que la endoglina podría tener una función importante en la patogenia de la fibrosis renal.…”

Section: Endoglina Y Fibrogénesisunclassified

Endoglina: estructura, funciones biológicas y papel en la fibrogénesis

García-Pozo

Miquilena-Colina

Lozano-Rodríguez

et al. 2008

Rev. esp. enferm. dig.

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INTRODUCCIÓNLa endoglina, también llamada CD105, se descubrió a finales de la década de 1980 como un marcador de células endoteliales humanas mediante un anticuerpo monoclonal, llamado 44G4, creado para combatir una línea de células leucémicas pre-B (1). Otros estudios mostraron que la endoglina se expresaba también en los macrófagos, los precursores eritroides, los sincitiotrofoblastos de la placenta terminal y en las células del estroma (2-5). El gen que codifica la endoglina se ha localizado en el brazo largo del cromosoma humano 9 (6) y las mutaciones de este gen son las responsables de un trastorno vascular autosómico dominante que se denomina telangiectasia hemorrágica hereditaria de tipo 1 (THH1) (7). La endoglina se une con gran afinidad a distintas isoformas del TGF-β en las células del endotelio (CE) humano (8) y desempeña un papel importante en la angiogénesis (9), pues los ratones con desactivación homozigótica del gen de la endoglina mueren en medio de la gestación por angiogénesis defectuosa y anomalías cardiovasculares graves, mientras que los heterozigóticos son viables, aunque están predispuestos a tener anomalías vasculares parecidas a la THH (10-12).Aparte de su importancia biológica en procesos fundamentales de las células endoteliales, el reconocimiento de la relevancia que posee la endoglina en medicina es cada vez mayor. En ese sentido, estudios tanto in vitro como in vivo han confirmado el enorme potencial de la endoglina como diana terapéutica del cáncer humano, observándose que los anticuerpos monoconales anti-CD105 conjugados con inmunotoxinas inducen supresiones duraderas del crecimiento tumoral y las metástasis en los modelos oncológicos animales (13,14). Por otra parte, cada vez son más las pruebas de que la endoglina podría desempeñar un papel importante en la fibrogénesis, ya que se ha observado una sobreexpresión de esta proteína en biopsias de pacientes con fibrosis renal y hepática (15,16). Esta revisión resume algunos de los últimos avances en el conocimiento de la estructura y las funciones biológicas de la endoglina, haciendo especial énfasis en su posible papel en la fibrogénesis. ESTRUCTURALa endoglina es una glicoproteína homodimérica transmembranosa de 180 kDa que contiene un dominio extracelular de 561 residuos aminoacídicos y una región citoplasmática rica en serina y treonina de 47 residuos aminoacídicos (17,18). Estructuralmente, la endoglina pertenece a la familia de proteínas extracelulares de la zona pelúcida (ZP), que poseen en común un doEndoglina: estructura, funciones biológicas y papel en la fibrogénesis

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Endoglin Expression in Human and Rat Mesangial Cells and Its Upregulation by TGF-β1

Cited by 47 publications

References 26 publications

Endoglin Differentially Modulates Antagonistic Transforming Growth Factor-β1 and BMP-7 Signaling

Endoglin Differentially Modulates Antagonistic Transforming Growth Factor-β1 and BMP-7 Signaling

Endoglin Upregulation in the Liver after Bile Duct Ligation in Rats

Endoglina: estructura, funciones biológicas y papel en la fibrogénesis

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