Tamoxifen ameliorates renal tubulointerstitial fibrosis by modulation of estrogen receptor α-mediated transforming growth factor-β1/Smad signaling pathway

Kim, Dal; Lee, Ae Sin; Jung, Yu Jin; Yang, Kyung‐Moo; Lee, Sik; Park, Sung Kwang; Kim, Won; Kang, Kyung Pyo

doi:10.1093/ndt/gfu240

Cited by 69 publications

(84 citation statements)

References 41 publications

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“…Among these, the expressions of fibronectin and TGF-␤1 are upregulated in the UUO model of obstructive nephropathy and may aid the progression to tubulointerstitial fibrosis (12,25,31,34,37,55,66,68). Understanding the regulatory pathways that control their production may be paramount to developing effective therapeutics to treat these diseases.…”

Section: Discussionmentioning

confidence: 99%

Cyclic stretch-induced TGF-β1 and fibronectin expression is mediated by β1-integrin through c-Src- and STAT3-dependent pathways in renal epithelial cells

Hamzeh

Sridhara

Alexander

2015

American Journal of Physiology-Renal Physiology

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Section: Discussionmentioning

confidence: 99%

Cyclic stretch-induced TGF-β1 and fibronectin expression is mediated by β1-integrin through c-Src- and STAT3-dependent pathways in renal epithelial cells

Hamzeh

Sridhara

Alexander

2015

American Journal of Physiology-Renal Physiology

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“…Transforming growth factor (TGF)-β is an important cytokine regulating apoptosis, cell cycle, differentiation and extracellular matrix accumulation (31)(32)(33). A large body of evidence has linked TGF-β/ Smad signaling to the development and progression of renal fibrosis (34)(35)(36).…”

Section: Sirt1 Reduces Fibrosis By Smad3 (Targeting Mothers Against Dmentioning

confidence: 99%

Sirtuin 1: A Target for Kidney Diseases

Kong

Zhou

et al. 2015

Mol Med

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Sirtuin 1 (SIRT1) is an evolutionarily conserved NAD + -dependent histone deacetylase that is necessary for caloric restriction-related lifespan extension. SIRT1, as an intracellular energy sensor, detects the concentration of intracellular NAD + and uses this information to adapt cellular energy output to cellular energy requirements. Previous studies on SIRT1 have confirmed its beneficial effects on cellular immunity to oxidative stress, reduction of fibrosis, suppression of inflammation, inhibition of apoptosis, regulation of metabolism, induction of autophagy and regulation of blood pressure. All of the above biological processes are involved in the pathogenesis of kidney diseases. Therefore, the activation of SIRT1 may become a therapeutic target to improve the clinical outcome of kidney diseases. In this review, we give an overview of SIRT1 and its molecular targets as well as SIRT1-modulated biological processes, with a particular focus on the role of SIRT1 in kidney diseases.

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“…Estos modelos sugieren que el TGF-β no tiene un papel crítico en la inmunidad de los ratones. Sin embargo, esta conclusión hay que tomarla con precaución pues, entre otras alteraciones, el tratamiento con dosis de tamoxifeno similares a las que se usan para la eliminación genética del TGF-βRII pueden tener efectos colaterales (Kim, et al, 2014). Considerando toda la evidencia disponible, podemos decir que en ninguno modelo se ha establecido claramente un rol inmunomodulador importante del TGF-β en una infección viral in vivo.…”

Section: Cd4dntgf-briiunclassified

Papel del TGF-β en la inmunidad contra los rotavirus

Franco-Cortés

2016

Rev. Acad. Colomb. Cienc. Ex. Fis. Nat.

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ResumenLa vía de entrada y el principal sitio de replicación de los rotavirus es el intestino delgado. En este órgano el TGF-β juega un papel muy importante para mantener la tolerancia a los alimentos y microorganismos comensales. Por esta razon, es probable que esta citocina juegue un papel modulador en esta infección. Experimentos in vitro de nuestro laboratorio han mostrado que células humanas epiteliales infectadas por rotavirus aumentan la secreción de TGF-β y promueven una baja respuesta de linfocitos T, la que es necesaria para la inmunidad antiviral. En este artículo de revisión se analiza en forma crítica la hipótesis que los rotavirus inducen la producción de TGF-β como mecanismo de evasión inmune.Palabras clave: rotavirus, inmunidad intestinal, factor de crecimiento transformante Beta, tolerancia inmunológica, evasión inmunológica de virus. Role of TGF-β in rotavirus immunity AbstractRotavirus enter their host and predominantly replicates in the small intestine. In this organ, TGF-β plays an important role in maintaining tolerance to commensal microorganisms and food. For this reason, it is probable that this citokine plays a role in modulating viral infection. Results from our laboratory have shown that in vitro human cells infected with rotavirus secrete increased levels of TGF-β and promote an attenuated T cell response, which is necessary for protective cellular immunity. In this review article, I will critically evaluate the hypothesis that rotavirus induce the production of TGF-β as an immune evasion mechanism.Key words: Rotavirus, intestinal immunity, transforming growth factor beta, immunological tolerance, viral immune evasion. Correspondencia:Manuel Antonio Franco-Cortés, mafranco@javeriana.edu.co Recibido: 25 de octubre de 2015 Aceptado: 15 de febrero de 2016 doi: http://dx.doi.org/10.18257/raccefyn.300 Ciencias biomédicas IntroducciónEl desarrollo de vacunas contra los rotavirus es un importante logro de la medicina moderna (Angel, et al., 2014). Sin embargo, las vacunas actualmente en uso son relativamente poco eficientes en los países en vías de desarrollo, donde son más útiles, y es importante entender mejor la inmunidad antiviral para mejorarlas (Angel, et al., 2014). La inmunidad que inducen los rotavirus no es esterilizante y en muchos casos es de corta duración (Angel, et al., 2012; Franco, et al., 2006). Es probable que durante el desarrollo de la respuesta inmune contra estos virus entren en juego mecanismos que favorecen una respuesta protectora, elementos reguladores negativos de la respuesta inmune y, por último, las estrategias que ha desarrollado el virus para escapar a ésta (Angel, et al., 2012). El sistema inmune cuenta, entre otros, con 3 poderosos reguladores negativos: La proteína "muerte programada 1" (PD-1), la interleucina 10 (IL-10) y el factor de crecimiento transformante beta (TGF-β) (Freeman, et al., 2014; Garidou, et al., 2012). Dado que la principal puerta de entrada y sitio de replicación de los rotavirus es el intestino delgado, donde el TGF-β juega un papel ...

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Tamoxifen ameliorates renal tubulointerstitial fibrosis by modulation of estrogen receptor α-mediated transforming growth factor-β1/Smad signaling pathway

Abstract: These findings indicate that tamoxifen has a beneficial effect on UUO-induced tubulointerstitial fibrosis by suppression of renal fibroblast activation via modulation of ERα-mediated renal TGF-β1/Smad signaling pathway.

Cited by 69 publications

References 41 publications

Cyclic stretch-induced TGF-β1 and fibronectin expression is mediated by β1-integrin through c-Src- and STAT3-dependent pathways in renal epithelial cells

Cyclic stretch-induced TGF-β1 and fibronectin expression is mediated by β1-integrin through c-Src- and STAT3-dependent pathways in renal epithelial cells

Sirtuin 1: A Target for Kidney Diseases

Papel del TGF-β en la inmunidad contra los rotavirus

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