Suppressor of cytokine signaling (SOCS) 1 is down-regulated in renal transplant recipients with rejection

Wu, Tsai-Hung; Lee, Hui-Ting; Lai, Cheng‐chung; Yang, An-Hang; Loong, Che‐Chuan; Wang, Hsin‐Kai; Yu, Chia‐Li; Tsai, Chang-Youh

doi:10.1016/j.trim.2016.07.001

Cited by 6 publications

(4 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Among those genes, suppressors of cytokine signaling 1 (Sosc1), a negative regulator, was chosen for the further experiment owing to its pivotal role in braking the overshooting of the proinflammatory reactions by resolution of inflammatory cascades and regulation of the immune system in transplantation as previously reported. 36,37 The prediction website miRanda showed the miR-155-5p binding sites in the 3′ UTR of Socs1 (Fig. 4D).…”

Section: Resultsmentioning

confidence: 99%

Targeted microRNA delivery by lipid nanoparticles and gas vesicle-assisted ultrasound cavitation to treat heart transplant rejection

Wang

Zhou

et al. 2023

Biomater. Sci.

View full text Add to dashboard Cite

show abstract

Section: Resultsmentioning

confidence: 99%

Targeted microRNA delivery by lipid nanoparticles and gas vesicle-assisted ultrasound cavitation to treat heart transplant rejection

Wang

Zhou

et al. 2023

Biomater. Sci.

View full text Add to dashboard Cite

show abstract

“…The profibrotic cytokine TGF‐β1 can cause the renal fibrosis through its binding to receptors at the cell surface and one study revealing that inhibition of TGF‐β1‐receptor posttranslational core fucosylation can alleviate the rat RIF . The down‐regulation of SOCS1 is regarded as a regulator for the early renal allograft rejection detection . Significantly enough, another study demonstrated that the SOCS‐1 is up‐regulated in human mesangial cells (HMCs) under high glucose conditions and can suppress the synthesis of TGF‐beta1 and fibronectin induced by high glucose in HMCs .…”

Section: Discussionmentioning

confidence: 99%

“…42 The down-regulation of SOCS1 is regarded as a regulator for the early renal allograft rejection detection. 43 Significantly enough, another study demonstrated that the SOCS-1 is up-regulated in human mesangial cells (HMCs) under high glucose conditions and can suppress the synthesis of TGF-beta1 and fibronectin induced by high glucose in HMCs. 44…”

Section: Groupsmentioning

confidence: 99%

Silencing of SOCS‐1 and SOCS‐3 suppresses renal interstitial fibrosis by alleviating renal tubular damage in a rat model of hydronephrosis

Zheng

Wang

Wen

et al. 2017

J of Cellular Biochemistry

View full text Add to dashboard Cite

Our study was performed to elucidate how SOCS-1/3 silencing suppresses renal interstitial fibrosis (RIF) by alleviating renal tubular damage in rat models affected by hydronephrosis. Male Wistar rats were randomly selected to establish hydronephrosis rat model, after which all rats were classified into normal, model, negative control (NC), siRNA-SOCS-1, siRNA-SOCS-3, and siRNA-SOCS-1 + siRNA-SOCS-3 groups. The levels of urine protein, serum creatinine (Scr), and blood urea nitrogen (BUN) were detected. ELISA was performed to determine levels of cystatin (CysC), β2-microglobulin (β2-MG), interleukin (IL)-6, and tumor necrosis factor (TNF)-α. RT-qPCR and Western blotting were used for mRNA and protein expressions of SOCS-1, SOCS-3, α-smooth muscle actin (α-SMA), and transforming Growth Factor (TGF)-β1. Compared with the normal group, the levels of Scr, BUN, urine protein, NAG, CysC, β2-MG, IL-6, and TNF-α were increased in other groups, as well as elevated mRNA and protein expressions of SOCS-1, SOCS-3, α-SMA, and TGF-β1. The siRNA-SOCS-1, siRNA-SOCS-3, and siRNA-SOCS-1 + siRNA-SOCS-3 groups were found with decreased levels of Scr, BUN, urine protein, NAG, CysC, β2-MG, IL-6, and TNF-α, as well as mRNA and protein expressions of SOCS-1, SOCS-3, α-SMA, and TGF-β1, including positive rates of SOCS-1 and SOCS-3 proteins in comparison with the model and NC groups. In comparison with the siRNA-SOCS-1 and siRNA-SOCS-3 groups, the siRNA-SOCS-1 + siRNA-SOCS-3 group exhibited decreased levels of Scr, BUN, urine protein, NAG, CysC, β2-MG, IL-6, and TNF-α. Our study demonstrated that silencing of SOCS-1/3 may suppress RIF by alleviating the renal tubular damage in rat models affected by hydronephrosis.

show abstract

“…The clinical role of the SHP-2 in the regulation of the GH signal transduction is confirmed by Noonan [93] and Leopard [94] syndromes. In addition, dual-specificity phosphatases (DUSPs), a family of type-I cysteine-based protein tyrosine phosphatases that act on both tyrosine and serine/theronine residues on a substrate, are also of interest for its ability to interact with STAT5b [95]. However, further studies are required to understand the mechanism of this interaction.…”

Section: Protein Phosphatases and Signal Regulatory Proteins (Sirps)mentioning

confidence: 99%

Control of Liver Gene Expression by Sex Steroids and Growth Hormone Interplay

Fernández-Pérez¹,

Mirecki-Garrido²,

Recio³

et al. 2020

Chemistry and Biological Activity of Steroids

View full text Add to dashboard Cite

Sex steroids have important physiological actions, which are not limited to reproductive organs, in both females and males. They exert important physiological roles, including the regulation of somatotropic-liver axis, intermediate metabolism, or gender dimorphism. This is in part because the liver is a sex steroid-responsive organ where sex steroid-and growth hormone (GH)-dependent signaling pathways connect to regulate complex gene expression networks. Sex steroids can impact liver gene expression by a direct, through hepatic estrogen receptor (ER)α and androgen receptor (AR), or indirect mechanisms, by modulation of pituitary GH secretion and/or interaction with the GHR-STAT5b signaling pathway. Therefore, deficiency of sex steroid-and GH-dependent signaling pathways might cause a dramatic impact on mammalian liver physiology. In this chapter, we will focus our attention on main concepts and paradigms involved in the role and interplay between sex steroid-and GH-dependent signaling to regulate gene expression networks in the mammalian liver. A better understanding of how sex steroids and interactions with GH-STAT5b signaling pathway influence physiological and pathological states in the liver will contribute to improve clinical management of patients with disorders in body growth, development, and metabolism.Chemistry and Biological Activity of Steroids 2 androgen/AR [6,7,[21][22][23][24][25] or signaling pathways in adults causes a similar metabolic-like syndrome (i.e., fatty liver, adiposity, insulin resistance), a phenotype that might be ameliorated by E2/T or GH replacement. Therefore, the interplay between sex steroids and GH is clinically relevant because of its importance in the regulation of endocrine, metabolic, and gender-differentiated actions on the mammalian liver [33]. A better understanding of this complex sex steroid-GH interplay in physiological and pathological states will contribute to prevent health damage and improve clinical management of patients with growth, developmental, and metabolic disorders. In this review, we will summarize the role of sex steroid-and GH-dependent signaling pathways on liver gene expression. The liver is as sex steroid-responsive organSex steroids can regulate liver gene transcription through direct and indirect mechanisms.

show abstract

Suppressor of cytokine signaling (SOCS) 1 is down-regulated in renal transplant recipients with rejection

Cited by 6 publications

References 40 publications

Targeted microRNA delivery by lipid nanoparticles and gas vesicle-assisted ultrasound cavitation to treat heart transplant rejection

Targeted microRNA delivery by lipid nanoparticles and gas vesicle-assisted ultrasound cavitation to treat heart transplant rejection

Silencing of SOCS‐1 and SOCS‐3 suppresses renal interstitial fibrosis by alleviating renal tubular damage in a rat model of hydronephrosis

Control of Liver Gene Expression by Sex Steroids and Growth Hormone Interplay

Contact Info

Product

Resources

About