Intracellular protein therapy with SOCS3 inhibits inflammation and apoptosis

Jo, Daewoong; Liu, Danya; Yao, Shanshan; Collins, Robert D.; Hawiger, Jacek

doi:10.1038/nm1269

Cited by 251 publications

(228 citation statements)

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“…The absence of proinflammatory cytokine induction could be partly due to the parallel elevation of the SOCS-3 mRNA after infection. The SOCS-3 is a potent inhibitor of cytokine signaling and its transgenic over-expression may inhibit inflammation and associated apoptosis in vivo (Auerhammer and Melmed, 2001;Jo et al, 2005). Accordingly, although infected mice had elevated basal pro-inflammatory cytokine levels (i.e.…”

Section: Discussionmentioning

confidence: 99%

“…In fact, the effect of infection on ischemic damage may largely depend on the regulation of reactive oxygen species by pro-inflammatory and anti-inflammatory cytokines as well as by the main antioxidant state regulators, namely superoxide dismutase (SOD) (Guegan et al, 1998;Murakami et al, 1998), glutathione (GSH) (Nicholls and Budd, 2000;Schulz et al, 2000;Droge, 2002), uncoupling protein-2 (UCP2) (Arsenijevic et al, 2000b;Mattiasson et al, 2003) and nerve growth factor (NGF) (Brodie, 1996;Guegan et al, 1999;Villoslada et al, 2000). In addition, the newly described suppressor of cytokine signaling (SOCS) proteins are induced in peripheral and central models of inflammation (Lebel et al, 2000;Bates et al, 2001;Larsen and Ropke, 2002;Wang and Campbell, 2002;Huang et al, 2003;Park et al, 2003;Jo et al, 2005). SOCS possibly interact with cellular redox determinants (Park et al, 2003) and transgenic SOCS expression has been shown to inhibit inflammation and apoptosis following lipopolysaccharide (LPS) injection (Jo et al, 2005).…”

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confidence: 99%

“…In addition, the newly described suppressor of cytokine signaling (SOCS) proteins are induced in peripheral and central models of inflammation (Lebel et al, 2000;Bates et al, 2001;Larsen and Ropke, 2002;Wang and Campbell, 2002;Huang et al, 2003;Park et al, 2003;Jo et al, 2005). SOCS possibly interact with cellular redox determinants (Park et al, 2003) and transgenic SOCS expression has been shown to inhibit inflammation and apoptosis following lipopolysaccharide (LPS) injection (Jo et al, 2005).…”

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Decreased infarct size after focal cerebral ischemia in mice chronically infected with Toxoplasma gondii

et al. 2007

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Abstract-To determine whether Toxoplasma gondii infection could modify biological phenomena associated with brain ischemia, we investigated the effect of permanent middle cerebral artery occlusion (MCAO) on neuronal survival, inflammation and redox state in chronically infected mice. Infected animals showed a 40% to 50% decrease of infarct size compared with non-infected littermates 1, 4 and 14 days after MCAO. The resistance of infected mice may be associated with increased basal levels of anti-inflammatory cytokines and/or a marked reduction of the MCAO-related brain induction of two pro-inflammatory cytokines, tumor necrosis factor-alpha and interferon-gamma (IFN␥). In addition, potential anti-inflammatory/neuroprotective factors such as nerve growth factor, suppressor of cytokine signaling-3, superoxide dismutase activity, uncoupling protein-2 and glutathione (GSH) were upregulated in the brain of infected mice. Consistent with a role of GSH in central cytokine regulation, GSH depletion by diethyl maleate inhibited Toxoplasma gondii lesion resistance by increasing the proinflammatory cytokine IFN␥ brain levels. Overall, these findings indicate that chronic toxoplasmosis decisively influences both the inflammatory molecular events and outcome of cerebral ischemia.

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Section: Discussionmentioning

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Decreased infarct size after focal cerebral ischemia in mice chronically infected with Toxoplasma gondii

et al. 2007

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“…Although SOCS3 knockout mice die in utero due to placental defects, conditional SOCS3 depletion induces inflammatory and metabolic disorder [49][50][51]. Thus, SOCS3 plays a role in cytokine as well as insulin signaling.…”

Section: Socs3mentioning

confidence: 99%

SOCS proteins in regulation of receptor tyrosine kinase signaling

Kazi

Kabir

Flores‐Morales

2014

Cell. Mol. Life Sci.

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SOCS proteins in regulation of receptor tyrosine kinase signaling.Uddin, Kazi; Kabir, Nuzhat N; Flores-Morales, Amilcar; Rönnstrand, Lars Link to publication Citation for published version (APA): Kazi, J. U., Kabir, N. N., Flores-Morales, A., & Rönnstrand, L. (2014). SOCS proteins in regulation of receptor tyrosine kinase signaling. Cellular and Molecular Life Sciences, 71(17), 3297-3310. DOI: 10.1007/s00018-014-1619-y General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from the public portal for the purpose of private study or research.• You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal Take down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. AbstractThe receptor tyrosine kinases (RTKs) are a family of cell surface receptors that play critical roles in signal transduction from extracellular stimuli. Many of this family of kinases are overexpressed or mutated in human malignancies and thus became attractive drug target for cancer treatment. The signaling mediated by RTKs must be tightly regulated by interacting proteins including protein-tyrosine phosphatases and ubiquitin ligases. The suppressor of cytokine signaling (SOCS) family proteins are well known negative regulators of cytokine receptors signaling consisting of eight structurally similar proteins, SOCS1-7 and CIS. A key feature of this family of proteins is the presence of an SH2 domain and a SOCS box. Recent studies suggest that SOCS proteins also play a role in RTK signaling. Activation of RTK results in transcriptional activation of SOCS encoding genes. These proteins associate with RTKs through their SH2 domains and subsequently recruit the E3 ubiquitin machinery through the SOCS box, and thereby limit receptor stability by inducing ubiquitination. In a similar fashion SOCS proteins negatively regulate mitogenic signaling by RTKs. It is also evident that RTKs sometimes can bypass SOCS regulation and SOCS proteins can even potentiate RTKs-mediated mitogenic signaling. Thus apart from negative regulation of receptor signaling, SOCS proteins may also influence signaling in other ways.

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“…Penetratin has been shown to cause uniform distribution and improve tumor retention of single-chain antibody marking an important step toward radio immunotherapy of solid tumors. Recombinant SOCS3-CPP has been shown to effectively inhibit the cytokine-mediated signal transduction associated with acute inflammation and liver apoptosis (67). Disulfide linkage between Tat and anti-tetanus antibody caused neutralization of the toxin and showed higher nuclear localization (68).…”

Section: Delivery Of Proteins As Cpp-cargo Complexmentioning

confidence: 99%

Cell‐penetrating peptides: Nanocarrier for macromolecule delivery in living cells

2010

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SummaryNovel classes and applications of cell-penetrating peptides (CPPs) are being constantly discovered since they were first identified 2 decades ago. These short cationic peptides (nanomolecules) either by covalent binding or by noncovalent binding can traverse cell membranes and deliver a variety of molecules that are unable to overcome the permeability barrier in their own capacity. The ability of the CPPs to deliver variety of macromolecules, such as oligonucleotides, therapeutic drugs, proteins, and medical imaging agents, by forming nanoparticulate carriers in a range of cells has led them to emerge as a potential tool for both macromolecule delivery application and to gain insight into the fundamentals of mechanism of cellular uptake across the plasma membrane. This review explores the recent advances, challenges, and future prospects in the field of CPP-mediated cargo delivery in mammalian and plant cells. Studies have been conducted into the peptide chemistry and stability of CPP-macromolecular complexes. Most of the CPPs have been shown to be nontoxic and do not interfere with the functionality of the macromolecules delivered across the cell membrane. The mechanism of uptake of CPP-cargo complexes and the uptake of CPPs alone across the plasma membrane remains unresolved. As the world of CPPs is rapidly advancing in both mammalian and plant system, there is a promising future for the various applications of transduction and transfection into intact cells.

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Intracellular protein therapy with SOCS3 inhibits inflammation and apoptosis

Cited by 251 publications

References 29 publications

Decreased infarct size after focal cerebral ischemia in mice chronically infected with Toxoplasma gondii

Decreased infarct size after focal cerebral ischemia in mice chronically infected with Toxoplasma gondii

SOCS proteins in regulation of receptor tyrosine kinase signaling

Cell‐penetrating peptides: Nanocarrier for macromolecule delivery in living cells

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