Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add more filters










Database
Language
Publication year range
1.
Mol Biol Rep ; 51(1): 351, 2024 Feb 24.
Article in English | MEDLINE | ID: mdl-38400865

ABSTRACT

The nervous system possesses the remarkable ability to undergo changes in order to store information; however, it is also susceptible to damage caused by invading pathogens or neurodegenerative processes. As a member of nucleotide-binding oligomerization domain-like receptor (NLR) family, the NLRP6 inflammasome serves as a cytoplasmic innate immune sensor responsible for detecting microbe-associated molecular patterns. Upon activation, NLRP6 can recruit the adapter protein apoptosis-associated speck-like protein (ASC) and the inflammatory factors caspase-1 or caspase-11. Consequently, inflammasomes are formed, facilitating the maturation and secretion of pro-inflammatory cytokines such as inflammatory factors-18 (IL-18) and inflammatory factors-1ß (IL-1ß). Precise regulation of NLRP6 is crucial for maintaining tissue homeostasis, as dysregulated inflammasome activation can contribute to the development of various diseases. Furthermore, NLRP6 may also play a role in the regulation of extraintestinal diseases. In cells of the brain, such as astrocytes and neurons, NLRP6 inflammasome are also present. Here, the assembly and subsequent activation of caspase-1 mediated by NLRP6 contribute to disease progression. This review aims to discuss the structure and function of NLRP6, explain clearly the mechanisms that induce and activate NLRP6, and explore its role within the central and peripheral nervous system.


Subject(s)
Inflammasomes , Nervous System Diseases , Humans , Inflammasomes/metabolism , Cytokines/metabolism , Caspase 1/metabolism , Apoptosis , Nervous System Diseases/genetics , Caspases , Intracellular Signaling Peptides and Proteins
2.
Cancer Lett ; 509: 26-38, 2021 07 01.
Article in English | MEDLINE | ID: mdl-33819529

ABSTRACT

Oncolytic adenovirus-mediated gene therapy shows promise for cancer treatment; however, the systemic delivery of oncolytic adenovirus to tumors remains challenging. Recently, mesenchymal stem cells (MSCs) have emerged as potential vehicles for improving delivery. Yet, because the oncolytic adenovirus replicates in MSCs, balancing MSC viability with viral load is key to achieving optimal therapeutic effect. We thus developed an all-in-one Tet-on system that can regulate replication of oncolytic adenovirus. Then, we loaded the novel oncolytic adenovirus carrying interleukin (IL)-24 and/or Endostatin in human umbilical cord blood-mesenchymal stem cells (hUCB-MSCs) for glioma therapy. In vitro assays demonstrated that this novel oncolytic adenovirus could efficiently replicate and kill glioma cells while sparing normal cells. Moreover, doxycycline effectively regulated oncolytic adenovirus replication in the hUCB-MSCs. The doxycycline induction group with dual expression of IL-24 and Endostatin exhibited significantly greater antitumor effects than other groups in a xenograft model of glioma. Thus, this strategy for systemic delivery of oncolytic adenovirus with its oncolytic activity controlled by a Tet-on system is a promising method for achieving antitumor efficacy in glioma, especially for metastatic tumors.


Subject(s)
Brain Neoplasms/therapy , Cord Blood Stem Cell Transplantation , Endostatins/biosynthesis , Genetic Therapy , Glioma/therapy , Interleukins/biosynthesis , Mesenchymal Stem Cell Transplantation , Mesenchymal Stem Cells/virology , Oncolytic Virotherapy , Oncolytic Viruses/genetics , Animals , Brain Neoplasms/genetics , Brain Neoplasms/metabolism , Brain Neoplasms/virology , Cell Death , Cell Line, Tumor , Cell Movement , Cell Proliferation , Endostatins/genetics , Female , Genetic Vectors , Glioma/genetics , Glioma/metabolism , Glioma/virology , Humans , Interleukins/genetics , Mice, Inbred BALB C , Mice, Nude , Oncolytic Viruses/growth & development , Tumor Burden , Virus Replication , Xenograft Model Antitumor Assays
SELECTION OF CITATIONS
SEARCH DETAIL
...