NLRP10 Affects the Stability of Abin-1 To Control Inflammatory Responses

Mirza, Nora; Sowa, Anna; Lautz, Katja; Kufer, Thomas A.

doi:10.4049/jimmunol.1800334

Cited by 15 publications

(9 citation statements)

References 54 publications

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“…ABIN‐1 has emerged as a key inflammation‐related regulator that has been implicated in multiple inflammatory diseases. In Shigella flexneri ‐infected epithelial cells, inhibition of ABIN‐1 resulted in the enhanced activation of proinflammatory signalling . Overexpression of ABIN‐1 inhibited IL‐17‐derived inflammation in fibroblasts and epithelial cells, indicating a potential therapeutic value of ABIN‐1 .…”

Section: Discussionmentioning

confidence: 99%

ABIN‐1 protects chondrocytes from lipopolysaccharide‐induced inflammatory injury through the inactivation of NF‐κB signalling

Peng

Lü

et al. 2020

Clin Exp Pharma Physio

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The A20-binding inhibitor of nuclear factor (NF)-κB-1 (ABIN-1) protein has recently been implicated as a key regulator of inflammation with involvement in multiple inflammatory diseases. However, the function of ABIN-1 in osteoarthritis (OA) remains unclear. In the current study, we explored the role of ABIN-1 in the regulation of lipopolysaccharide (LPS)-induced inflammatory injury of chondrocytes, which served as an in vitro model of OA. Results revealed that ABIN-1 expression was induced by chondrocyte exposure to LPS. ABN-1 silencing exacerbated LPS-induced apoptosis and the inflammatory response, while ABIN-1 overexpression alleviated the inflammatory response and LPS-induced apoptosis in chondrocytes. Moreover, ABIN-1 overexpression resulted in significantly decreased LPS-induced NF-κB activation.Notably, activation of NF-κB signalling significantly reversed ABIN-1-mediated inhibitory effects on LPS-induced inflammatory injury in chondrocytes. Taken together, these results demonstrate that ABIN-1 protects chondrocytes against LPS-induced inflammatory injury through the suppression of NF-κB signalling. Our study suggests a potential role for ABIN-1 in OA. Further, we show that ABIN-1 may serve as a potential target for controlling joint inflammation. protects chondrocytes from lipopolysaccharide-induced inflammatory injury through the inactivation of NF-κB signalling.

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Section: Discussionmentioning

confidence: 99%

ABIN‐1 protects chondrocytes from lipopolysaccharide‐induced inflammatory injury through the inactivation of NF‐κB signalling

Peng

Lü

et al. 2020

Clin Exp Pharma Physio

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“…TNIP1 (Log 2 Fold 1.05) has been implicated by genome wide association studies to be important for psor-iatic arthiritis, systemic sclerosis, systemic lupus erythematosus, and psoriasis [55]. Interestingly, the protein product of Tnip1, whose function is largely anti-inflammatory, can form a complex with Nlrp10 (Log 2 Fold 1.04), which is also upregulated in the dataset and can negatively regulate protein levels of Tnip1 upon infection [56]. Nlrp10 −/ − mice have also revealed that it is highly important for establishing an adaptive immune response [57].…”

Section: Differential Gene Expression In the Hematopoietic Cell Populmentioning

confidence: 99%

Investigating global gene expression changes in a murine model of cherubism

Sharma

Cotney

Singh

et al. 2020

Bone

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Cherubism is a rare genetic disorder caused primarily by mutations in SH3BP2 resulting in excessive bone resorption and fibrous tissue overgrowth in the lower portions of the face. Bone marrow derived cell cultures derived from a murine model of cherubism display poor osteogenesis and spontaneous osteoclast formation. To develop a deeper understanding for the potential underlying mechanisms contributing to these phenotypes in mice, we compared global gene expression changes in hematopoietic and mesenchymal cell populations between cherubism and wild type mice. In the hematopoietic population, not surprisingly, upregulated genes were significantly enriched for functions related to osteoclastogenesis. However, these upregulated genes were also significantly enriched for functions associated with inflammation including arachidonic acid/prostaglandin signaling, regulators of coagulation and autoinflammation, extracellular matrix remodeling, and chemokine expression. In the mesenchymal population, we observed down regulation of osteoblast and adventitial reticular cell marker genes. Regulators of BMP and Wnt pathway associated genes showed numerous changes in gene expression, likely implicating the down regulation of BMP signaling and possibly the activation of certain Wnt pathways. Analyses of the cherubism derived mesenchymal population also revealed interesting *

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“…S. flexneri 5a M90T, along with S. flexneri 2a, is one of the most commonly employed laboratory reference strain for S. flexneri in many independent research groups across the globe [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27]. Indeed, much of our knowledge of the molecular mechanisms of Shigella pathogenesis has been obtained using S. flexneri M90T as a model.…”

Section: Introductionmentioning

confidence: 99%

Complete genome sequence and annotation of the laboratory reference strain Shigella flexneri serotype 5a M90T and genome-wide transcriptional start site determination

2020

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Background: Shigella is a Gram-negative facultative intracellular bacterium that causes bacillary dysentery in humans. Shigella invades cells of the colonic mucosa owing to its virulence plasmid-encoded Type 3 Secretion System (T3SS), and multiplies in the target cell cytosol. Although the laboratory reference strain S. flexneri serotype 5a M90T has been extensively used to understand the molecular mechanisms of pathogenesis, its complete genome sequence is not available, thereby greatly limiting studies employing high-throughput sequencing and systems biology approaches. Results: We have sequenced, assembled, annotated and manually curated the full genome of S. flexneri 5a M90T. This yielded two complete circular contigs, the chromosome and the virulence plasmid (pWR100). To obtain the genome sequence, we have employed long-read PacBio DNA sequencing followed by polishing with Illumina RNA-seq data. This provides a new hybrid strategy to prepare gapless, highly accurate genome sequences, which also cover AT-rich tracks or repetitive sequences that are transcribed. Furthermore, we have performed genome-wide analysis of transcriptional start sites (TSS) and determined the length of 5′ untranslated regions (5′-UTRs) at typical culture conditions for the inoculum of in vitro infection experiments. We identified 6723 primary TSS (pTSS) and 7328 secondary TSS (sTSS). The S. flexneri 5a M90T annotated genome sequence and the transcriptional start sites are integrated into RegulonDB (http://regulondb.ccg.unam. mx) and RSAT (http://embnet.ccg.unam.mx/rsat/) databases to use their analysis tools in the S. flexneri 5a M90T genome. Conclusions: We provide the first complete genome for S. flexneri serotype 5a, specifically the laboratory reference strain M90T. Our work opens the possibility of employing S. flexneri M90T in high-quality systems biology studies such as transcriptomic and differential expression analyses or in genome evolution studies. Moreover, the catalogue of TSS that we report here can be used in molecular pathogenesis studies as a resource to know which genes are transcribed before infection of host cells. The genome sequence, together with the analysis of transcriptional start sites, is also a valuable tool for precise genetic manipulation of S. flexneri 5a M90T. Further, we present a new hybrid strategy to prepare gapless, highly accurate genome sequences. Unlike currently used hybrid strategies combining long-and short-read DNA sequencing technologies to maximize accuracy, our workflow using long-read DNA sequencing and short-read RNA sequencing provides the added value of using non-redundant technologies, which yield distinct, exploitable datasets.

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NLRP10 Affects the Stability of Abin-1 To Control Inflammatory Responses

Cited by 15 publications

References 54 publications

ABIN‐1 protects chondrocytes from lipopolysaccharide‐induced inflammatory injury through the inactivation of NF‐κB signalling

ABIN‐1 protects chondrocytes from lipopolysaccharide‐induced inflammatory injury through the inactivation of NF‐κB signalling

Investigating global gene expression changes in a murine model of cherubism

Complete genome sequence and annotation of the laboratory reference strain Shigella flexneri serotype 5a M90T and genome-wide transcriptional start site determination

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