Tyrosine phosphatase SHP2 negatively regulates NLRP3 inflammasome activation via ANT1-dependent mitochondrial homeostasis

Guo, Wenjie; Li, Wen; Chen, Zhe; Gu, Yanhong; Peng, Shuang; Shen, Lihong; Shen, Yan; Wang, Xingqi; Feng, Gen‐Sheng; Sun, Yang; Xu, Qiang

doi:10.1038/s41467-017-02351-0

Cited by 106 publications

(79 citation statements)

References 47 publications

(46 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our findings provide a better understanding of MDSCs accumulation and activation by tumor cells and its contribution to lung cancer development. Previous studies have proved a complex process for MDSCs accumulation and activation, including two groups of signals . One is for the expansion of immature myeloid cells, such as GM‐CSF and STAT3.…”

Section: Discussionmentioning

confidence: 99%

CARD9 prevents lung cancer development by suppressing the expansion of myeloid‐derived suppressor cells and IDO production

Liu

et al. 2019

Intl Journal of Cancer

View full text Add to dashboard Cite

Caspase recruitment domain‐containing protein 9 (CARD9) is an adaptor protein and highly expressed in myeloid cells. Our previous study demonstrates a critical protective effect of CARD9 in the development of colitis‐associated colon cancer. Nevertheless, the effect of CARD9 in lung cancer remains unclear. Here, using a mouse Lewis lung cancer model, we found the tumor burden of CARD9−/− mice was much heavier than that in wild‐type (WT) mice. More myeloid‐derived suppressor cells (MDSCs) were accumulated and less cytotoxicity T lymphocyte was found in tumor tissues of CARD9−/− mice, compared to WT mice. Depleting MDSCs using anti‐Gr1 antibody can significantly decrease tumor burden in CARD9−/− mice. Furthermore, the noncanonical nuclear factor‐kappaB (NF‐κB) pathway was activated in CARD9−/− mice‐derived MDSCs. Deficiency of CARD9 enhanced expression of indoleamine 2,3‐dioxygenase (IDO) in MDSCs via noncanonical NF‐κB pathway. Moreover, correlations between CARD9 expressions and MDSCs relative genes (IDO, iNOS‐2 and arginase 1 [ARG‐1]) were further confirmed in tumor tissues from lung cancer patients. Taken together, we showed a CARD9‐NF‐κB‐IDO pathway in MDSCs which can inhibit the suppressive function of MDSCs and prevent lung cancer development.

show abstract

Section: Discussionmentioning

confidence: 99%

CARD9 prevents lung cancer development by suppressing the expansion of myeloid‐derived suppressor cells and IDO production

Liu

et al. 2019

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

“…Guo et al . recently reported that ANT1 regulated the NLRP3 inflammasome in macrophages . Therefore, in addition to the inflammasome, we hypothesized that ANT1 also regulates inflammatory cytokine expression.…”

Section: Resultsmentioning

confidence: 92%

“…These results suggest that ANT1 knockdown has little influence on cell viability of macrophages. Previous work has shown that ANT1 regulates the inflammasome [13]. We hypothesized that ANT1 regulated not only the inflammasome but also cytokine expression.…”

Section: Discussionmentioning

confidence: 94%

“…The level of ANT1 expression in macrophages is unknown. However, it was recently reported that ANT1 regulates the inflammasome in a macrophage‐like cell line . In the present study, we first compared the amount of ANT1 in macrophages and cardiac muscle.…”

Section: Discussionmentioning

confidence: 95%

“…Previous work has shown that ANT1 regulates the inflammasome . We hypothesized that ANT1 regulated not only the inflammasome but also cytokine expression.…”

Section: Discussionmentioning

confidence: 95%

See 2 more Smart Citations

The inner mitochondrial membrane protein ANT1 modulates IL‐6 expression via the JNK pathway in macrophages

et al. 2018

View full text Add to dashboard Cite

Mitochondria are increasingly associated with inflammation. Here, we focus on the relationship between inflammation and adenine nucleotide translocator type 1 (ANT1), which is localized in the mitochondrial inner membrane. ANT1 plays an important role in oxidative phosphorylation, and mutations in the ANT1 gene are responsible for mitochondrial diseases. Ample studies have demonstrated that ANT1 has a critical role in cardiomyocytes and neurons, but little has been reported on its functions in immune cells. We knocked down ANT1 expression in macrophages and examined inflammatory cytokine expression after lipopolysaccharide stimulation. ANT1 knockdown reduces the expression of IL‐6. JNK, upstream of IL‐6, is downregulated, but other MAP kinases and the NF‐κB signaling remain unchanged. These results suggest that ANT1 modulates IL‐6 expression through JNK in macrophages.

show abstract

Crosstalk of NLRP3 inflammasome and noncoding RNAs in cardiomyopathies

Jafari,

Shahabi Rabori,

Zolfi Gol

et al. 2023

Cell Biochemistry & Function

View full text Add to dashboard Cite

Cardiovascular diseases (CVDs) identified as a serious public health problem. Although there is a lot of evidence that inflammatory processes play a significant role in the progression of CVDs, however, the precise mechanism is not fully understood. Nevertheless, recent studies have focused on inflammation and its related agents. Nucleotide oligomerization domain‐, leucine‐rich repeat‐, and pyrin domain‐containing protein 3 (NLRP3) is a type of pattern recognition receptor (PRR) that can recognize pathogen‐associated molecular patterns and trigger innate immune response. NLRP3 is a component of the NOD‐like receptor (NLR) family and have a pivotal role in detecting damage to cardiovascular tissue. It is suggested that activation of NLRP3 inflammasome leads to initiating and propagating the inflammatory response in cardiomyopathy. So, late investigations have highlighted the NLRP3 inflammasome activation in various forms of cardiomyopathy. On the other side, it was shown that noncoding RNAs (ncRNAs), particularly, microRNAs, lncRNAs, and circRNAs possess a regulatory function in the immune system's inflammatory response, implicating their involvement in various inflammatory disorders. In addition, their role in different cardiomyopathies was indicated in recent studies. This review article provides a summary of recent advancements focusing on the function of the NLRP3 inflammasome in common CVDs, especially cardiomyopathy, while also discussing the therapeutic potential of inhibiting the NLRP3 inflammasome regulated by ncRNAs.

show abstract

Tyrosine phosphatase SHP2 negatively regulates NLRP3 inflammasome activation via ANT1-dependent mitochondrial homeostasis

Cited by 106 publications

References 47 publications

CARD9 prevents lung cancer development by suppressing the expansion of myeloid‐derived suppressor cells and IDO production

CARD9 prevents lung cancer development by suppressing the expansion of myeloid‐derived suppressor cells and IDO production

The inner mitochondrial membrane protein ANT1 modulates IL‐6 expression via the JNK pathway in macrophages

Crosstalk of NLRP3 inflammasome and noncoding RNAs in cardiomyopathies

Contact Info

Product

Resources

About