NLRC3 inhibits PDGF‐induced PASMCs proliferation via PI3K‐mTOR pathway

Zha, Lihuang; Zhou, Jun; Tan, Yilong; Guo, Shuzhen; Zhang, Men‐qiu; Li, Sheng; Peng, Yan; Yu, Zaixin

doi:10.1002/jcp.29763

Cited by 15 publications

(8 citation statements)

References 38 publications

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“…The Hipk gene family were also found to have flatfish-specific expansion in previous study [37]. Besides, two new genes associated with cell proliferation were also highly expressed on the right side, including Nlrc3-like [42] (Figure 3C) and Trim25 [43] (Figure 3D). Asymmetric expression of these three new genes may have potential functions in the formation of the asymmetry of the left and right sides of the Japanese flounder.…”

Section: Asymmetric Expression Of Some New Genes May Play Roles In the Formation Of The Unique Body Plan Of Flatfishesmentioning

confidence: 56%

Pattern of New Gene Origination in a Special Fish Lineage, the Flatfishes

Chen

Wang

et al. 2021

Genes

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Origination of new genes are of inherent interest of evolutionary geneticists for decades, but few studies have addressed the general pattern in a fish lineage. Using our recent released whole genome data of flatfishes, which evolved one of the most specialized body plans in vertebrates, we identified 1541 (6.9% of the starry flounder genes) flatfish-lineage-specific genes. The origination pattern of these flatfish new genes is largely similar to those observed in other vertebrates, as shown by the proportion of DNA-mediated duplication (1317; 85.5%), RNA-mediated duplication (retrogenes; 96; 6.2%), and de novo–origination (128; 8.3%). The emergence rate of species-specific genes is 32.1 per Mya and the whole average level rate for the flatfish-lineage-specific genes is 20.9 per Mya. A large proportion (31.4%) of these new genes have been subjected to selection, in contrast to the 4.0% in primates, while the old genes remain quite similar (66.4% vs. 65.0%). In addition, most of these new genes (70.8%) are found to be expressed, indicating their functionality. This study not only presents one example of systematic new gene identification in a teleost taxon based on comprehensive phylogenomic data, but also shows that new genes may play roles in body planning.

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Section: Asymmetric Expression Of Some New Genes May Play Roles In the Formation Of The Unique Body Plan Of Flatfishesmentioning

confidence: 56%

Pattern of New Gene Origination in a Special Fish Lineage, the Flatfishes

Chen

Wang

et al. 2021

Genes

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“…Similarly, nucleotide oligomerization domain-like receptors with caspase activation and recruitment domain 3 (NLRC3) is essential for immune responses in ALI, which is upregulated in rats with ventilator-induced ALI [ 24 ]. Besides, NLRC3 could prohibit PI3K phosphorylation in pulmonary artery smooth muscle cells [ 25 ]. Our results showed that TILRR suppressed phosphorylation of PI3K and AKT in HPMVECs under LPS condition.…”

Section: Discussionmentioning

confidence: 99%

TILRR Aggravates Sepsis-Induced Acute Lung Injury by Suppressing the PI3K/Akt Pathway

Wang

Lin²,

Guo

2022

Evidence-Based Complementary and Alternative Medicine

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Acute lung injury (ALI) is a life-threatening lung change, and 40% of ALI cases result from sepsis. However, the effective treatment for sepsis-induced ALI is limited. It is urgent to explore novel therapeutic targets for ALI caused by sepsis. Anti-inflammatory therapy is a potential effective treatment for sepsis-induced ALI. Toll-like/Interleukin-1 receptor regulator (TILRR) could trigger aberrant inflammatory responses. Nevertheless, the role of TILRR in sepsis-induced ALI remains unknown. Besides, the phosphatidylinositol 3′kinase/protein kinase B (PI3K/Akt) pathway exerts protective effect on sepsis-induced ALI. Thus, the primary aim of the current study was to investigate whether TILRR contributed to sepsis-induced ALI by the PI3K/Akt pathway. To construct the sepsis-induced ALI model, human pulmonary microvascular endothelial cells (HPMVECs) were treated with lipopolysaccharide (LPS). Besides, the mRNA levels and protein levels were determined by quantitative reverse transcription-PCR (qPCR) and Western blot (WB), respectively. Moreover, cell proliferation was identified by the Cell Counting Kit-8 (CCK-8) assay and Annexin V was utilized to detect apoptosis. Furthermore, levels of proinflammatory cytokines and oxidative stress were tested by the enzyme-linked immunosorbent assay (ELISA) while reactive oxygen species (ROS) was determined by the flow cytometer. Results indicated that TILRR was upregulated to suppress the proliferation and induce apoptosis of HPMVECs under LPS treatment. Besides, TILRR induced aberrant inflammatory responses and oxidative stress in HPMVECs under LPS treatment. Mechanistically, TILRR regulated proliferation, apoptosis, inflammatory responses, and oxidative stress in LPS-treated HPMVECs through inactivating the PI3K/Akt pathway. In summary, TILRR aggravated sepsis-induced ALI by suppressing the PI3K/Akt pathway. These results could provide novel therapy targets for sepsis-induced ALI.

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“…The animal experiment evidence suggested that NLRC3 inhibited the proliferation, migration, and inflammation of PASMCs and improved the symptoms of PH. Further, in the presence of agonists of PI3K-mTOR signal pathway, the beneficial effect of NLRC3 in the PH model were reversed ( 72 , 73 ). Thus, we can conclude that, NLRC3 improves the prognosis of PH by negatively regulating the PI3K-mTOR signaling pathway to suppress the proliferation, migration, and inflammation of PASMCs, NLRC3 may be the therapeutic target, diagnostic index, or prognostic index for PH.…”

Section: Role Of Nlrc3 In Immune-related Diseasesmentioning

confidence: 99%

Negative regulator NLRC3: Its potential role and regulatory mechanism in immune response and immune-related diseases

Sun

Zhang

et al. 2022

Front. Immunol.

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NLRC3 is a member of the pattern recognition receptors nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) family, and plays a pivotal regulatory role in modulating the activation of immune cells. In macrophages, NLRC3 inhibits the activation of the NF-κB signaling pathway, the STING/TBK1 signaling pathway, and the formation of the inflammasome. In the context of T cells immune response, NLRC3 prevents the activation of T cells by regulating the function of dendritic cells and directly influencing the function of T cells. Different from other pattern recognition receptors, NLRC3 is more closely associated with regulatory activity than pathogens recognition, it influences the fates of cells, for example, prevents proliferation, promotes apoptosis and inhibits pyroptosis. These cellular functions regulated by NLRC3 are involved in the development processes of a variety of diseases, such as infectious disease, sterile inflammatory diseases, and cancer. However, its characteristics, function and regulatory mechanism in immune response and immune-related diseases have not been addressed fully. In this review, we elaborate the potential roles of NLRC3 from several different levels, include molecular mechanism, cellular functions in the immune-related diseases.

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NLRC3 inhibits PDGF‐induced PASMCs proliferation via PI3K‐mTOR pathway

Cited by 15 publications

References 38 publications

Pattern of New Gene Origination in a Special Fish Lineage, the Flatfishes

Pattern of New Gene Origination in a Special Fish Lineage, the Flatfishes

TILRR Aggravates Sepsis-Induced Acute Lung Injury by Suppressing the PI3K/Akt Pathway

Negative regulator NLRC3: Its potential role and regulatory mechanism in immune response and immune-related diseases

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