international-expert-consensus-recommendations-for-neonatal

International Expert Consensus and Recommendations for Neonatal Pneumothorax Ultrasound Diagnosis and Ultrasound-guided Thoracentesis Procedure

Pneumothorax (PTX) represents accumulation of the air in the pleural space. A large or tension pneumothorax can collapse the lung and cause hemodynamic ...

gene-knock-crisprcas9-cell-sorting-macrophage-t-cell

Gene Knock-in by CRISPR/Cas9 and Cell Sorting in Macrophage and T Cell Lines

Functional genomics studies of the immune system require genetic manipulations that involve both deletion of target genes and addition of elements to ...

Beijing Chaoyang District Maternal and Child Healthcare Hospital

Fifth Medical Center of Chinese PLA General Hospital

Xinxiang medical university

During foam cell formation and atherosclerosis development, the scavenger receptor CD36 plays critical roles in lipid uptake and triggering of atherogenicity via the activation of Vav molecules. The Vav family includes three highly conserved members known as Vav1, Vav2, and Vav3. As Vav1 and Vav3 were found to exert function in atherosclerosis development, it remains thus to decipher whether Vav2 also plays a role in the development of atherosclerosis. In this study we found that Vav2 deficiency in RAW264.7 macrophages significantly diminished oxidized LDL uptake and CD36 signaling, demonstrating that each Vav protein family member was required for foam cell formation. Genetic disruption of Vav2 in ApoE-deficient C57BL/6 mice significantly inhibited the severity of atherosclerosis. Strikingly, we further found that the genetic deletion of each member of the Vav protein family by CRISPR/Cas9 resulted in a similar alteration of transcriptomic profiles of macrophages. The three members of the Vav proteins were found to form complexes, and genetic ablation of each single Vav molecule was sufficient to prevent endocytosis of CD36. The functional interdependence of the three Vav family members in foam cell formation was due to their indispensable roles in transcriptomic programing, lipid uptake, and activation of the JNK kinase in macrophages.

The three members of the Vav family proteins form complexes that concur to foam cell formation and atherosclerosis.

 is associated with high mortality among immunocompromised patients. Resistance to and toxic side effects of antifungal drugs require the development of alternative antifungal agents. AMP-17 is a novel antimicrobial peptide derived from  that exerts excellent antifungal effects against the  species. In this article, we discuss the potential mechanism of AMP-17 against  from the perspective of affecting the latter's cell external structure.

Antimicrobial Peptide AMP-17 Affects  by Disrupting Its Cell Wall and Cell Membrane Integrity.

NF-κB activation is essential in mediating the induction of pro-inflammatory cytokines and also plays a key role in regulating the inflammatory response through intricate mechanisms. In this study, loss of Gfi1 was found to be associated with transcriptomic profiles related to NF-κB activation, including an increase in pro-inflammatory cytokines. Genetically inactivating the IKK/NF-κB signaling pathway in macrophages showed that Gfi1 deficiency led to pro-inflammatory cytokine production requiring NF-κB activation. More importantly, we revealed that one of the under-researched mechanisms, involving Gfi1 and Zc3h12c exerted negative regulation on NF-κB activation. Both Gfi1 and Zc3h12c were found to inhibit NF-κB activation, and double knockout exhibited additive roles of Gfi1 and Zc3h12c in preventing proinflammatory cytokine production. The loss of Gfi1 upregulated Zc3h12c which in turn inhibited NF-κB activation. Therefore, this study delineates the function of Zc3h12c in enhancing the negative regulation of Gfi1 through NF-κB activation during inflammation in macrophages.

Gfi1 and Zc3h12c orchestrate a negative feedback loop that inhibits NF-kB activation during inflammation in macrophages.

Atherosclerosis, a progressive inflammatory disease characterized by elevated inflammation and lipid accumulation in the aortic endothelium, arises in part from the infiltration of inflammatory cells into the vascular wall. However, it is not fully defined how inflammatory cells, especially macrophages, affect the pathogenesis of atherosclerosis. Schlafen4 (Slfn4) mRNA is remarkably upregulated upon ox-LDL stimulation in macrophages. Nonetheless, the role of Slfn4 in foam cell formation remains unclear.

Slfn4 deficiency improves MAPK-mediated inflammation, oxidative stress, apoptosis and abates atherosclerosis progression in apolipoprotein E-deficient mice.

ArticleTotal : 2	Year
Publication title Cited by 30	2020
Publication title Cited by 7	2021

Article	Year
The three members of the Vav family proteins form complexes that concur to foam cell formation and atherosclerosis. Journal of lipid research\| PubMed ID: 31570505	2019
Antimicrobial Peptide AMP-17 Affects by Disrupting Its Cell Wall and Cell Membrane Integrity. Infection and drug resistance\| PubMed ID: 32801789	2020
Gfi1 and Zc3h12c orchestrate a negative feedback loop that inhibits NF-kB activation during inflammation in macrophages. Molecular immunology\| PubMed ID: 33157351	2020
Slfn4 deficiency improves MAPK-mediated inflammation, oxidative stress, apoptosis and abates atherosclerosis progression in apolipoprotein E-deficient mice. Atherosclerosis\| PubMed ID: 34757313	2021

Guo Guo

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