Proteome Profiling of PMJ2-R and Primary Peritoneal Macrophages

Русанов, А. Л.; Кожин, П. М.; Tikhonova, Olga V.; Zgoda, Victor G.; Loginov, Dmitry S.; Chlastáková, Adéla; Selinger, Martin; Štěrba, Ján; Grubhoffer, Libor; Лузгина, Н. Г.

doi:10.3390/ijms22126323

Cited by 9 publications

(6 citation statements)

References 72 publications

(86 reference statements)

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“…After centrifugation, the milk-white mononuclear cells in the second layer were transferred to a new centrifuge tube, washed with cleaning solution, and resuspended in RPMI (Roswell Park Memorial Institute) 1640 medium supplemented with 10% FBS. Primary peritoneal macrophages were derived from 12-week male WT and FcγRⅢ −/− mice fed a control diet or adenine diet as described in a previous study 37 and cultured in RPMI 1640 medium with 10% FBS at 37 °C in 5% CO 2 . Bone marrow–derived macrophages were isolated from the tibias and femurs of 8-week male C57BL/6J mice.…”

Section: Methodsmentioning

confidence: 99%

Urate-Lowering Therapy Inhibits Thoracic Aortic Aneurysm and Dissection Formation in Mice

Liu

Luo

et al. 2023

ATVB

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Background: Thoracic aortic aneurysm and dissection (TAAD) is a highly lethal vascular disease without effective drug therapy. Whether elevated serum concentrations of uric acid are involved in TAAD development remains unclear. Methods: Serum uric acid levels were detected in different TAAD mouse models and patients. The urate-lowering drug allopurinol was administered in the drinking water of TAAD mice. Adenine diet–induced mice were established to investigate the role of hyperuricemia in TAAD formation and RNA-sequencing of thoracic aortas from these mice was performed. Results: We found serum uric acid levels were elevated in various mouse TAAD models, including mice fed a β-aminopropionitrile diet, Marfan mice with fibrillin-1 haploinsufficiency (Fbn1 C1041G/+ ), and ApoE −/− mice infused with Ang II (angiotensin II), as well as in patients with TAAD. Administration of urate-lowering drug allopurinol in the drinking water significantly alleviated TAAD formation in β-aminopropionitrile–treated mice, Fbn1 C1041G/+ mice, and Ang II–infused ApoE −/− mice. Moreover, an adenine diet was used to induce hyperuricemia in mice. Intriguingly, a 4-week adenine diet feeding directly induced TAAD formation characterized by increased maximal thoracic aortic diameters and severe elastin degradation, which were ameliorated by allopurinol. Unbiased RNA-sequencing in mouse thoracic aortas suggested that FcγR (Fc gamma receptor) was upregulated upon adenine diet, but reciprocally repressed by allopurinol. Mechanistically, hyperuricemia activated FcγR-mediated ERK1/2 (extracellular signal-regulated kinase 1/2) phosphorylation to induce macrophage inflammation and TAAD development, which was abrogated by allopurinol or FcγR deficiency. Conclusions: This study uncovered an important and previously unrecognized role of hyperuricemia in mediating the pathogenesis of TAAD, and uric acid–lowering drug may represent a promising therapeutic approach for TAAD.

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Section: Methodsmentioning

confidence: 99%

Urate-Lowering Therapy Inhibits Thoracic Aortic Aneurysm and Dissection Formation in Mice

Liu

Luo

et al. 2023

ATVB

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“…High-performance liquid chromatography and mass spectrometry analysis was performed similarly to Rusanov et al (2021) with minimal changes.…”

Section: Methodsmentioning

confidence: 99%

“…The isolation width for precursor ions was 2 m/z. Precursors with a charge state of 1+ and more than 5+ were rejected, and all measured precursors were dynamically excluded from triggering of a subsequent MS/MS for 20 s ( Rusanov et al, 2021 ).…”

Section: Methodsmentioning

confidence: 99%

Some structural features of the peptide profile of myelin basic protein-hydrolyzing antibodies in schizophrenic patients

Zavialova

Parshukova

Kazieva

et al. 2023

PeerJ

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The antibodies of schizophrenic patients that hydrolyze myelin basic protein (MBP) have been actively studied recently, but the mechanism of the catalytic properties of immunoglobulin molecules remains unknown. Determination of specific immunoglobulin sequences associated with the high activity of MBP proteolysis will help to understand the mechanisms of abzyme catalysis. In the course of comparative mass spectrometric analysis of IgG peptides from the blood serum of patients with acute schizophrenia and healthy people, 12 sequences were identified, which were found only in antibodies that hydrolyze MBP. These sequences belong to IgG heavy chains and κ- and λ-type light chains, with eight of them belonging to variable domains. The content of peptides from the variable regions of the light chains does not correlate with the proteolytic activity of IgG to MBP in patients with schizophrenia, whereas for two sequences from the variable regions of the heavy chains (FQ(+0.98)GWVTMTR and *LYLQMN(+0.98)SLR), an increase in activity with increasing their concentration. The results suggest that these sequences may be involved in one way or another in MBP hydrolysis.

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“…Cells were cultured in an atmosphere at 24°C. Extraction and purification of primary macrophages were modified and optimized based on a previous protocol (51,52), and its effectiveness was verified by our group.…”

Section: Hepatocyte Cell Line Of Chinese Tongue Sole Was From China Y...mentioning

confidence: 99%

SHP-1 interacts with NFκB1 to inhibit its phosphorylation and nuclear translocation to suppress excessive bacterial inflammation

Wang,

Tan,

Wang

et al. 2024

Preprint

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The protein tyrosine phosphatase SHP-1 is a key negative regulator in cancer by dephosphorylating multiple target molecules. Specially in the NFκB signaling, where NFκB1/Rela dimer translocate to the nucleus and activate target gene transcription, SHP-1 inhibits the phosphorylation of Rela, while its regulation on NFκB1 has been unknown, especially in pathogen-induced inflammation. Chinese tongue sole, a representative flatfish, has been widely used as a genomics and disease model. Using the teleost and cellular model, we revealed for the first time that SHP-1 inhibits NFκB1 phosphorylation and nuclear translocation by interacting with NFκB1, thereby suppressing NFκB signaling to inhibit bacterial inflammation. In addition, we showed that SHP-1 decreased mortality and alleviated histopathological deterioration, manifested in the inhibition of immune-related pathways and secretion of pro- inflammatory cytokines. Using cellular model, SHP-1 overexpression reduced macrophages M1 polarization, phagocytosis, and oxidative stress, while silencing SHP- 1 exhibited opposite effects. Our findings systematically dissect the functions of SHP- 1 and provide mechanistic insights into the control of inflammation-related diseases.TeaserSHP-1 help maintain the cellular and individual homeostasis by inhibiting the excessive inflammation and immunity via regulating the NFκB signaling.

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Proteome Profiling of PMJ2-R and Primary Peritoneal Macrophages

Cited by 9 publications

References 72 publications

Urate-Lowering Therapy Inhibits Thoracic Aortic Aneurysm and Dissection Formation in Mice

Urate-Lowering Therapy Inhibits Thoracic Aortic Aneurysm and Dissection Formation in Mice

Some structural features of the peptide profile of myelin basic protein-hydrolyzing antibodies in schizophrenic patients

SHP-1 interacts with NFκB1 to inhibit its phosphorylation and nuclear translocation to suppress excessive bacterial inflammation

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