Inverse Correlation of TRIM32 and Protein Kinase C ζ in T Helper Type 2–Biased Inflammation

Wang, Zhiping; Yoo, Yeon Jung; Torre, R. De La; Topham, Christina; Hanifin, Jon M.; Simpson, Eric L.; Messing, Robert O.; Kulesz‐Martin, Molly; Liu, Yuangang

doi:10.1016/j.jid.2020.09.021

Cited by 5 publications

(5 citation statements)

References 41 publications

(53 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ubiquitinating and deubiquitinating can change intracellular homeostasis and modulate the cellular cycle, proliferation, and survival ( Kwon and Ciechanover, 2017 ). Notably, current studies confirmed that E3 ubiquitin ligases and DUBs play roles in the AD pathophysiology ( Fang et al, 2002 ; Loeser and Penninger, 2007a ; Mohapatra et al, 2013a ; G’Sell et al, 2015 ; Theivanthiran et al, 2015 ; Liu et al, 2017 ; Salva et al, 2017 ; Tang et al, 2018 ; Devos et al, 2019 ; Harirchian et al, 2019 ; Sundberg et al, 2020 ; Wang et al, 2021 ).…”

Section: Involvement Of Post-translational Modifications In Adssupporting

confidence: 70%

“…According to the down-regulation of Trim32 and Sharpin in AD patients, similar findings were observed that Trim32-deficient mice present T H 2-biased inflammation spontaneously developed in imiquimod-induced psoriatic dermatitis ( Liu et al, 2017 ; Wang et al, 2021 ), while KCs-specific Sharpin knockout mice developed more severe inflammatory AD lesions compared to normal ones ( Sundberg et al, 2020 ). Transmembrane protein 79 (TMEM79, a predisposition gene for AD) can specifically inhibit ubiquitin-specific peptidase 8 deubiquitination, and its deficiency shows more susceptible to developing skin inflammation, compromised barrier function, and spontaneous dermatitis ( Lim et al, 2013 ; Sasaki et al, 2013 ; Saunders et al, 2013 ; Chen et al, 2020 ).…”

Section: Involvement Of Post-translational Modifications In Adssupporting

confidence: 69%

See 1 more Smart Citation

Post-Translational Modifications in Atopic Dermatitis: Current Research and Clinical Relevance

Luo

et al. 2022

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Atopic dermatitis (AD) is a chronic and relapsing cutaneous disorder characterized by compromised immune system, excessive inflammation, and skin barrier disruption. Post-translational modifications (PTMs) are covalent and enzymatic modifications of proteins after their translation, which have been reported to play roles in inflammatory and allergic diseases. However, less attention has been paid to the effect of PTMs on AD. This review summarized the knowledge of six major classes (including phosphorylation, acetylation, ubiquitination, SUMOylation, glycosylation, o-glycosylation, and glycation) of PTMs in AD pathogenesis and discussed the opportunities for disease management.

show abstract

Section: Involvement Of Post-translational Modifications In Adssupporting

confidence: 70%

Section: Involvement Of Post-translational Modifications In Adssupporting

confidence: 69%

Post-Translational Modifications in Atopic Dermatitis: Current Research and Clinical Relevance

Luo

et al. 2022

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

show abstract

“…Lower expression of CXCL12, CXCL2, CXCL16 and CCR3 in LCAL dairy cows further confirmed a reduced capacity for recruitment and migration of PMNL to the inflammation site ( 15 , 16 ). LCAL dairy cows had lower expression of PRKCZ, a calcium and diacylglycerol independent serine/threonine-protein kinase, confirming that hypocalcemia reduced PRKCZ kinase activity to decrease transendothelial migration ( 17 , 18 ), thus, increasing the risk of infectious diseases.…”

Section: Resultsmentioning

confidence: 80%

Transcriptomics of circulating neutrophils in dairy cows with subclinical hypocalcemia

Zhang

Ma²,

Huang³

et al. 2022

Front. Vet. Sci.

View full text Add to dashboard Cite

Hypocalcemia is closely associated with inflammatory diseases in dairy cows. Recent research has underscored the key role of calcium in the adaptations of the innate immune system during this period. The main objective in the present study was to compare the transcriptome profiles and analyze differences in the expression of neutrophil (PMNL) immune function-related genes and calcium binding-related genes in hypocalcemic cows. At 2 days postpartum, a concentration >2.10 mmol Ca2+/L was used to classify cows as controls (CON), and a concentration <2.00 mmol Ca2+/L used to classify cows as low-calcium (LCAL) (n = 8 in each group). A routine medical examination was conducted by the attending veterinarian to ensure there were no other complications and that the blood β-hydroxybutyrate was <1.2 mmol/L. Blood was collected from the tail vein (20 mL) to isolate PMNL, and 5 cows in each group were used for RNA sequencing and statistical analysis of gene expression differences. Transcriptome RNA-seq sequencing analysis was via omicsstudio using the R package edgeR. GO and KEGG enrichment analysis were used for bioinformatics. The remaining 3 cows in each group were used for validation of RNA sequencing data via quantitative PCR, which confirmed the observed responses. Compared with CON, 158 genes in LCAL were significantly up-regulated and 296 genes were down-regulated. The downregulation of Interleukin-12 (CXCL12), Tubulin beta chain (TUBB1), L1 cell adhesion molecule (L1CAM), and Myeloperoxidase (MPO) indicated a decrease in immune function of PMNL in LCAL cows. The decreased expression of calcium-binding pathway-related genes in PMNL of LCAL cows indicated a decrease in immune function of PMNL likely related to calcium ions. For example, cartilage acid protein 1 (CRTAC1) and calcium/calmodulin-dependent kinase 4 (CAMK4) were significantly reduced in LCAL cows. The upregulation of Cyclin dependent kinase inhibitor 1A (CDKN1A), Perforin 1 (PRF1), and Homeodomain interacting protein kinase 3 (HIPK3) indicated that LCAL led to greater cell apoptosis and senescence. Overall, the analyses indicated that the reduction in PMNL immune function during hypocalcemia is associated with downregulation of intracellular Ca2+ related genes and upregulation of genes controlling apoptosis and senescence. Together, these alterations contribute to an immunosuppressive state during the transition period.

show abstract

“…RhoA is a GTPase plays an essential role in the migration and activation of T cells (73). PRKCZ is a protein kinase C family member that is highly expressed in Th2 CD4+ T cells (74). PARD3 and PARD6A have been shown regulate the RhoA signaling pathway (75).…”

Section: Discussionmentioning

confidence: 99%

Lymphocyte-Specific Biomarkers Associated With Preterm Birth and Bronchopulmonary Dysplasia

et al. 2021

View full text Add to dashboard Cite

Many premature babies who are born with neonatal respiratory distress syndrome (RDS) go on to develop Bronchopulmonary Dysplasia (BPD) and later Post-Prematurity Respiratory Disease (PRD) at one year corrected age, characterized by persistent or recurrent lower respiratory tract symptoms frequently related to inflammation and viral infection. Transcriptomic profiles were generated from sorted peripheral blood CD8+ T cells of preterm and full-term infants enrolled with consent in the NHLBI Prematurity and Respiratory Outcomes Program (PROP) at the University of Rochester and the University at Buffalo. We identified outcome-related gene expression patterns following standard methods to identify markers for oxygen utilization and BPD as outcomes in extremely premature infants. We further identified predictor gene sets for BPD based on transcriptomic data adjusted for gestational age at birth (GAB). RNA-Seq analysis was completed for CD8+ T cells from 145 subjects. Among the subjects with highest risk for BPD (born at <29 weeks gestational age (GA); n=72), 501 genes were associated with oxygen utilization. In the same set of subjects, 571 genes were differentially expressed in subjects with a diagnosis of BPD and 105 genes were different in BPD subjects as defined by physiologic challenge. A set of 92 genes could predict BPD with a moderately high degree of accuracy. We consistently observed dysregulation of TGFB, NRF2, HIPPO, and CD40-associated pathways in BPD. Using gene expression data from both premature and full-term subjects (n=116), we identified a 28 gene set that predicted the PRD status with a moderately high level of accuracy, which also were involved in TGFB signaling. Transcriptomic data from sort-purified peripheral blood CD8+ T cells from 145 preterm and full-term infants identified sets of molecular markers of inflammation associated with independent development of BPD in extremely premature infants at high risk for the disease and of PRD among the preterm and full-term subjects.

show abstract

Inverse Correlation of TRIM32 and Protein Kinase C ζ in T Helper Type 2–Biased Inflammation

Cited by 5 publications

References 41 publications

Post-Translational Modifications in Atopic Dermatitis: Current Research and Clinical Relevance

Post-Translational Modifications in Atopic Dermatitis: Current Research and Clinical Relevance

Transcriptomics of circulating neutrophils in dairy cows with subclinical hypocalcemia

Lymphocyte-Specific Biomarkers Associated With Preterm Birth and Bronchopulmonary Dysplasia

Contact Info

Product

Resources

About