CD99-like 2 (CD99L2)-deficient mice are defective in the acute inflammatory response

Rutledge, Nakisha S.; Weber, Evan W.; Winger, Ryan C.; Tourtellotte, Warren G.; Park, Seong Hoe; Müller, William A.

doi:10.1016/j.yexmp.2015.08.011

Cited by 5 publications

(3 citation statements)

References 21 publications

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“…PPP1R13L is significantly induced during in vitro trophectoderm differentiation [75], and ARPC2 supports endothelial barrier during angiogenesis [76]. RNA editing site was also localized within 3’UTR of CD99L2 , that is mostly expressed on leukocytes, endothelial cells and plays a role in extravasation of neutrophils under inflammatory conditions [77]. Selection and maturation of T-cells are regulated by both LCK proto-oncogene, Src family tyrosine kinase ( LCK ) and tyrosine kinases ( ZAP70 ), as key signaling molecules essential for lymphokine production [78,79], moreover, LCK affects trophoblast invasion and decidualization [80,81].…”

Section: Discussionmentioning

confidence: 99%

Placenta Transcriptome Profiling in Intrauterine Growth Restriction (IUGR)

Majewska

Lipka

Paukszto

et al. 2019

IJMS

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Intrauterine growth restriction (IUGR) is a serious pathological complication associated with compromised fetal development during pregnancy. The aim of the study was to broaden knowledge about the transcriptomic complexity of the human placenta by identifying genes potentially involved in IUGR pathophysiology. RNA-Seq data were used to profile protein-coding genes, detect alternative splicing events (AS), single nucleotide variant (SNV) calling, and RNA editing sites prediction in IUGR-affected placental transcriptome. The applied methodology enabled detection of 37,501 transcriptionally active regions and the selection of 28 differentially-expressed genes (DEGs), among them 10 were upregulated and 18 downregulated in IUGR-affected placentas. Functional enrichment annotation indicated that most of the DEGs were implicated in the processes of inflammation and immune disorders related to IUGR and preeclampsia. Additionally, we revealed that some genes (S100A13, GPR126, CTRP1, and TFPI) involved in the alternation of splicing events were mainly implicated in angiogenic-related processes. Significant SNVs were overlapped with 6533 transcripts and assigned to 2386 coding sequence (CDS), 1528 introns, 345 5’ untranslated region (UTR), 1260 3’UTR, 918 non-coding RNA (ncRNA), and 10 intergenic regions. Within CDS regions, 543 missense substitutions with functional effects were recognized. Two known mutations (rs4575, synonymous; rs3817, on the downstream region) were detected within the range of AS and DEG candidates: PA28β and PINLYP, respectively. Novel genes that are dysregulated in IUGR were detected in the current research. Investigating genes underlying the IUGR is crucial for identification of mechanisms regulating placental development during a complicated pregnancy.

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Section: Discussionmentioning

confidence: 99%

Placenta Transcriptome Profiling in Intrauterine Growth Restriction (IUGR)

Majewska

Lipka

Paukszto

et al. 2019

IJMS

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“…Among them, hsa_circ_091692, hsa_circ_102296 and hsa_circ_029965 were up‐regulated in active TB plasma. Hsa_circ_091692 is encoded by the CD99L2 (CD99‐Like 2) gene, the protein product expressed on leucocytes and play an important role in various acute and chronic inflammatory diseases . Hsa_circ_102296 aligns with ANKRD12 (Ankyrin repeat domain 12), which encodes a 224 kD nuclear protein associated with colorectal cancer .…”

Section: Discussionmentioning

confidence: 99%

Dysregulated circRNAs in plasma from active tuberculosis patients

Gao

et al. 2018

J Cellular Molecular Medi

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Endogenous circular RNAs (circRNAs) have been reported in various diseases. However, their role in active TB remains unknown. The study was aimed to determine plasma circRNA expression profile to characterize potential biomarker and improve our understanding of active TB pathogenesis. CircRNA expression profiles were screened by circRNA microarrays in active TB plasma samples. Dysregulated circRNAs were then verified by qRT‐PCR. CircRNA targets were predicted based on analysis of circRNA‐miRNA‐mRNA interaction. GO and KEGG pathway analyses were used to predict the function of circRNA. ROC curve was calculated to evaluate diagnostic value for active TB. A total of 75 circRNAs were significantly dysregulated in active TB plasma. By further validation, hsa_circRNA_103571 exhibited significant decrease in active TB patients and showed potential interaction with active TB‐related miRNAs such as miR‐29a and miR‐16. Bioinformatics analysis revealed that hsa_circRNA_103571 was primarily involved in ras signalling pathway, regulation of actin cytoskeleton, T‐ and B‐cell receptor signalling pathway. ROC curve analysis suggested that hsa_circRNA_103571 had significant value for active TB diagnosis. Circulating circRNA dysregulation may play a role in active TB pathogenesis. Hsa_circRNA_103571 may be served as a potential biomarker for active TB diagnosis, and hsa_circRNA_103571‐miRNA‐mRNA interaction may provide some novel mechanism for active TB.

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“…When leukocytes reach the site of transmigration, the homophilic interactions between PECAM-1 on leukocytes with PECAM-1 on the endothelium causes a transient increase in cytosolic calcium in ECs which guide the leukocytes to the junctions ( Ley, 2007 ; Muller, 2011 ). Like PECAM-1, CD99 ( Schenkel et al, 2002 ) and CD99L2, expressed at EC junctions and on leukocytes, rely on a homophilic interactions to promote leukocyte extravasation ( Schenkel et al, 2002 ; Seelige et al, 2013 ; Rutledge et al, 2015 ). In ECs, the major functional component of the adherent junction is VE-cadherin.…”

Section: The Molecular Processes Of Leukocyte Recruitment In Inflammamentioning

confidence: 99%

Dysregulation of Leukocyte Trafficking in Type 2 Diabetes: Mechanisms and Potential Therapeutic Avenues

Pezhman

Tahrani

Chimen

2021

Front. Cell Dev. Biol.

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Type 2 Diabetes Mellitus (T2DM) is a chronic inflammatory disorder that is characterized by chronic hyperglycemia and impaired insulin signaling which in addition to be caused by common metabolic dysregulations, have also been associated to changes in various immune cell number, function and activation phenotype. Obesity plays a central role in the development of T2DM. The inflammation originating from obese adipose tissue develops systemically and contributes to insulin resistance, beta cell dysfunction and hyperglycemia. Hyperglycemia can also contribute to chronic, low-grade inflammation resulting in compromised immune function. In this review, we explore how the trafficking of innate and adaptive immune cells under inflammatory condition is dysregulated in T2DM. We particularly highlight the obesity-related accumulation of leukocytes in the adipose tissue leading to insulin resistance and beta-cell dysfunction and resulting in hyperglycemia and consequent changes of adhesion and migratory behavior of leukocytes in different vascular beds. Thus, here we discuss how potential therapeutic targeting of leukocyte trafficking could be an efficient way to control inflammation as well as diabetes and its vascular complications.

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CD99-like 2 (CD99L2)-deficient mice are defective in the acute inflammatory response

Cited by 5 publications

References 21 publications

Placenta Transcriptome Profiling in Intrauterine Growth Restriction (IUGR)

Placenta Transcriptome Profiling in Intrauterine Growth Restriction (IUGR)

Dysregulated circRNAs in plasma from active tuberculosis patients

Dysregulation of Leukocyte Trafficking in Type 2 Diabetes: Mechanisms and Potential Therapeutic Avenues

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