A single–cell type transcriptomics map of human tissues

Karlsson, Max; Zhang, Cheng Cheng; Méar, Loren; Zhong, Wen; Digre, Andreas; Katona, Borbala; Sjöstedt, Evelina; Butler, Lynn M.; Odeberg, Jacob; Dusart, Philip; Edfors, Fredrik; Oksvold, Per; Feilitzen, Kalle von; Zwahlén, Martin; Arif, Muhammad; Altay, Özlem; Li, Xiangyu; Özcan, Mehmet; Mardinoğlu, Adil; Fagerberg, Linn; Mulder, Jan; Luo, Yonglun; Pontén, Fredrik; Uhlén, Mathias; Lindskog, Cecilia

doi:10.1126/sciadv.abh2169

Cited by 902 publications

(912 citation statements)

References 34 publications

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“…Transcripts in blood could indicate expression by blood cells or could reflect the presence of circulating EC. In 2 body-wide human single-cell atlases 48 , 49 and 1 single-cell database (of both mouse and human studies), 50 the majority of the 38 candidates were enriched in EC; 20/38 (53%) in 2 or all, with 25/38 (66%) in at least 1 (Table I, Tab_5, Table A, column O, P, Q in the Data Supplement ). Transcripts encoding for 13/38 candidates (34%) were enriched in immortalized EC, versus other cell lines (Table I, Tab_5, Table A, column S in the Data Supplement ).…”

Section: Resultsmentioning

confidence: 99%

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Identification of Endothelial Proteins in Plasma Associated With Cardiovascular Risk Factors

Iglesias

Kruse

Sánchez-Rivera

et al. 2021

ATVB

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Objective: Endothelial cell (EC) dysfunction is a well-established response to cardiovascular disease risk factors, such as smoking and obesity. Risk factor exposure can modify EC signaling and behavior, leading to arterial and venous disease development. Here, we aimed to identify biomarker panels for the assessment of EC dysfunction, which could be useful for risk stratification or to monitor treatment response. Approach and Results: We used affinity proteomics to identify EC proteins circulating in plasma that were associated with cardiovascular disease risk factor exposure. Two hundred sixteen proteins, which we previously predicted to be EC-enriched across vascular beds, were measured in plasma samples (N=1005) from the population-based SCAPIS (Swedish Cardiopulmonary Bioimage Study) pilot. Thirty-eight of these proteins were associated with body mass index, total cholesterol, low-density lipoprotein, smoking, hypertension, or diabetes. Sex-specific analysis revealed that associations predominantly observed in female- or male-only samples were most frequently with the risk factors body mass index, or total cholesterol and smoking, respectively. We show a relationship between individual cardiovascular disease risk, calculated with the Framingham risk score, and the corresponding biomarker profiles. Conclusions: EC proteins in plasma could reflect vascular health status.

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Section: Resultsmentioning

confidence: 99%

“…Data from human single-cell atlases 48 , 49 and the Panglao database ( https://panglaodb.se ) 50 were used to provide EC protein expression information in Table I, Tab 5 in the Data Supplement .…”

Section: Methodsmentioning

confidence: 99%

Identification of Endothelial Proteins in Plasma Associated With Cardiovascular Risk Factors

Iglesias

Kruse

Sánchez-Rivera

et al. 2021

ATVB

Self Cite

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“…Regarding the cardiovascular system, cardiomyocytes, endothelial cells, fibroblasts, smooth muscle cells and immune cells are relevant. Several enzymes are expressed in these cells, for detailed information see Supplement Table healthy human tissues (Supplement Table 1) according to transcriptomics datasets of www.proteinatlas.org (28). The ratelimiting IDO expression is not detected in cardiomyocytes, fibroblasts and dendritic cells, and expression is low in endothelial, smooth muscle and T cells, and high in macrophages and monocytes (Supplement Table 1) in healthy persons.…”

Section: The Kynurenine Pathwaymentioning

confidence: 99%

Kynurenine Pathway Metabolites as Potential Clinical Biomarkers in Coronary Artery Disease

et al. 2022

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Coronary artery disease (CAD) is one of the leading cause of mortality worldwide. Several risk factors including unhealthy lifestyle, genetic background, obesity, diabetes, hypercholesterolemia, hypertension, smoking, age, etc. contribute to the development of coronary atherosclerosis and subsequent coronary artery disease. Inflammation plays an important role in coronary artery disease development and progression. Pro-inflammatory signals promote the degradation of tryptophan via the kynurenine pathway resulting in the formation of several immunomodulatory metabolites. An unbalanced kynurenic pathway has been implicated in the pathomechanisms of various diseases including CAD. Significant improvements in detection methods in the last decades may allow simultaneous measurement of multiple metabolites of the kynurenine pathway and such a thorough analysis of the kynurenine pathway may be a valuable tool for risk stratification and determination of CAD prognosis. Nevertheless, imbalance in the activities of different branches of the kynurenine pathway may require careful interpretation. In this review, we aim to summarize clinical evidence supporting a possible use of kynurenine pathway metabolites as clinical biomarkers in various manifestations of CAD.

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“…In this study, we found that knocking out the PIGS and HRD1 genes caused the accumulation of CD55 precursor proteins, which enabled us to reveal the speci c role of the GPI attachment signal peptide of CD55 in GPI biosynthesis. It is reasonable to postulate that CD55 acts as a regulator because it is widely expressed in diverse organs and cells 52 . Moreover, we found that the GPI attachment signal peptide of CD48 functioned similarly to that of CD55.…”

Section: Discussionmentioning

confidence: 99%

Precursors of select GPI-anchored proteins positively regulate GPI biosynthesis under the control of ERAD

Liu¹,

Wang²,

Zhou³

et al. 2021

Preprint

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We previously reported that glycosylphosphatidylinositol (GPI) biosynthesis is regulated by endoplasmic reticulum associated degradation (ERAD); however, the underlying mechanistic basis remains unclear. Based on a genome-wide CRISPR–Cas9 screen, we show that a widely expressed GPI-anchored protein CD55 precursor and ER-resident ARV1 together upregulate GPI biosynthesis under ERAD-deficient conditions. In cells defective in GPI transamidase, GPI-anchored protein precursors fail to obtain GPI, remaining the uncleaved GPI-attachment signal at the C-termini. We show that ERAD deficiency causes accumulation of the CD55 precursor, which in turn upregulates GPI biosynthesis, where the GPI-attachment signal peptide is the active element. Among the 32 GPI-anchored proteins tested, only the GPI-attachment signal peptides of CD55 and CD48 enhance GPI biosynthesis. ARV1 is essential for the GPI upregulation by CD55 precursor. Our data demonstrate an ARV1-dependent regulatory connection between GPI biosynthesis and precursors of select GPI-anchored proteins that are under the control of ERAD.

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A single–cell type transcriptomics map of human tissues

Cited by 902 publications

References 34 publications

Identification of Endothelial Proteins in Plasma Associated With Cardiovascular Risk Factors

Identification of Endothelial Proteins in Plasma Associated With Cardiovascular Risk Factors

Kynurenine Pathway Metabolites as Potential Clinical Biomarkers in Coronary Artery Disease

Precursors of select GPI-anchored proteins positively regulate GPI biosynthesis under the control of ERAD

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