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HGNC Genes

SARS-CoV-2 proteins

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    Excessive matrix metalloproteinase-1 HGNC and hyperactivation of endothelial cells occurred in COVID-19 MESHD patients and were associated with the severity of COVID-19 MESHD

    Authors: Fahim Syed; Wei Li; Ryan F Relich; Patrick M Russell; Shanxiang Zhang; Michelle K Zimmerman; Qigui Yu

    doi:10.1101/2021.01.19.21250115 Date: 2021-01-20 Source: medRxiv

    COVID-19 MESHD starts as a respiratory disease MESHD that can progress to pneumonia MESHD, severe acute respiratory syndrome MESHD (SARS), and multi-organ failure MESHD. Growing evidence suggests that COVID-19 MESHD is a systemic illness that primarily injures the vascular endothelium, yet the underlying mechanisms remain unknown. SARS-CoV-2 infection MESHD is believed to trigger a cytokine storm that plays a critical role in the pathogenesis of endothelialitis and vascular injury MESHD, eventually leading to respiratory and multi-organ failure MESHD in COVID-19 MESHD patients. We used a multiplex immunoassay to systematically profile and compare 65 inflammatory cytokines/chemokines/growth factors in plasma samples from 24 hospitalized (severe/critical) COVID-19 MESHD patients, 14 mild/moderate cases, and 13 healthy controls (HCs). Patients with severe/critical and mild/moderate COVID-19 MESHD had significantly higher plasma levels of 20 analytes than HCs. Surprisingly, only one cytokine ( MIF HGNC) was among these altered analytes, while the rest were chemokines and growth factors. In addition, only MMP-1 HGNC and VEGF-A HGNC were significantly elevated in hospitalized COVID-19 MESHD patients when compared to mild/moderate cases. Given that excessive MMP-1 HGNC plays a central role in tissue destruction in a wide variety of vascular diseases MESHD and that elevated VEGF-A HGNC, an EC activation marker, increases vascular permeability, we further studied MMP-1 HGNC enzymatic activity and other EC activation markers such as soluble forms of CD146 HGNC, ICAM-1 HGNC, and VCAM-1 HGNC. We found that plasma MMP-1 HGNC enzymatic activity and plasma levels of MMP-1 HGNC and EC activation markers were highly dysregulated in COVID-19 MESHD patients. Some dysregulations MESHD were associated with patients age or gender, but not with race. Our results demonstrate that COVID-19 MESHD patients have distinct inflammatory profiles that are distinguished from the cytokine storms in other human diseases. Excessive MMP-1 HGNC and hyperactivation of ECs occur in COVID-19 MESHD patients and are associated with the severity of COVID-19 MESHD.

    The aging whole blood transcriptome reveals a potential role of FASLG HGNC in COVID-19 MESHD

    Authors: Luiz Gustavo Chuffa Sr.; Jeferson dos Santos Souza Sr.; Mariana Costa de Mello; Mario de Oliveira Neto Sr.; Robson Francisco Carvalho Sr.; Kevin S. Cashman; Richard P. Ramonell; Shuya Kyu; Ankur Singh Saini; Monica Cabrera-Mora; Andrew Derrico; David Alter; John D. Roback; Michael Horwath; Henry M. Wu; An-Kwok Ian Wong; Alexandra W. Dretler; Ria Gripaldo; Andrea N. Lane; Hao Wu; Saeyun Lee; Mindy Hernandez; Vanessa Engineer; John Varghese; Sang Le; Iñaki Sanz; John L. Daiss; Frances Eun-Hyung Lee

    doi:10.1101/2020.12.04.412494 Date: 2020-12-06 Source: bioRxiv

    The risk for severe illness from COVID-19 MESHD increases with age as older patients are at the highest risk. Although it is still unclear whether the virus is blood-transmitted, the viral RNA is detected in serum. Identifying how Severe Acute Respiratory Syndrome Coronavirus 2 MESHD (SARS-CoV-2) interacts with specific blood components during aging is expected to guide proper therapies. Considering that all human coronavirus require host cellular molecules to promote infection, we investigated the aging whole blood transcriptome from the Genotype-Tissue Expression (GTEx) database to explore differentially expressed genes (DEGs) translated into proteins potentially interacting with viral proteins. From a total of 22 DEGs in aged blood, five genes ( FASLG HGNC, CTSW HGNC, CTSE HGNC, VCAM1 HGNC, and BAG3 HGNC) changed expression during aging. These age-related genes are involved in immune response, inflammation MESHD, cell component and cell adhesion, and platelet activation/aggregation. Both males and females older than 50 overexpress FASLG HGNC compared with younger adults (20-30 years old), possibly inducing a hyper-inflammatory cascade that activates specific immune cells. Furthermore, the expression of cathepsins ( CTSW HGNC and CTSE HGNC) and the anti-apoptotic co-chaperone molecule BAG3 HGNC was significantly increased throughout aging in both gender. By exploring publicly available Single-Cell RNA-Sequencing (scRNA-Seq) data on peripheral blood of SARS-CoV-2-infected MESHD patients, we found FASLG HGNC and CTSW HGNC expressed mainly in natural killer (NK) cells and CD8+ (cytotoxic) T lymphocytes whereas BAG3 HGNC was expressed in CD4+ T cells, naive T cells, and CD14 HGNC+ monocytes. The increased expression of FASLG HGNC in blood during aging may explain why older patients are more prone to severe acute viral infection complications MESHD. These results indicate FASLG HGNC as a prognostic candidate and potential therapeutic target for more aggressive clinical manifestation of COVID-19 MESHD.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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