Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Single cell transcriptomics profiling of the stromal cells in the pathologic association of ribosomal proteins in the ischemic myocardium and epicardial fat.

Thai A., Doescher C., Kamal N., Teramoto D., Fung C., Cha E.

Animal Study on Cardiovascular Disease, Chronic Inflammation, published in Cell Tissue Res (2024) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Cell Tissue Res (2024)
Country
Germany
Reported sample size
—
Source database
PubMed
PMID
39641799
DOI
10.1007/s00441-024-03933-3

Abstract (original English)

Sustenance of ischemia in the surviving cardiac tissue following myocardial infarction (MI) elicits a proinflammatory milieu resulting in subsequent pathological episodes. Also, the activation and release of ribosomal proteins under ischemic insults have been unveiled; however, their extra ribosomal functions are unknown. We identified the ribosomal proteins including RPL10A, RPL14, RPL30, RPS18, FAU-40 (RPS30), and RPSA (Laminin Receptor, LR) in the vesicles of ischemia challenged epicardial adipose tissue derived stromal cells (EATDS). The present study aimed to assess the association of these proteins in the epicardial adipose tissues (EAT) and left ventricular (LV) myocardium and isolated stromal cells (EATDS and LVSCs) from hyperlipidemic (HL), MI and coronary artery bypass graft (CABG) swine models. The findings revealed an upregulation of RPL10A, RPL14, RPL30, RPS18, RPS30, and RPSA in the LV tissues of CABG and HL swine with a concomitant reduction in the MI group. RPS30 displayed similar upregulation in EAT, whereas the expression of other ribosomal proteins was not significantly altered. Additionally, the ischemic LVSCs and EATDS displayed altered expression status of these genes compared to the control. Also, the RPS18 + , RPL30 + and RPSA + LVSCs favored ischemia and revealed similar anti-inflammatory and regenerative sub-phenotypes reflecting the protective/surviva

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
AnimalsRibosomal ProteinsSwineMyocardial IschemiaAdipose TissuePericardiumStromal CellsMyocardiumGene Expression ProfilingSingle-Cell Analysis

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