Evidence map›Paper›PMID 35436627›Full record

ArticleBiochemical and biophysical research communications2022

Attenuated cell-cycle division protein 2 and elevated mitotic roles of polo-like kinase 1 characterize deficient myoblast fusion in peripheral arterial disease.

Ricardo Ferrari, Guangzhi Cong, Ansuman Chattopadhyay, B Xie, E Assaf, K Morder, Michael J Calderon, Simon C Watkins, Ulka Sachdev

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biochemical and biophysical research communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 59% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Ricardo FerrariUniversity of Pittsburgh Medical Center Department of Surgery, Division of Vascular Surgery, USA.
Guangzhi CongUniversity of Pittsburgh Medical Center Department of Surgery, Division of Vascular Surgery, USA; Department of Cardiology, Cardiovascular Institute, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China.
Ansuman ChattopadhyayHealth Sciences Library System, University of Pittsburgh School of Medicine, USA.
B XieUniversity of Pittsburgh Medical Center Department of Surgery, Division of Vascular Surgery, USA.
E AssafUniversity of Pittsburgh Medical Center Department of Surgery, Division of Vascular Surgery, USA.
K MorderUniversity of Pittsburgh Medical Center Department of Surgery, Division of Vascular Surgery, USA.
Michael J CalderonCenter for Biologic Imaging @ University of Pittsburgh, USA.
Simon C WatkinsCenter for Biologic Imaging @ University of Pittsburgh, USA.
Ulka SachdevUniversity of Pittsburgh Medical Center Department of Surgery, Division of Vascular Surgery, USA. Electronic address: Sachdevu2@upmc.edu.
University of Pittsburgh Medical Center · USUniversity of Pittsburgh · USNingxia Medical University · CN

Funding

Mechanisms of HMGB1 Release from Ischemic Muscle in Peripheral Arterial DiseaseR01HL136556 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SACHDEV, ULKA · 2018 to 2022
$2.0M
NHLBI NIH HHS R01 HL136556
6 · The paper itself

Abstract

introductionWe propose that MuSC-derived myoblasts in PAD have transcriptomic differences that can highlight underlying causes of ischemia-induced myopathy.

methodsDifferentiation capacity among perfused and ischemic human myoblasts was compared. Following next generation sequencing of mRNA, Ingenuity Pathway Analysis (IPA) was performed for canonical pathway enrichment. Live cell imaging and immunofluorescence were performed to determine myocyte fusion index and protein expression based on insights from IPA, specifically concerning cell cycle regulators including cell-division cycle protein 2 (CDC2) and polo-like kinase 1 (PLK1).

resultsIschemic myoblasts formed attenuated myotubes indicative of reduced fusion. Additionally, myoblasts from ischemic segments showed significant differences in canonical pathways associated with PLK1 (upregulated) and G2/M DNA damage checkpoint regulation (downregulated). PLK1 inhibition with BI2536 did not affect cell viability in any group over 24 h but deterred fusion more significantly in PAD myoblasts. Furthermore, PLK1 inhibition reduced the expression of checkpoint protein CDC2 in perfused but not ischemic cells.

conclusionDifferentiating myoblasts derived from ischemic muscle have significant differences in gene expression including those essential to DNA-damage checkpoint regulation and cell cycle progress. DNA-damage checkpoint dysregulation may contribute to myopathy in PAD.

Indexed as

Cell Cycle ProteinsPeripheral Arterial DiseaseCDC2 Protein KinaseCell CycleDNADNA DamageHumansMitosisMyoblastsPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsCDC2 Protein KinaseCDK1 protein, humanCell Cycle ProteinsDNAPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsCell cycle regulationIschemiaMyopathyPeripheral arterial diseasePolo-like kinaseRNA sequencing

Identifiers

PMID35436627
PMCPMC10687717
OpenAlexW4224014540

What Socratic holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.