Evidence mapPaperPMID 30452888Full record

ArticleTranslational research : the journal of laboratory and clinical medicine2019

Small molecule inhibition of dipeptidyl peptidase-4 enhances bone marrow progenitor cell function and angiogenesis in diabetic wounds.

Alexander J Whittam, Zeshaan N Maan, Dominik Duscher, Janos A Barrera, Michael S Hu, Lauren H Fischer, Sacha Khong, Sun Hyung Kwon, Victor W Wong, Graham G Walmsley and 5 more

Open access · greenAbstract read
In one paragraph

Article in Translational research : the journal of laboratory and clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. Review
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  6. A Narrative Review of Diabetic Macroangiopathy: From Molecular Mechanism to Therapeutic Approaches.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. DPP4 as a Potential Candidate in Cardiovascular Disease.Journal of inflammation research · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. 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

15 authors at 3 institutions in 1 country.

Alexander J WhittamDepartment of Surgery, Stanford University School of Medicine, Stanford, California. Electronic address: alexander.whittam@gmail.com.
Zeshaan N MaanDepartment of Surgery, Stanford University School of Medicine, Stanford, California. Electronic address: zmaan@stanford.edu.
Dominik DuscherDepartment of Surgery, Stanford University School of Medicine, Stanford, California. Electronic address: dominikduscher@me.com.
Janos A BarreraDepartment of Surgery, Stanford University School of Medicine, Stanford, California. Electronic address: janosbarrera@gmail.com.
Michael S HuDepartment of Surgery, Stanford University School of Medicine, Stanford, California. Electronic address: mhu2@stanford.edu.
Lauren H FischerDepartment of Surgery, Stanford University School of Medicine, Stanford, California. Electronic address: lhf7@stanford.edu.
Sacha KhongDepartment of Surgery, Stanford University School of Medicine, Stanford, California. Electronic address: skhong@stanford.edu.
Sun Hyung KwonDepartment of Surgery, Stanford University School of Medicine, Stanford, California. Electronic address: kwonsunh@stanford.edu.
Victor W WongDepartment of Surgery, Stanford University School of Medicine, Stanford, California. Electronic address: vicw.wong@gmail.com.
Graham G WalmsleyDepartment of Surgery, Stanford University School of Medicine, Stanford, California. Electronic address: 3gwalmsley@gmail.com.
Ferdinando GiaccoDiabetes Research Center, Albert Einstein College of Medicine, New York, New York. Electronic address: giacco.ferdinando@gmail.com.
Michael JanuszykDepartment of Surgery, Stanford University School of Medicine, Stanford, California. Electronic address: mjanuszyk@mednet.ucla.edu.
Michael BrownleeDiabetes Research Center, Albert Einstein College of Medicine, New York, New York. Electronic address: brownlee@aecom.yu.edu.
Michael T LongakerDepartment of Surgery, Stanford University School of Medicine, Stanford, California. Electronic address: longaker@stanford.edu.
Geoffrey C GurtnerDepartment of Surgery, Stanford University School of Medicine, Stanford, California. Electronic address: ggurtner@stanford.edu.
Stanford Medicine · USStanford University · USAlbert Einstein College of Medicine · US

Funding

Progenitor Cell Dysfunction and Impaired VasculogenesisR01DK074095 · UNIVERSITY OF ARIZONA · 2005 to 2025
$743k
NIDDK NIH HHS R01 DK074095NIDDK NIH HHS R56 DK074095
6 · The paper itself

Abstract

In diabetes, stromal cell-derived factor-1 (SDF-1) expression and progenitor cell recruitment are reduced. Dipeptidyl peptidase-4 (DPP-4) inhibits SDF-1 expression and progenitor cell recruitment. Here we examined the impact of the DPP-4 inhibitor, MK0626, on progenitor cell kinetics in the context of wound healing. Wildtype (WT) murine fibroblasts cultured under high-glucose to reproduce a diabetic microenvironment were exposed to MK0626, glipizide, or no treatment, and SDF-1 expression was measured with ELISA. Diabetic mice received MK0626, glipizide, or no treatment for 6 weeks and then were wounded. Immunohistochemistry was used to quantify neovascularization and SDF-1 expression. Gene expression was measured at the RNA and protein level using quantitative polymerase chain reaction and ELISA, respectively. Flow cytometry was used to characterize bone marrow-derived mesenchymal progenitor cell (BM-MPC) population recruitment to wounds. BM-MPC gene expression was assayed using microfluidic single cell analysis. WT murine fibroblasts exposed to MK0626 demonstrated increased SDF-1 expression. MK0626 treatment significantly accelerated wound healing and increased wound vascularity, SDF-1 expression, and dermal thickness in diabetic wounds. MK0626 treatment increased the number of BM-MPCs present in bone marrow and in diabetic wounds. MK0626 had no effect on BM-MPC population dynamics. BM-MPCs harvested from MK0626-treated mice exhibited increased chemotaxis in response to SDF-1 when compared to diabetic controls. Treatment with a DPP-4 inhibitor significantly improved wound healing, angiogenesis, and endogenous progenitor cell recruitment in the setting of diabetes.

Indexed as

Neovascularization, PathologicAnimalsChemokine CXCL12Diabetes Mellitus, ExperimentalDipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsGlipizideHematopoietic Stem CellsMiceMice, Inbred C57BLTriazolesWound HealingWounds and InjuriesChemokine CXCL12Cxcl12 protein, mouseDipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsDpp4 protein, mouseGlipizideMK0626TriazolesBM-MPC = bone marrow-derived mesenchymal progenitor cellDMEM = Dulbecco's Modified Eagle MediumDPP-4 = dipeptidyl peptidase-4FBS = fetal bovine serumMPC = mesenchymal progenitor cellNIH = National Institute of HealthPBS = phosphate buffered salineqRT-PCR = quantitative reverse transcription polymerase chain reactionSDF-1 = stromal cell-derived factor-1VEGF = vascular endothelial growth factorWT = wild type

Identifiers

PMID30452888
PMCPMC7252504
OpenAlexW2898858369

What Socratic holds

Textmetadata
LicenceTDM
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.