Evidence map›Paper›PMID 25891676›Full record

ArticleThe Journal of surgical research2015

Paclitaxel impairs adipose stem cell proliferation and differentiation.

Rachel L Choron, Shaohua Chang, Sophia Khan, Miguel A Villalobos, Ping Zhang, Jeffrey P Carpenter, Thomas N Tulenko, Yuan Liu

Abstract read
In one paragraph

Article in The Journal of surgical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 36 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Rachel L ChoronDepartment of Surgery, Cooper University Hospital, Camden, New Jersey. Electronic address: Rachel.Choron@gmail.com.
Shaohua ChangDepartment of Surgical Research, Cooper University Hospital, Camden, New Jersey.
Sophia KhanDepartment of Surgery, Cooper University Hospital, Camden, New Jersey.
Miguel A VillalobosDepartment of Surgery, Cooper University Hospital, Camden, New Jersey.
Ping ZhangDepartment of Surgical Research, Cooper University Hospital, Camden, New Jersey.
Jeffrey P CarpenterDepartment of Surgery, Cooper University Hospital, Camden, New Jersey.
Thomas N TulenkoDepartment of Surgical Research, Cooper University Hospital, Camden, New Jersey.
Yuan LiuDepartment of Plastic Surgery, Cooper University Hospital, Camden, New Jersey.
Cooper University Hospital · US

Funding

Dietary Cholesterol and Defects in Cholesterol SynthesisR01HL073980 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI STEINER, ROBERT DAVID · 2003 to 2013
$4.5M
SMOOTH MUSCLE CELL MEMBRANE DURING ATHEROGENESISR01HL066273 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI TULENKO, THOMAS N. · 2000 to 2003
$1.4M
NHLBI NIH HHS 7R01HL073980-10NHLBI NIH HHS R01 HL066273NHLBI NIH HHS R01 HL073980
6 · The paper itself

Abstract

backgroundCancer patients with chemotherapy-induced immunosuppression have poor surgical site wound healing. Prior literature supports the use of human adipose-derived stem cell (hASC) lipoinjection to improve wound healing. It has been established that multipotent hASCs facilitate neovascularization, accelerate epithelialization, and quicken wound closure in animal models. Although hASC wound therapy may benefit surgical cancer patients, the chemotherapeutic effects on hASCs are unknown. We hypothesized that paclitaxel, a chemotherapeutic agent, impairs hASC growth, multipotency, and induces apoptosis.

methodshASCs were isolated and harvested from consented, chemotherapy and radiation naive patients. Growth curves, MTT (3-(4,5-Dimethylthiazol-2-Yl)-2,5-Diphenyltetrazolium Bromide), and EdU (5-ethynyl-2-deoxyguridine) assays measured cytotoxicity and proliferation. Oil Red O stain, Alizarin Red stain, matrigel tube formation assay, and quantitative polymerase chain reaction analyzed hASC differentiation. Annexin V assay measured apoptosis. Immunostaining and Western blot determined tumor necrosis factor α (TNF-α) expression.

resultshASCs were selectively more sensitive to paclitaxel (0.01-30 μM) than fibroblasts (P < 0.05). After 12 d, paclitaxel caused hASC growth arrest, whereas control hASCs proliferated (P = 0.006). Paclitaxel caused an 80.6% reduction in new DNA synthesis (P < 0.001). Paclitaxel severely inhibited endothelial differentiation and capillary-like tube formation. Differentiation markers, lipoprotein lipase (adipogenic), alkaline phosphatase (osteogenic), CD31, and van Willebrand factor (endothelial), were significantly decreased (all P < 0.05) confirming paclitaxel impaired differentiation. Paclitaxel was also found to induce apoptosis and TNF-α was upregulated in paclitaxel-treated hASCs (P < 0.001).

conclusionsPaclitaxel is more cytotoxic to hASCs than fibroblasts. Paclitaxel inhibits hASC proliferation, differentiation, and induces apoptosis, possibly through the TNF-α pathway. Paclitaxel's severe inhibition of endothelial differentiation indicates neovascularization disruption, possibly causing poor wound healing in cancer patients receiving chemotherapy.

Indexed as

Adipose TissueAdult Stem CellsAntineoplastic Agents, PhytogenicApoptosisCell DifferentiationCell LineCell ProliferationEndothelial CellsFibroblastsHumansOsteogenesisPaclitaxelTumor Necrosis Factor-alphaAntineoplastic Agents, PhytogenicPaclitaxelTumor Necrosis Factor-alphaCancer therapyChronic woundsHuman adipose–derived stem cellsNeovascularizationPaclitaxelWound healing

Identifiers

PMID25891676
PMCPMC4442730
OpenAlexW2116875654

What OpenQuestion holds

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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 OpenQuestion graph.