Evidence map›Paper›PMID 31821371›Full record

ArticlePloS one2019

PTH1-34 improves bone healing by promoting angiogenesis and facilitating MSCs migration and differentiation in a stabilized fracture mouse model.

Xin Jiang, Cuidi Xu, Hongli Shi, Qun Cheng

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

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
2.0field-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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.

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  7. Mutanobactin-D, aInternational journal of molecular sciences · 2025
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  10. CD90's role in vascularization and healing of rib fractures: insights from Dll4/notch regulation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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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

4 authors at 1 institution in 1 country.

Xin JiangDepartment of Osteoporosis and Bone Disease, Huadong Hospital Affiliated to Fudan University, Research Section of Geriatric Metabolic Bone Disease, Shanghai Geriatric Institute, Shanghai, China.
Cuidi XuDepartment of Osteoporosis and Bone Disease, Huadong Hospital Affiliated to Fudan University, Research Section of Geriatric Metabolic Bone Disease, Shanghai Geriatric Institute, Shanghai, China.
Hongli ShiDepartment of Osteoporosis and Bone Disease, Huadong Hospital Affiliated to Fudan University, Research Section of Geriatric Metabolic Bone Disease, Shanghai Geriatric Institute, Shanghai, China.
Qun ChengDepartment of Osteoporosis and Bone Disease, Huadong Hospital Affiliated to Fudan University, Research Section of Geriatric Metabolic Bone Disease, Shanghai Geriatric Institute, Shanghai, China.ORCID 0000-0001-5604-1504
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivePTH1-34 (parathyroid hormone 1-34) is the only clinical drug to promote osteogenesis. MSCs (mesenchymal stem cells) have multidirectional differentiation potential and are closely related to fracture healing. This study was to explore the effects of PTH1-34 on proliferation and differentiation of endothelial cells and MSCs in vitro, and on angiogenesis, and MSCs migration during fracture healing in vivo.

methodsMice with stabilized fracture were assigned to 4 groups: CON, PTH (PTH1-34 40 μg/kg/day), MSC (transplanted with 105 MSCs), PTH+MSCs. Mice were sacrificed 14 days after fracture, and callus tissues were harvested for microCT scan and immunohistochemistry analysis. The effects of PTH1-34 on angiogenesis, and MSCs differentiation and migration were assessed by wound healing, tube formation and immunofluorescence staining.

resultsTreatment with either PTH1-34, or MSCs promoted bone healing and vascular formation in fracture callus. The callus bone mass, bone volume, and bone mineral density were all greater in PTH and/or MSC groups than they were in CON (p<0.05). PTH1-34 increased small vessels formation (diameter ≤50μm), whereas MSCs increased the large ones (diameter >50μm). Expression of CD31 within calluses and trabecular bones were significantly higher in PTH1-34 treated group than that of not (p<0.05). Expression of CD31, VEGFR, VEGFR2, and vWF was upregulated, and wound healing and tube formation were increased in MSCs treated with PTH1-34 compared to that of control.

conclusionsPTH1-34 improved the proliferation and differentiation of endothelial cells and MSCs, enhancing migration of MSCs to bone callus to promote angiogenesis and osteogenesis, and facilitating fracture healing.

Indexed as

AnimalsCell MovementCell ProliferationDisease Models, AnimalFemaleFracture HealingFractures, BoneMesenchymal Stem CellsMiceNeovascularization, PhysiologicOsteogenesisParathyroid HormoneParathyroid Hormone

Identifiers

PMID31821371
PMCPMC6903750
OpenAlexW2995650209

What OpenQuestion holds

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LicenceCC BY
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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.