Evidence map›Paper›PMID 31502302›Full record

ArticleCell proliferation2019

GIT1 regulates angiogenic factor secretion in bone marrow mesenchymal stem cells via NF-κB/Notch signalling to promote angiogenesis.

Linwei Li, Pengyu Tang, Zheng Zhou, Qian Wang, Tao Xu, Shujie Zhao, Yifan Huang, Fanqi Kong, Wei Liu, Lin Cheng and 9 more

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

18 citing papers in PubMed, 23 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

19 authors at 2 institutions in 1 country.

Linwei LiDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Pengyu TangDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zheng ZhouDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Qian WangDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Tao XuDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Shujie ZhaoDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yifan HuangDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Fanqi KongDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Wei LiuDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Lin ChengDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zhimin ZhouDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Xuan ZhaoDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Changjiang GuDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yongjun LuoDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Gaojian TaoDepartment of Pain, Affiliated Drum Tower Hospital, Medical School of Nanjing University, Nanjing, China.
Dingfei QianDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jian ChenDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jin FanDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Guoyong YinDepartment of Orthopedic, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.ORCID https://orcid.org/0000-0002-7268-5374
Jiangsu Province Hospital · CNNanjing Drum Tower Hospital · CN

Funding

Jiangsu Committee of Science and Technology-Social Development Plan BE2017755Jiangsu Six Talents Peak WSN-011Medical Science and technology development Foundation from Nanjing Department of Health YKK17060Nanjing Committee of Science and Technology 201505005National Natural Science Foundation of China 814National Natural Science Foundation of China 81472080National Natural Science Foundation of China 81520108018National Natural Science Foundation of China 81772351National Natural Science Foundation of China 81772352Research Innovation Program for Academic Degree College Graduates of Jiangsu KYLX16_1105
6 · The paper itself

Abstract

objectivesOsteogenesis is coupled with angiogenesis during bone remodelling. G-protein-coupled receptor (GPCR) kinase 2-interacting protein-1 (GIT1) is an important protein that participates in fracture healing by regulating angiogenesis. This study investigated whether GIT1 could affect bone mesenchymal stem cells (BMSCs) to secrete angiogenic factors to enhance fracture healing by promoting angiogenesis and its possible mechanism. MATERIALS AND

methodsThe angiogenesis of mice post-fracture was detected by micro-CT and immunofluorescence. Subsequently, vascular endothelial growth factor (VEGF) level in mouse and human BMSCs (hBMSCs) under TNF-α stimulation was detected. The hBMSCs were transfected with GIT1 shRNAs to further explore the relationship between GIT1 and VEGF and angiogenesis in vitro. Furthermore, based on previous research on GIT1, possible signal pathways were investigated.

resultsGIT1 knockout mice exhibited impaired angiogenesis and delayed fracture healing. And GIT1 deficiency remarkably reduced the expression of VEGF mRNA in BMSCs, which affected the proliferation and migration of human umbilical vein endothelial cells. GIT1 knockdown inhibited the activation of Notch and NF-κB signals by decreasing nuclear transportation of NICD and P65/P50, respectively. Overexpression of the canonical NF-κB subunits P65 and P50 markedly increased NICD-dependent activation of recombination signal-binding protein-jκ reporter. Finally, GIT1 enhanced the affinity of NF-κB essential modulator (NEMO) for K63-linked ubiquitin chains via interaction with NEMO coiled-coil 2 domains.

conclusionThese data revealed a positive role for GIT1 by modulating the Notch/NF-κB signals which promoting paracrine of BMSCs to enhance angiogenesis and fracture healing.

Indexed as

Adaptor Proteins, Signal TransducingAngiogenesis Inducing AgentsCell Cycle ProteinsHumansHuman Umbilical Vein Endothelial CellsMesenchymal Stem CellsNeovascularization, PathologicNF-kappa BReceptors, NotchSignal TransductionAdaptor Proteins, Signal TransducingAngiogenesis Inducing AgentsCell Cycle ProteinsGIT1 protein, humanNF-kappa BReceptors, Notchangiogenesisfracture healingGIT1NF-κBNotch

Identifiers

PMID31502302
PMCPMC6869488
OpenAlexW2972534595

What OpenQuestion holds

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Registered trials

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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.