Evidence map›Paper›PMID 32213190›Full record

ArticleStem cell research & therapy2020

LAMA2 regulates the fate commitment of mesenchymal stem cells via hedgehog signaling.

Yuan Zhu, Xiao Zhang, Ranli Gu, Xuenan Liu, Siyi Wang, Dandan Xia, Zheng Li, Xiaomin Lian, Ping Zhang, Yunsong Liu and 1 more

Abstract read
In one paragraph

Article in Stem cell research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Article
  2. [Whole genome sequencing and analysis of familial nonsyndromic congenital tooth agenesis].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2026
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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

11 authors.

Yuan ZhuDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, National Laboratory for Digital and Material Technology of Stomatology, Beijing Key Laboratory of Digital Stomatology, National Clinical Research Center for Oral Diseases, 22 Zhongguancun South Avenue, Beijing, 100081, People's Republic of China.
Xiao ZhangDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, National Laboratory for Digital and Material Technology of Stomatology, Beijing Key Laboratory of Digital Stomatology, National Clinical Research Center for Oral Diseases, 22 Zhongguancun South Avenue, Beijing, 100081, People's Republic of China.
Ranli GuDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, National Laboratory for Digital and Material Technology of Stomatology, Beijing Key Laboratory of Digital Stomatology, National Clinical Research Center for Oral Diseases, 22 Zhongguancun South Avenue, Beijing, 100081, People's Republic of China.
Xuenan LiuDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, National Laboratory for Digital and Material Technology of Stomatology, Beijing Key Laboratory of Digital Stomatology, National Clinical Research Center for Oral Diseases, 22 Zhongguancun South Avenue, Beijing, 100081, People's Republic of China.
Siyi WangDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, National Laboratory for Digital and Material Technology of Stomatology, Beijing Key Laboratory of Digital Stomatology, National Clinical Research Center for Oral Diseases, 22 Zhongguancun South Avenue, Beijing, 100081, People's Republic of China.
Dandan XiaDepartment of Materials Science and Engineering, College of Engineering, Peking University, Beijing, 100871, People's Republic of China.
Zheng LiDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, National Laboratory for Digital and Material Technology of Stomatology, Beijing Key Laboratory of Digital Stomatology, National Clinical Research Center for Oral Diseases, 22 Zhongguancun South Avenue, Beijing, 100081, People's Republic of China.
Xiaomin LianDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, National Laboratory for Digital and Material Technology of Stomatology, Beijing Key Laboratory of Digital Stomatology, National Clinical Research Center for Oral Diseases, 22 Zhongguancun South Avenue, Beijing, 100081, People's Republic of China.
Ping ZhangDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, National Laboratory for Digital and Material Technology of Stomatology, Beijing Key Laboratory of Digital Stomatology, National Clinical Research Center for Oral Diseases, 22 Zhongguancun South Avenue, Beijing, 100081, People's Republic of China. zhangping332@bjmu.edu.cn.
Yunsong LiuDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, National Laboratory for Digital and Material Technology of Stomatology, Beijing Key Laboratory of Digital Stomatology, National Clinical Research Center for Oral Diseases, 22 Zhongguancun South Avenue, Beijing, 100081, People's Republic of China. liuyunsong@hsc.pku.edu.cn.
Yongsheng ZhouDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, National Laboratory for Digital and Material Technology of Stomatology, Beijing Key Laboratory of Digital Stomatology, National Clinical Research Center for Oral Diseases, 22 Zhongguancun South Avenue, Beijing, 100081, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBone defects are a common clinical condition that has gained an increasing amount of attention in recent years. Causes of bone defect include tumors, inflammation, and fractures. Bone tissue engineering is a novel treatment of bone defect, and human mesenchymal stem cells (hMSCs) are the ideal seed cells for bone tissue engineering due to their multi-lineage differentiation potential and immunogenicity. The laminin α2 (LAMA2) gene encodes the α2 subunit of laminins. Mutations in this gene have been reported to cause muscular dystrophy, but thus far no studies have elucidated the role of LAMA2 in the fate choices of MSCs. Here, we aimed to investigate the critical role of LAMA2 in the osteogenesis and adipogenesis of mesenchymal stem cells (MSCs).

methodsWe investigated LAMA2 function in osteogenic and adipogenic differentiation of MSCs in vitro and in vivo through loss- and gain-of-function experiments. In addition, molecular mechanism was clarified by Western blot and siRNA.

resultsOur results demonstrated that LAMA2 was a critical regulator for fate commitment of MSCs. Both in vitro and in vivo studies indicate that LAMA2 inhibits osteogenesis and promotes adipogenesis. Mechanistically, we found that LAMA2 regulated osteogenesis and adipogenesis of MSCs by modulating the hedgehog signaling pathway.

conclusionsThe present work confirms that LAMA2 is a new molecular target for MSC-based bone regeneration.

Indexed as

Mesenchymal Stem CellsAdipogenesisCell DifferentiationCells, CulturedHedgehog ProteinsHumansLamininOsteogenesisHedgehog ProteinsLamininlaminin alpha 2Hedgehog signalingHuman mesenchymal stem cellsLAMA2Osteogenic differentiation

Identifiers

PMID32213190
PMCPMC7093965

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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.