Evidence map›Paper›PMID 30185660›Full record

ArticleJCI insight2018

1,25-Dihydroxyvitamin D suppresses M1 macrophages and promotes M2 differentiation at bone injury sites.

Samiksha Wasnik, Charles H Rundle, David J Baylink, Mohammad Safaie Yazdi, Edmundo E Carreon, Yi Xu, Xuezhong Qin, Kin-Hing William Lau, Xiaolei Tang

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.7field-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

42 citing papers in PubMed, 79 citations in OpenAlex.

  1. Extracellular Vesicles and Their Role in Osteogenesis.Bioengineering (Basel, Switzerland) · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Dual effects of 1α,25-dihydroxyvitamin DJournal of dental sciences · 2026
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Role of 1,25-dihydroxyvitamin DWorld journal of gastrointestinal oncology · 2025
    Article
  12. Vitamin DScientific reports · 2024
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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

9 authors at 2 institutions in 1 country.

Samiksha WasnikDivision of Regenerative Medicine, Department of Medicine, Loma Linda University, Loma Linda, California, USA.
Charles H RundleMusculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, California, USA.
David J BaylinkDivision of Regenerative Medicine, Department of Medicine, Loma Linda University, Loma Linda, California, USA.
Mohammad Safaie YazdiDivision of Regenerative Medicine, Department of Medicine, Loma Linda University, Loma Linda, California, USA.
Edmundo E CarreonDivision of Regenerative Medicine, Department of Medicine, Loma Linda University, Loma Linda, California, USA.
Yi XuDivision of Regenerative Medicine, Department of Medicine, Loma Linda University, Loma Linda, California, USA.
Xuezhong QinDivision of Regenerative Medicine, Department of Medicine, Loma Linda University, Loma Linda, California, USA.
Kin-Hing William LauDivision of Regenerative Medicine, Department of Medicine, Loma Linda University, Loma Linda, California, USA.
Xiaolei TangDivision of Regenerative Medicine, Department of Medicine, Loma Linda University, Loma Linda, California, USA.
Loma Linda University · USJerry L. Pettis Memorial VA Medical Center · US

Funding

BLR&D Research Career Scientist AwardIK6BX003782 · VA · VA LOMA LINDA HEALTHCARE SYSTEM · PI LAU, KIN-HING WILLIAM · 2017 to 2021
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BLRD VA IK6 BX003782
6 · The paper itself

Abstract

An indispensable role of macrophages in bone repair has been well recognized. Previous data have demonstrated the copresence of M1 macrophages and mesenchymal stem cells (MSCs) during the proinflammatory stage of bone repair. However, the exact role of M1 macrophages in MSC function and bone repair is unknown. This study aimed to define the role of M1 macrophages at bone injury sites via the function of 1,25-Dihydroxyvitamin D (1,25[OH]2D) in suppressing M1 but promoting M2 differentiation. We showed that 1,25(OH)2D suppressed M1 macrophage-mediated enhancement of MSC migration. Additionally, 1,25(OH)2D inhibited M1 macrophage secretion of osteogenic proteins (i.e., Oncostatin M, TNF-α, and IL-6). Importantly, the 1,25(OH)2D-mediated suppression of osteogenic function in M1 macrophages at the proinflammatory stage was associated with 1,25(OH)2D-mediated reduction of MSC abundance, compromised osteogenic potential of MSCs, and impairment of fracture repair. Furthermore, outside the proinflammatory stage, 1,25(OH)2D treatment did not suppress fracture repair. Accordingly, our data support 2 conclusions: (a) M1 macrophages are important for the recruitment and osteogenic priming of MSCs and, hence, are necessary for fracture repair, and (b) under vitamin D-sufficient conditions, 1,25(OH)2D treatment is unnecessary and can be detrimental if provided during the proinflammatory stage of fracture healing.

Indexed as

AnimalsBone and BonesCell DifferentiationCell MovementCytokinesHumansImmunity, CellularInterleukin-6MacrophagesMaleMesenchymal Stem CellsMiceOncostatin MOsteogenesisRAW 264.7 CellsTumor Necrosis Factor-alpha1,25-dihydroxyvitamin DCytokinesInterleukin-6Oncostatin MTumor Necrosis Factor-alphaVitamin DAdult stem cellsBone BiologyBone diseaseCellular immune response

Identifiers

PMID30185660
PMCPMC6171806
OpenAlexW2889905349

What OpenQuestion holds

Textmetadata
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.