Evidence map›Paper›PMID 34193023›Full record

ArticleBioengineered2021

Platelet-rich plasma regulating the repair of ultraviolet B-induced acute tissue inflammation: adjusting macrophage polarization through the activin receptor-follistatin system.

Gajin Park, Wen Qian, Mei-Jie Zhang, Yi-He Chen, Li-Wen Ma, Ni Zeng, Qian Lu, Yue-Yue Li, Wei-Wei Ma, Xu-Feng Yin and 2 more

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
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

12 authors at 1 institution in 1 country.

Gajin ParkDepartment of Dermatology, the First Affiliated of Nanjing Medical University, Nanjing, China.
Wen QianDepartment of Dermatology, the First Affiliated of Nanjing Medical University, Nanjing, China.
Mei-Jie ZhangDepartment of Dermatology, the First Affiliated of Nanjing Medical University, Nanjing, China.
Yi-He ChenDepartment of Dermatology, the First Affiliated of Nanjing Medical University, Nanjing, China.
Li-Wen MaDepartment of Dermatology, the First Affiliated of Nanjing Medical University, Nanjing, China.
Ni ZengDepartment of Dermatology, the First Affiliated of Nanjing Medical University, Nanjing, China.
Qian LuDepartment of Dermatology, the First Affiliated of Nanjing Medical University, Nanjing, China.
Yue-Yue LiDepartment of Dermatology, the First Affiliated of Nanjing Medical University, Nanjing, China.
Wei-Wei MaDepartment of Dermatology, the First Affiliated of Nanjing Medical University, Nanjing, China.
Xu-Feng YinDepartment of Dermatology, the First Affiliated of Nanjing Medical University, Nanjing, China.
Bing-Rong ZhouDepartment of Dermatology, the First Affiliated of Nanjing Medical University, Nanjing, China.
Dan LuoDepartment of Dermatology, the First Affiliated of Nanjing Medical University, Nanjing, China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ultraviolet B (UVB) is one of the most common exogenous factors in skin aging, especially photoaging. Once a large amount of UVB accumulates within a short period of time, skin tissue can become inflamed. It has also been found in clinics that platelet-rich plasma (PRP) can promote wound repair; therefore, the aim of this study was to identify the mechanism by which PRP repairs UVB-induced skin photodamage. We used PRP of Sprague-Dawley rats with the two-spin technique in the established acute UVB radiation photodamage model and harvested the corresponding skin after 1, 7, and 28 d. Hematoxylin and eosin staining was used to observe tissue inflammation. We found that PRP reduces inflammation in the early stages of UVB-induced acute skin damage, and then promotes the proliferation of collagen in the middle and late stages. Moreover, PRP can stimulate Act A and M1 polarization in the early stage, while inhibiting activin A (Act A) and inducing M2 polarization in the middle and late stages. In conclusion, this study demonstrates that PRP plays an important regulatory role in helping reduce UVB-induced acute skin tissue inflammation by adjusting macrophage polarization, which alleviates skin inflammation and stimulates collagen regeneration.

Indexed as

Skin AgingActivin ReceptorsAnimalsDisease Models, AnimalFemaleFollistatinInflammationMacrophagesPlatelet-Rich PlasmaRatsRats, Sprague-DawleySkinUltraviolet RaysActivin ReceptorsFollistatinactivininflammationmacrophage polarizationPlatelet-rich plasmaUVB-induced acute photodamage

Identifiers

PMID34193023
PMCPMC8806634
OpenAlexW3176450068

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.