Evidence map›Paper›PMID 39153095›Full record

ArticleArchives of dermatological research2024

Adipose-derived mesenchymal stem cells suppress fibroblast proliferation of hypertrophic scar through CCL5 and CXCL12.

Bo Chen, Xiongxiang Zhu, Dongmei Zhang, Zhensen Zhu, Qian Ye, Jingdong Guo

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In one paragraph

Article in Archives of dermatological research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–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

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

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4 · The record

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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

6 authors.

Bo ChenDepartment of Burns and Plastic Surgery, Shenzhen Hospital of Southern Medical University, No.1333, Xinhu Road, Baoan District, Shenzhen, 518000, Guangdong, China.
Xiongxiang ZhuDepartment of Burns and Plastic Surgery, Shenzhen Hospital of Southern Medical University, No.1333, Xinhu Road, Baoan District, Shenzhen, 518000, Guangdong, China.
Dongmei ZhangDepartment of Burns and Plastic Surgery, Shenzhen Hospital of Southern Medical University, No.1333, Xinhu Road, Baoan District, Shenzhen, 518000, Guangdong, China.
Zhensen ZhuDepartment of Burns and Plastic Surgery, Shenzhen Hospital of Southern Medical University, No.1333, Xinhu Road, Baoan District, Shenzhen, 518000, Guangdong, China.
Qian YeDepartment of Orthopaedics, Shenzhen Hospital of Southern Medical University, Shenzhen, 518000, Guangdong, China.
Jingdong GuoDepartment of Burns and Plastic Surgery, Shenzhen Hospital of Southern Medical University, No.1333, Xinhu Road, Baoan District, Shenzhen, 518000, Guangdong, China. guojingdong1996@163.com.

Funding

Medical Scientific Research Foundation of Guangdong Province B2022034
6 · The paper itself

Abstract

BACKGROUND AND

objectiveAdipose-derived mesenchymal stem cells (ADSCs) can accelerate wound healing, reduce scar formation, and inhibit hypertrophic scar (HTS). ADSCs can secrete a large amount of CCL5, and CCL5 has been proved to be pro-inflammatory and pro-fibrotic. CXCL12 (SDF-1) is a key chemokine that promotes stem cell migration and survival. Therefore, this study selected normal skin and HTS conditioned medium to simulate different microenvironments, and analyzed the effects of different microenvironments on the expression of CCL5 and CXCL12 in human ADSCs (hADSCs). MATERIALS AND

methodshADSCs with silenced expression of CCL5 and CXCL12 were co-cultured with hypertrophic scar fibroblasts to verify the effects of CCL5 and CXCL12 in hADSCs on the proliferation ability of hypertrophic scar fibroblasts. A mouse model of hypertrophic scar was established to further confirm the effect of CCL5 and CXCL12 in hADSCs on hypertrophic scar formation.

resultsCCL5 level was found to be significantly high in hADSCs cultured in HTS conditioned medium. CXCL12 in HTS group was prominently lowly expressed compared with the normal group. Inhibition of CCL5 in hADSCs enhanced the effects of untreated hADSCs on proliferation of HTS fibroblasts while CXCL12 knockdown exerted the opposite function. Inhibition of CCL5 in hADSCs increased the percentage of HTS fibroblasts in the G0/G1 phase while down-regulation of CXCL12 decreased those. Meanwhile, the down-regulated levels of fibroblast markers including collagen I, collagen III, and α-SMA induced by CCL5 knockdown were significantly up-regulated by CXCL12 inhibition. hADSCs alleviate the HTS of mice through CCL5 and CXCL12.

conclusionIn summary, our results demonstrated that hADSCs efficiently cured HTS by suppressing proliferation of HTS fibroblasts, which may be related to the inhibition of CXCL12 and elevation of CCL5 in hADSCs, suggesting that hADSCs may provide an alternative therapeutic approach for the treatment of HTS.

Indexed as

Cell ProliferationChemokine CCL5Chemokine CXCL12Cicatrix, HypertrophicFibroblastsMesenchymal Stem CellsAdipose TissueAdultAnimalsCells, CulturedCoculture TechniquesCulture Media, ConditionedDisease Models, AnimalFemaleHumansMaleCCL5 protein, humanChemokine CCL5Chemokine CXCL12Culture Media, ConditionedCXCL12 protein, humanAdipose derived mesenchymal stem cellCCL5CXCL12FibroblastHypertrophic scar

Identifiers

PMID39153095

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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.