Evidence map›Paper›PMID 35000526›Full record

ArticleBioengineered2022

Up-regulation of caveolin 1 mediated by chitosan activates Wnt/ β-catenin pathway in chronic refractory wound diabetic rat model.

Jie Gao, Jiayuan Zhang, Lianheng Xia, Xuewei Liang, Wukun Ding, Meiyu Song, Linggen Li, Zhen Jia

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.3field-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

4 citing papers in PubMed, 11 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

8 authors at 2 institutions in 1 country.

Jie GaoDepartment of peripheral vascular diseases, First Affiliated hospital, Heilongjiang University of Traditional Chinese Medicine, Harbin City, Heilongjiang, China.
Jiayuan ZhangSchool of Stomatology, Qiqihar Medical University, Qiqihar, China.
Lianheng XiaDepartment of peripheral vascular diseases, First Affiliated hospital, Heilongjiang University of Traditional Chinese Medicine, Harbin City, Heilongjiang, China.
Xuewei LiangDepartment of peripheral vascular diseases, First Affiliated hospital, Heilongjiang University of Traditional Chinese Medicine, Harbin City, Heilongjiang, China.
Wukun DingDepartment of peripheral vascular diseases, First Affiliated hospital, Heilongjiang University of Traditional Chinese Medicine, Harbin City, Heilongjiang, China.
Meiyu SongDepartment of peripheral vascular diseases, First Affiliated hospital, Heilongjiang University of Traditional Chinese Medicine, Harbin City, Heilongjiang, China.
Linggen LiDepartment of peripheral vascular diseases, First Affiliated hospital, Heilongjiang University of Traditional Chinese Medicine, Harbin City, Heilongjiang, China.
Zhen JiaDepartment of peripheral vascular diseases, First Affiliated hospital, Heilongjiang University of Traditional Chinese Medicine, Harbin City, Heilongjiang, China.ORCID 0000-0001-8207-3366
First Affiliated Hospital of Heilongjiang University of Chinese Medicine · CNQiqihar Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus (DM) can be implicated in the perturbations of vascular integrity and the dysfunction of angiogenesis. Chitosan has the advantage of promoting the vascular endothelial cell proliferation. However, the molecular mechanism of action in the promotion of wound healing by chitosan derivatives is still debated. In the current study, DM with chronic wound (CW) model rats were prepared and treated with chitosan. Vascular endothelial cells isolated from granulation tissues were conducted by RNA sequencing. Two thousand three hundred and sixteen genes were up-regulated, while 1,864 genes were down-regulated after chitosan treatment compared to CW group. Here, we observed that caveolin 1 (CAV1) was highly expressed induced by chitosan. Furthermore, we observed that CAV1 knockdown could compromise the activation of Wnt pathway by reduction of β-catenin in rat aortic endothelial cells (RAOECs) and brain endothelium four cells (RBE4s). Moreover, we determined a direct interaction between CAV1 and β-catenin by IP assay. The C-terminus of CAV1 and β-catenin (24 to 586 amino acids) contributed to the interaction of these two proteins. Finally, the protein docking analysis indicated that the fragments of β-catenin (253-261 'FYAITTLHN' and 292-303 'KFLAITTDCLQI') might have affected the structure by CAV1 and facilitated the resistance to degradation. Taken together, our study demonstrates that chitosan can up-regulate CAV1 expression, and CAV1 can interact with β-catenin for promotion of canonical Wnt signaling pathway activity. Our results deepens the molecular mechanism of the Wnt pathway in vascular endothelial cells and is beneficial to developing new targets to assist in enhancing the pharmacological effect of chitosan on wound healing and angiogenesis against DM.

Indexed as

Animalsbeta CateninBinding SitesCaveolin 1Cell LineChitosanDiabetes ComplicationsDisease Models, AnimalGene Expression ProfilingGene Expression RegulationIndenesMaleMolecular Docking SimulationProtein BindingRatsSequence Analysis, RNAbeta CateninCaveolin 1ChitosanIndenesN-(5-(6-fluoro-3-pyridinyl)-2,3-dihydro-1H-inden-2-yl)-2-propanesulfonamideSulfonamidesangiogenesisCAV1chitosandiabetes mellitusWnt pathwayβ-catenin

Identifiers

PMID35000526
PMCPMC8805831
OpenAlexW4205382844

What Socratic 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 Socratic graph.