Evidence map›Paper›PMID 31732563›Full record

ArticleThe Journal of biological chemistry2019

Inhibition of CD44 induces apoptosis, inflammation, and matrix metalloproteinase expression in tendinopathy.

Po-Ting Wu, Wei-Ren Su, Chia-Lung Li, Jeng-Long Hsieh, Ching-Hou Ma, Chao-Liang Wu, Li-Chieh Kuo, I-Ming Jou, Shih-Yao Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

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  16. Fullerenol inhibits tendinopathy by alleviating inflammation.Frontiers in bioengineering and biotechnology · 2023
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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

9 authors at 4 institutions in 1 country.

Po-Ting WuDepartment of Orthopaedics, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Wei-Ren SuDepartment of Orthopaedics, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Chia-Lung LiDepartment of Orthopaedics, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Jeng-Long HsiehDepartment of Nursing, College of Nursing, Chung Hwa University of Medical Technology, Tainan, Taiwan.
Ching-Hou MaDepartment of Orthopedics, E-Da Hospital, Kaohsiung, Taiwan.
Chao-Liang WuDepartment of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Li-Chieh KuoMedical Device Innovation Center, National Cheng Kung University, Tainan, Taiwan.
I-Ming JouDepartment of Orthopedics, E-Da Hospital, Kaohsiung, Taiwan jming@mail.ncku.edu.tw.
Shih-Yao ChenDepartment of Nursing, College of Nursing, Chung Hwa University of Medical Technology, Tainan, Taiwan leonlai50@gmail.com.ORCID 0000-0003-4929-855X
National Cheng Kung University Hospital · TWChung Hwa University of Medical Technology · TWE-Da Hospital · TWNational Cheng Kung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis has emerged as a primary cause of tendinopathy. CD44 signaling pathways exert anti-apoptotic and -inflammatory effects on tumor cells, chondrocytes, and fibroblast-like synoviocytes. The aim of this study was to examine the association among CD44, apoptosis, and inflammation in tendinopathy. Expression of CD44 and apoptotic cell numbers in tendon tissue from patients with long head of biceps (LHB) tendinopathy were determined according to the histological grades of tendinopathy. Primary tenocytes from Achilles tendon of Sprague-Dawley rats 1 week after collagenase injection were cultured with an antagonizing antibody against CD44. Treatment responses were determined by evaluating cell viability and expression of tendon-related proliferation markers, inflammatory mediators, and apoptosis. The expression of CD44 and apoptosis were positively correlated with the severity of tendinopathy in the human LHB tendinopathy. Furthermore, CD44 expression and apoptotic cells were co-stained in tendinopathic tendon. Blocking the CD44 signaling pathways in rat primary tenocytes by OX-50 induced cell apoptosis and the elevated levels of cleaved caspase-3. Furthermore, they had decreased cell viability and expression of collagen type I, type III, tenomodulin, and phosphorylated AKT. In contrast, there were elevated levels of inflammatory mediators, including interleukin (IL)-1β, IL-6, tumor necrosis factor-α, cyclooxygenase-2, and phosphorylated NF-κB, as well as matrix metalloproteinase (MMP) family members including MMP-1, -3, -9, and -13 in tenocytes upon OX-50 treatment. This study is the first to demonstrate the association of CD44 and apoptosis in tendinopathy. Our data imply that CD44 may play a role in tendinopathy via regulating apoptosis, inflammation, and extracellular matrix homeostasis.

Indexed as

ApoptosisActinsAnimalsAntibodiesCells, CulturedCyclooxygenase 2HumansHyaluronan ReceptorsInflammation MediatorsMaleMatrix MetalloproteinasesRatsRats, Sprague-DawleySignal TransductionSilicon DioxideTendinopathyActa2 protein, ratActinsAntibodiesCyclooxygenase 2Hyaluronan ReceptorsInflammation MediatorsMatrix MetalloproteinasesSilicon DioxideTumor Necrosis Factor-alphaapoptosisCD44cytokine inductioninflammationmatrix metalloproteinase (MMP)tendinopathytendon

Identifiers

PMID31732563
PMCPMC6937571
OpenAlexW2986614333

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.