Evidence map›Paper›PMID 37713069›Full record

ArticleGenes & genomics2024

HPF1 regulates tendon stem/progenitor cell senescence and tendon repair via PARP1-mediated poly-ADP ribosylation of HuR.

Weifeng Han, Dongqiang Gu, Hongguang Chen, Xu Tao, Lei Chen

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Article in Genes & genomics, 2024. 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
0.9field-weighted citation impact, top 20% 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

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 4 citations in OpenAlex.

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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

5 authors at 3 institutions in 1 country.

Weifeng HanDepartment of Orthopaedics, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Dongqiang GuSenior Department of Orthopedics, The Fourth Medical Center of PLA General Hospital, No. 51 Fucheng Road, Beijing, 10048, China.
Hongguang ChenSenior Department of Orthopedics, The Fourth Medical Center of PLA General Hospital, No. 51 Fucheng Road, Beijing, 10048, China.
Xu TaoSports Medicine Center, The First Affiliated Hospital of Military Medical University of the Army, Chongqing, 400038, China. taoux@hotmail.com.
Lei ChenSenior Department of Orthopedics, The Fourth Medical Center of PLA General Hospital, No. 51 Fucheng Road, Beijing, 10048, China. 18501219257@163.com.
Chinese PLA General Hospital · CNArmy Medical University · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTendon stem/progenitor cells (TSPCs) play a vital role in tendon repair, regeneration and homeostasis. However, the specific mechanism of TSPCs aging is still unclear.

objectiveThis study aims to explore the role and molecular mechanism of HPF1 in the aging of TSPCs.

methodsYoung and aged TSPCs (Y-TSPCs and A-TSPCs) were acquired from 3 to 4 and 24-26-month-old Sprague-Dawley male rats, TSPCs (Y-TSPCs and A-TSPCs) were subjected to senescence-associated β-galactosidase (SA-β-Gal))staining and telomerase activity detection, p16, p21, Scx, Tnmd, Col1, Col3HPF1 and PAPR1 expression levels were detected by Western blot or Reverse Transcription-quantitative Polymerase Chain Reaction (RT-qPCR), Reciprocal co-immunoprecipitation (co-IP) was used to explore the interaction between HPF1 and PARP1. Ribonucleoprotein immunoprecipitation (RNP-IP) was used to analyze the binding of HuR to the senescence marker gene mRNAs, IP was used to perform HPF1 to the PARylation of HuR, and the half-life of p16 and p21 were detected. Finally, we established an in vivo model, and the tendon tissue was used to perform hematoxylin and eosin (HE) and masson's trichrome staining, as well as the immunohistochemical analysis of Col I and TNMD.

resultsCompared with Y-TSPCs, A-TSPCs had significantly enhanced cell senescence and significantly reduced tendon differentiation ability, and significantly increased the expression of HPF1 and PARP1. In addition, HPF1 and PARP1 interacted and coordinated the senescence and differentiation of TSPCs, HPF1 could also regulate the expression of p21 and p21, the interaction of p16 or p21 with HuR, and the poly-ADP ribosylation of PARP1 to HuR. HPF1 overexpression and siHuR co-transfection significantly reduced the half-life of p16 and p21, and HPF1 and PARP1 regulated the mRNA levels of p16 and p21 through HuR. Finally, in vivo experiments have shown that HPF1 or PARP1 overexpression could both inhibit the ability of tendon differentiation and promote cell senescence.

conclusionsHPF1 promoted the senescence of TSPCs and inhibits the tendon differentiation of TSPCs through PARP1-mediated poly-ADP ribosylation of HuR.

Indexed as

Cellular SenescencePoly ADP RibosylationAnimalsMaleRatsRats, Sprague-DawleyStem CellsTendonsCell senescenceHPF1mRNA stabilityTendon-derived stem/progenitor cells (TSPCs)Tendon repair

Identifiers

PMID37713069
OpenAlexW4386757999

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Registered trials

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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.