miR-135a modulates tendon stem/progenitor cell senescence via suppressing ROCK1

Chen, Lei; Wang, Guodong; Liu, Junpeng; Wang, Hua-Song; Liu, Ximing; Wang, Qing; Cai, Xianhua

doi:10.1016/j.bone.2014.11.001

Cited by 49 publications

(53 citation statements)

References 39 publications

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“…Their data show that the IL-33/ST2 system functions in early tendon disease by triggering the production of inflammatory mediators and switching collagen pro-duction away from Col1 and towards Col3, which is known to be present in increased quantities in tendinopathic tissue. Most pertinent to this investigation was their finding that miR-29a acts to regulate Chitosan improves tendon healing after surgery and is reduced by increased expression of miR-29b and down-regulation of TGF-B1/Smad3 level Kawanishi et al 36 miR-210 Rats Patellar tendon miR-210 healed damaged meniscus through upregulation of VGEF and FGF2 from synovial cells Millar et al 22 miR29a Human Hamstring Downregulation of miR29a induces an increase in Col3 expression Mendias et al 21 miR140 Rats Achilles tendon TGF-B1 treatment increases miR-140 while mechanical loading decreases miR-140 Chen et al 23 miR-140-5p Human Achilles tendon miR-140-5p regulated Pin1 expression by targeting its 3 0 UTR, which acts as regulator of TSPC aging Chen et al 18 miR-135a Human Achilles tendon ROCK1 mediates the effects of mirR-135a in TSPCs (downregulated in young TSPCs compared to old TSPCs) Yatsenko et al 37 miR-9a Drosaphilia Tendon cells miR-9a-expressing tendons lack Dg expression, allowing proper muscle-tendon attachments Wang et al 19 miR-124 Human Tendon tissue (ACLR)…”

Section: Discussionmentioning

confidence: 99%

Effect of micro‐RNA on tenocytes and tendon‐related gene expression: A systematic review

Dubin

Greenberg

Iglinski-Benjamin

et al. 2018

Journal Orthopaedic Research

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The purpose of the review was to synthesize the current literature regarding the effect of miRNA on biological processes known to be involved in tendon and tenocyte development and homeostasis. Using multiple databases, a systematic review was performed with a customized search term crafted to identify any study examining micro-RNA in relation to tendon and/or tenocytes. Results were classified based on the following categories: Gene expression, tenocyte development and differentiation, tendon tissue repair, and tenocyte senescence. A total of 3,112 potentially relevant studies were reviewed, and after exclusion criteria was applied, 15 investigations were included in the final analysis. There were 14 specific miRNA included in this review, with 11 studies reporting on tendon-related gene expression, five reporting on tendon development and/or tenocyte differentiation, six reporting on tendon tissue repair, and five reporting on tenocyte senescence. The miR-29 family was the most commonly reported micro-RNA in the investigation. We also report on a number of micro-RNA which are associated with both positive and negative effects on tendon homeostasis. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res.

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Section: Discussionmentioning

confidence: 99%

Effect of micro‐RNA on tenocytes and tendon‐related gene expression: A systematic review

Dubin

Greenberg

Iglinski-Benjamin

et al. 2018

Journal Orthopaedic Research

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“…These effects of miR-135a were shown to be mediated by Rho-associated coiled-coil protein kinase 1 (ROCK1). 58 …”

Section: Cellular Senescence and Its Biological Impact On Tendon mentioning

confidence: 99%

“…These effects of miR-135a were shown to be mediated by Rho-associated coiled-coil protein kinase 1 (ROCK1). 58 The group agreed that further studies on the mechanisms underlying the regulation of TSPCs by aging will propel this area of research in a new direction. The new findings could provide clues to understand TSPC survival, stress response, function and fate determination, which are critical for the intervention of injuries and diseases, especially those related to aging.…”

Section: These Findings Highlight the Detrimental Effects Of Aging Onmentioning

confidence: 99%

Biology and mechano‐response of tendon cells: Progress overview and perspectives

Sun

Schaniel

Leong

et al. 2015

Journal Orthopaedic Research

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In this review, we summarize the group discussions on Cell Biology & Mechanics from the 2014 ORS/ISMMS New Frontiers in Tendon Research Conference. The major discussion topics included: 1) the biology of tendon stem/progenitor cells (TSPCs) and the potential of stem cell-based tendon therapy using TSPCs and other types of stem cells, namely, embryonic and/or induced pluripotent stem cells (iPSCs), 2) the biological concept and potential impact of cellular senescence on tendon aging, tendon injury repair and the development of degenerative disease, and 3) the effects of tendon cells’ mechano-response on tendon cell fate and metabolism. For each topic, a brief overview is presented which summarizes the major points discussed by the group participants. The focus of the discussions ranged from current research progress, challenges and opportunities, to future directions on these topics. In the preparation of this manuscript, authors consulted relevant references as a part of their efforts to present an accurate view on the topics discussed.

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“…Recently, Choi et al reported that miR-135a induced cytotoxic effects in mouse Sertoli cells with a concomitant increase in reactive oxygen species, and suggested this as a new mechanism of apoptosis by miR-135a [26]. So far, all the reported examples of miR-135a -induced apoptosis have been p53-independent [23, 27], and Chen et al suggested that miR-135a might prevent senescence by suppressing ROCK1 [28], the specific mechanism remained elusive. Until recently, it was unclear whether replicative apoptosis could also be induced by GC cells.…”

Section: Discussionmentioning

confidence: 99%

miR-135a promotes gastric cancer progression and resistance to oxaliplatin

Yan

Chen

et al. 2016

Oncotarget

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Resistance to oxaliplatin (OXA)-based chemotherapy regimens continues to be a major cause of gastric cancer (GC) recurrence and metastasis. We analyzed GC samples and matched non-tumorous control stomach tissues from 280 patients and found that miR-135a was overexpressed in GC samples relative to control tissues. Tumors with high miR-135a expression were more likely to have aggressive characteristics (high levels of carcino-embryonic antigen, vascular invasion, lymphatic metastasis, and poor differentiation) than those with low levels. Patients with greater tumoral expression of miR-135a had shorter overall survival times and times to disease recurrence. Furthermore, miR-135a, which promotes the proliferation and invasion of OXA-resistant GC cells, inhibited E2F transcription factor 1 (E2F1)-induced apoptosis by downregulating E2F1 and Death-associated protein kinase 2 (DAPK2) expression. Our results indicate that higher levels of miR-135a in GC are associated with shorter survival times and reduced times to disease recurrence. The mechanism whereby miR-135a promotes GC pathogenesis appears to be the suppression of E2F1 expression and Sp1/DAPK2 pathway signaling.

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miR-135a modulates tendon stem/progenitor cell senescence via suppressing ROCK1

Cited by 49 publications

References 39 publications

Effect of micro‐RNA on tenocytes and tendon‐related gene expression: A systematic review

Effect of micro‐RNA on tenocytes and tendon‐related gene expression: A systematic review

Biology and mechano‐response of tendon cells: Progress overview and perspectives

miR-135a promotes gastric cancer progression and resistance to oxaliplatin

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