The transcriptional coactivator YAP1 is overexpressed in osteoarthritis and promotes its progression by interacting with Beclin-1

Zhang, Qiang; Fang, Xin; Zhao, Wei; Liang, Qiong

doi:10.1016/j.gene.2018.11.068

Cited by 22 publications

(29 citation statements)

References 47 publications

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“…Several studies have confirmed that YAP1 is overexpressed in OA animal model tissues, and the YAP1 content increases with the severity of OA (Nie et al, 2019;Zhang et al, 2019;Kania et al, 2020). Gong et al (2019) reached the same conclusion in studies with an OA mouse model and human OA tissue:…”

Section: Yap1 Is An Important Promoter Of Oamentioning

confidence: 63%

“…YAP1 has been reported to be a negative regulator of chondrogenesis, and the level of YAP1 expression has been shown to be a key element in maintaining chondrocyte function in vitro (Karystinou et al, 2015;Kania et al, 2020). Zhang et al (2019) observed through qPCR and Western blotting analyses that YAP1 overexpression significantly downregulates the expression of Runx2, osteocalcin, and collagen I related to ATDC5 cell differentiation, while inhibition of YAP1 significantly enhances the expression of Runx2, osteocalcin, and collagen I. Notably, YAP1 also promotes early chondrocyte proliferation by regulating SOX6 expression and inhibiting collagen type X (COL10A1) expression by interacting with Runx2 during chondrocyte maturation, thereby inhibiting chondrocyte maturation (Deng et al, 2016;Ying et al, 2018).…”

Section: High Yap1 Expression Inhibits Chondrocyte Differentiation In Oamentioning

confidence: 99%

“…Since YAP1 is a promoter in the development of OA, and downregulation of YAP1 contributes to chondrocyte differentiation and the maintenance of the chondrocyte phenotype in OA, the downregulation of YAP1 activity may be an effective way to treat OA. Interestingly, commonly used anti-OA drugs can inhibit YAP1 expression in different ways in OA mouse models, including paracetamol, diacerein, 99Tc-MDP, DSG, O3, vitamin C, and rapamycin (Zhang et al, 2019). Verteporfin, an inhibitor of YAP1, is also a good choice, as it can disrupt the YAP1-TEAD interaction and thereby inhibit YAP1 activity (Brodowska et al, 2014).…”

Section: Targeting Yap1 In Orthopedic Degenerative Diseases (Oa and Op)mentioning

confidence: 99%

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Yes-Associated Protein 1: Role and Treatment Prospects in Orthopedic Degenerative Diseases

Xie

Xiao

Tang

et al. 2020

Front. Cell Dev. Biol.

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The Hippo/yes-associated protein 1 signaling pathway is an evolutionarily conserved signaling pathway. This signaling pathway is primarily involved in the regulation of stem cell self-renewal, organ size and tissue regeneration by regulating cell proliferation, differentiation and apoptosis. It plays an important role in embryonic development and tissue organ formation. Yes-associated protein 1 (YAP1) is a key transcription factor in the Hippo signaling pathway and is negatively regulated by this pathway. Changes in YAP1 expression levels affect the occurrence and development of a variety of tumors, but the specific mechanism associated with this phenomenon has not been thoroughly studied. Recently, several studies have described the role of YAP1 in osteoarthritis (OA). Indeed, YAP1 is involved in orthopedic degenerative diseases such as osteoporosis (OP) in addition to OA. In this review, we will summarize the significance of YAP1 in orthopedic degenerative diseases and discuss the potential of the targeted modulation of YAP1 for the treatment of these diseases.

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Section: Yap1 Is An Important Promoter Of Oamentioning

confidence: 63%

Section: High Yap1 Expression Inhibits Chondrocyte Differentiation In Oamentioning

confidence: 99%

Section: Targeting Yap1 In Orthopedic Degenerative Diseases (Oa and Op)mentioning

confidence: 99%

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Yes-Associated Protein 1: Role and Treatment Prospects in Orthopedic Degenerative Diseases

Xie

Xiao

Tang

et al. 2020

Front. Cell Dev. Biol.

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“…We found 737 significantly downregulated genes in the AB uninjured group compared to the VEH uninjured group. These genes included regulators of skeletal development ( Alpl [ 37 ], Col6a1 [ 54 ], Col6a2 [ 55 ], Sox9 [ 37 ], Sox11 [ 56 ], and Wnt9a [ 57 ]), Hippo signaling ( Tead1 , Tead4 [ 58 ], and Yap1 [ 59 ]), muscle contraction ( Myh8 , Myh2 , and Myom2 ), and inflammatory response ( Tlr5 [ 60 ], Ccl8 [ 61 ], Cxcl13 [ 37 ], C5ar1 [ 62 ], Cxcr1 [ 63 ], and Foxo6 [ 64 ]). Inflammatory gene comparison between AB injured and uninjured groups compared to the corresponding VEH groups are shown in Figure 5 A and Table 1 .…”

Section: Resultsmentioning

confidence: 99%

Antibiotic Treatment Prior to Injury Improves Post-Traumatic Osteoarthritis Outcomes in Mice

Mendez

Murugesh

Sebastian

et al. 2020

IJMS

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Osteoarthritis (OA) is a painful and debilitating disease characterized by the chronic and progressive degradation of articular cartilage. Post-traumatic OA (PTOA) is a secondary form of OA that develops in ~50% of cases of severe articular injury. Inflammation and re-occurring injury have been implicated as contributing to the progression of PTOA after the initial injury. However, there is very little known about external factors prior to injury that could affect the risk of PTOA development. To examine how the gut microbiome affects PTOA development we used a chronic antibiotic treatment regimen starting at weaning for six weeks prior to ACL rupture, in mice. A six-weeks post-injury histological examination showed more robust cartilage staining on the antibiotic (AB)-treated mice than the untreated controls (VEH), suggesting slower disease progression in AB cohorts. Injured joints also showed an increase in the presence of anti-inflammatory M2 macrophages in the AB group. Molecularly, the phenotype correlated with a significantly lower expression of inflammatory genes Tlr5, Ccl8, Cxcl13, and Foxo6 in the injured joints of AB-treated animals. Our results indicate that a reduced state of inflammation at the time of injury and a lower expression of Wnt signaling modulatory protein, Rspo1, caused by AB treatment can slow down or improve PTOA outcomes.

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“…OA is considered the most prevalent degenerative disease in joints and chondrocytes play an important role in the development. However, the pathogenesis of OA remains to be elucidated (Zhang, Fang, Zhao, & Liang, ). Circular RNAs (circRNAs) are a large class of noncoding RNAs that exist ubiquitously in the cytoplasm of eukaryotic cells (Conn et al, ; Salzman, Gawad, Wang, Lacayo, & Brown, ).…”

Section: Discussionmentioning

confidence: 99%

Upregulation of microRNA‐9‐5p inhibits apoptosis of chondrocytes through downregulating Tnc in mice with osteoarthritis following tibial plateau fracture

Chen

Yang

Tan³

2019

Journal Cellular Physiology

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Osteoarthritis (OA) is a common degenerative joint disease which is typically progressed with age, affecting smaller joints of hands, lower limbs, and the vertebral column. It has been reported that microRNAs could regulate the biological processes of OA. Therefore, the purpose of this study was to elucidate miR-9-5p's role in regulating cartilage remodeling of OA mice following tibial plateau fracture (TPF) through regulation of tenascin C (Tnc). Initially, we determined the expression of miR-9-5p and Tnc in mice with OA and then testified their relationship. The results displayed a high expression of Tnc, but a poor expression of miR-9-5p with high methylation in OA. Tnc was confirmed to be a target gene of miR-9-5p. Moreover, based on gain-and loss-function experiments, an increase of miR-9-5p and loss of Tnc had the potential to inhibit cell apoptosis, while facilitating cell proliferation, migration, invasion, and cartilage remodeling of mice with OA following TPF. This was further demonstrated by a higher expression of type II collagen, lower type X collagen, and protogenin expression. Subsequently, downregulation of miR-9-5p aggravated the pathological changes of mice, illustrated by an increase in the Mankin score. In conclusion, the present study proved that overexpression of miR-9-5p suppressed chondrocytes apoptosis and promoted cartilage remodeling through downregulating of Tnc in mice with OA.

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The transcriptional coactivator YAP1 is overexpressed in osteoarthritis and promotes its progression by interacting with Beclin-1

Cited by 22 publications

References 47 publications

Yes-Associated Protein 1: Role and Treatment Prospects in Orthopedic Degenerative Diseases

Yes-Associated Protein 1: Role and Treatment Prospects in Orthopedic Degenerative Diseases

Antibiotic Treatment Prior to Injury Improves Post-Traumatic Osteoarthritis Outcomes in Mice

Upregulation of microRNA‐9‐5p inhibits apoptosis of chondrocytes through downregulating Tnc in mice with osteoarthritis following tibial plateau fracture

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