miR-27 regulates chondrogenesis by suppressing focal adhesion kinase during pharyngeal arch development

Kara, Nergis; Wei, Chunyao; Commanday, Alexander C.; Patton, James G.

doi:10.1016/j.ydbio.2017.06.013

Cited by 14 publications

(13 citation statements)

References 77 publications

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“…Integrin-ECM interactions promote osteogenic differentiation while inhibiting chondrogenesis in mesenchymal stem cells (17). Increased FAK activation prevents chondrogenesis (39), and intrinsic FAK expression is actively down-regulated in developing chondrocytes (59), which we also confirmed in chondrogenic hBMSCs ( fig. S6A).…”

Section: Discussionsupporting

confidence: 76%

ITGBL1 modulates integrin activity to promote cartilage formation and protect against arthritis

et al. 2018

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Developing and mature chondrocytes constantly interact with and remodel the surrounding extracellular matrix (ECM). Recent research indicates that integrin-ECM interaction is differentially regulated during cartilage formation (chondrogenesis). Integrin signaling is also a key source of the catabolic reactions responsible for joint destruction in both rheumatoid arthritis and osteoarthritis. However, we do not understand how chondrocytes dynamically regulate integrin signaling in such an ECM-rich environment. Here, we found that developing chondrocytes express integrin-β–like 1 (Itgbl1) at specific stages, inhibiting integrin signaling and promoting chondrogenesis. Unlike cytosolic integrin inhibitors, ITGBL1 is secreted and physically interacts with integrins to down-regulate activity. We observed that Itgbl1 expression was strongly reduced in the damaged articular cartilage of patients with osteoarthritis (OA). Ectopic expression of Itgbl1 protected joint cartilage against OA development in the destabilization of the medial meniscus–induced OA mouse model. Our results reveal ITGBL1 signaling as an underlying mechanism of protection against destructive cartilage disorders and suggest the potential therapeutic utility of targeting ITGBL1 to modulate integrin signaling in human disease.

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Section: Discussionsupporting

confidence: 76%

ITGBL1 modulates integrin activity to promote cartilage formation and protect against arthritis

et al. 2018

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“…There is some evidence to suggest that miRNA expression changed the across different species from miRNAs in many models of myocardial I/R injury, demonstrating the pivotal role of miRNAs in myocardial ischemic injury . It has been proposed that miR‐27 regulates cell differentiation in many diseases . It has conclusively been shown that miR‐27 may be involved in occurrence and development of atherosclerosis .…”

Section: Discussionmentioning

confidence: 99%

“…1,18 It has been proposed that miR-27 regulates cell differentiation in many diseases. 19,20 It has conclusively been shown that miR-27 may be involved in occurrence and development of atherosclerosis. 19 However, there were no reports on miR-27 acting a role in myocardial ischemic injury.…”

Section: Downregulated Expression Of Mir-27 In Myocardial Ischemiamentioning

confidence: 99%

“…19,20 It has conclusively been shown that miR-27 may be involved in occurrence and development of atherosclerosis. 19 However, there were no reports on miR-27 acting a role in myocardial ischemic injury. Previous reports hint us to hypothesis that miR-27 may have an effect on cardiomyocyte injury.…”

Section: Downregulated Expression Of Mir-27 In Myocardial Ischemiamentioning

confidence: 99%

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MiR‐27 alleviates myocardial cell damage induced by hypoxia/reoxygenation via targeting TGFBR1 and inhibiting NF‐κB pathway

Zhang

2019

The Kaohsiung J of Med Scie

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MiR‐27 prevents atherosclerosis by inhibiting inflammatory responses induced by lipoprotein lipase. Overexpression of miR‐27b attenuates angiotensin‐induced atrial fibrosis. Nevertheless, studies have rarely investigated on the effect of miR‐27 in cardiomyocyte injury. H9c2 cells were transfected with miR‐27 mimic/inhibitor. Then the cell proliferation was tested by MTT assay and the cell apoptosis was detected by flow cytometry. The luciferase activity assay was utilized to analyze the relationship between miR‐27 and TGFBR1. Quantificational real‐time polymerase chain reaction and western blot were utilized to detect the cardiomyocyte differentiation marker and nuclear factor kappa B (NF‐κB) pathway. Our outcomes demonstrated that miR‐27 expression was downregulated cardiomyocyte injury subjected to hypoxia/reoxygenation (H/R). Additionally, overexpression of miR‐27 could significantly alleviate cardiomyocyte injury by regulating cell activity and apoptosis. The luciferase activity assay confirmed that transforming growth factor ß receptor 1 (TGFBR1) is a direct hallmark of miR‐27. Besides, overexpression of miR‐27 promoted the expression of TGFBR1 in H/R model. After transfection with miR‐27 mimic/inhibitor, the expression of NF‐κB pathway‐related proteins was decreased/increased. Taken together, our data manifested that miR‐27 repressed cardiomyocyte injury induced by H/R via mediating TGFBR1 and inhibiting NF‐κB signaling pathway. Furthermore, miR‐27/ TGFBR1 might be utilized as hopeful biomarkers for myocardial ischemia diagnosis and treatment.

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“…Accumulating evidence reveals that miRNAs are implicated in several physiological and pathological processes, such as inflammation, carcinogenesis, and chondrogenesis, though binding to the 3′UTR of target genes (Jiang, Wang, & Shi, ; Kara, Wei, Commanday, & Patton, ; Li et al, ; Shen et al, ). In particular, miR141‐3p is considered to regulate OA features including apoptosis, inflammation, neurogenesis, drug resistance, and development of the disease (Jiang et al, ; Jin et al, ; Li et al, ; Saha, Choudhury, & Ain, ; Shen et al, ; Yu et al, ).…”

Section: Discussionmentioning

confidence: 99%

Glucose enhances aggrecan expression in chondrocytes via the PKCα/p38‐miR141‐3p signaling pathway

Fong¹,

Lin

Huang³

et al. 2018

Journal Cellular Physiology

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Aggrecan is a high molecular weight proteoglycan that plays a critical role in cartilage structure and the function of joints, providing intervertebral disc and cartilage with the ability to resist compressive loads. Aggrecan degradation in articular cartilage is a significant event in early-stage osteoarthritis (OA). Currently, no effective treatment exists for OA other than pain relief. Dextrose (D-glucose) prolotherapy has shown promising activity in the treatment of different musculoskeletal disorders, including OA. However, little is known about the molecular mechanism of the glucose effect in OA and on the regulation of chondrogenesis. We show for the first time that glucose upregulates aggrecan expression and subsequent chondrogenesis in ATDC5 cells. Moreover, we found that glucose-induced aggrecan expression is mediated through the protein kinase Cα (PKCα)- and p38-dependent pathway. As demonstrated by microRNA (miR) and luciferase analyses, the glucose-induced PKCα/p38 signaling axis is responsible for downregulating miR141-3p which targets to the 3'untranslated region of aggrecan. In summary, we show that glucose enhances chondrogenesis by upregulating aggrecan expression via the PKCα-p38-miR141-3p signaling pathway. This result provides new insights into the mechanism of glucose on chondrogenesis.

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miR-27 regulates chondrogenesis by suppressing focal adhesion kinase during pharyngeal arch development

Cited by 14 publications

References 77 publications

ITGBL1 modulates integrin activity to promote cartilage formation and protect against arthritis

ITGBL1 modulates integrin activity to promote cartilage formation and protect against arthritis

MiR‐27 alleviates myocardial cell damage induced by hypoxia/reoxygenation via targeting TGFBR1 and inhibiting NF‐κB pathway

Glucose enhances aggrecan expression in chondrocytes via the PKCα/p38‐miR141‐3p signaling pathway

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