Bax Targeted by miR-29a Regulates Chondrocyte Apoptosis in Osteoarthritis

Miao, Guiqiang; Xuehui, Zang; Hou, Huige; Sun, Hui; Wang, Lihui; Zhang, Ting; Tan, Yongtao; Liu, Wenzhou; Ye, Pei; Gao, Lihua; Zha, Zhengang

doi:10.1155/2019/1434538

Cited by 25 publications

(17 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MicroRNAs (miRNAs) play roles in a variety of physiological functions and disease processes by mediating cleavage and destabilization of mRNA [7]. Zhixi Duan et al have illustrated that miR-15a-5p motivates the degeneration and proliferation of chondrocytes through PTHrP inhibition [8].…”

Section: Introductionmentioning

confidence: 99%

Potential of miR-25-3p in protection of chondrocytes: emphasis on osteoarthritis

Deng

2021

Folia Histochem Cytobiol.

View full text Add to dashboard Cite

Introduction. Osteoarthritis (OA) is the most prevailing musculoskeletal dysfunction triggered by lesions in synovial membranes and articular cartilage. MicroRNAs (miRNAs) have emerged as crucial regulators participated in many biological courses, such as osteoarthritis. This study was undertaken to address the role of miR-25-3p in the apoptosis of rat chondrocytes under an OA-like condition and its underlying mechanism. Material and methods. OA cellular model was established in rat chondrocytes by TNF-α induction. Then, qRT-PCR and Western blotting were utilized for evaluation of the expressions of miR-25-3p and insulin-like growth factor-binding protein 7 (IGFBP7), CCK-8 assay for inspection of chondrocyte viability, flow cytometry for assessment of cell apoptosis rate, Western blotting for the detection of cleaved caspase-3 level and dual-luciferase reporter gene assay for verification of the targeting relationship between miR-25-3p and IGFBP7. Results. The miR-25-3p expression was decreased and IGFBP7 was elevated in TNF-α-induced rat chondrocytes. The miR-25-3p inhibited chondrocyte apoptosis and IGFBP7 promoted apoptosis as evidenced by enhanced cell viability and suppressed cell apoptosis in OA chondrocytes after miR-25-3p overexpression or IGFBP7 knockdown. The miR-25-3p facilitated chondrocyte viability and repressed cell apoptosis in OA by negatively regulating IGFBP7. Conclusions. MiR-25-3p negatively regulates IGFBP7 to promote chondrocyte proliferation and restrain chondrocyte apoptosis. Our findings suggest that the regulation of IGFBP7 by miR-25-3p may emerge as a novel therapeutic regimen for OA.

show abstract

Section: Introductionmentioning

confidence: 99%

Potential of miR-25-3p in protection of chondrocytes: emphasis on osteoarthritis

Deng

2021

Folia Histochem Cytobiol.

View full text Add to dashboard Cite

show abstract

“…MiRNAs are well known for their capability to inhibit expression of target genes via binding complementarily to 3′‐UTRs of target mRNAs (Cao et al., 2013; Shukla et al., 2011). Previous studies also reported that several miRNAs, including miR‐573, miR‐208b and miR‐29a, inhibit apoptosis via negative regulation of BAX expression (Miao et al., 2019; Wang et al., 2019; Zhou et al., 2018). In our previous studies, the expression levels of many mRNAs were found to be significantly modulated by miRNAs in GiCF cells during CyHV‐2 infection (Fei, Feng, et al., 2020; Lu, Xu, Shen, et al., 2018).…”

Section: Discussionmentioning

confidence: 96%

Expression and regulation of ccBAX by miR‐124 in the caudal fin cell of C. auratus gibelio upon cyprinid herpesvirus 2 infection

Chen

Chu

et al. 2021

Journal of Fish Diseases

View full text Add to dashboard Cite

Bcl2 family proteins play a critical role in cell death or survival. BAX, the death‐promoting protein of bcl2 family, mediated mitochondrial pathway inducing cells’ apoptosis in mammal. MiRNAs have been implicated as negative regulators down‐regulating genes’ expression after post‐transcriptional level. At present, little is known about the regulatory mechanism of miRNA on the Bcl2 family proteins during CyHV‐2 infection in silver crucian carp (Carassius auratus gibelio). In this study, the ccBAX (silver crucian carp BAX) gene was cloned and expressed, and polyclonal antibodies were raised in mouse against the purified ccBAX‐GST fusion protein. The structure analysis indicated that ccBAX protein included four conserve domains (BH1, BH2, BH3 and transmembrane domains) and the expression of ccBAX protein occurred throughout the cells. Furthermore, two miRNAs (miR‐124 and miRNA‐29b) were identified to negatively regulate ccBAX gene expression in GiCF cell. miR‐124 was found to suppress the expression of WT‐ccBAX (wild type), but not the MT‐ccBAX (mutant). Overall, the results demonstrated that the expression of the ccBAX gene was significantly down‐regulated by miR‐124 in silver crucian carp (Carassius auratus gibelio) during CyHV‐2 infection.

show abstract

“…Caspase-3, a member of cysteine proteases family, is responsible for most of the proteolysis during apoptosis [ 21 ]. Bax is a pro-apoptotic protein in the Bcl-2 family, which is upregulated in chondrocytes of patients with OA [ 22 ]. Bcl2 is an anti-apoptosis protein, whose alteration plays a key role in OA development [ 23 , 24 ].…”

Section: Discussionmentioning

confidence: 99%

HDAC2 interacts with microRNA-503-5p to regulate SGK1 in osteoarthritis

et al. 2021

View full text Add to dashboard Cite

Background Osteoarthritis (OA) is a disabling joint disease that causes articular cartilage degeneration. It has been implicated that altered expression of histone deacetylase 2 (HDAC2) is found in patients with OA. However, the specific role of HDAC2 in the development of OA still remains enigmatic. Hence, we sought to characterize the functional relevance of HDAC2 in the development of OA. Methods Anterior cruciate ligament surgery was performed to generate the rat model of OA. Luciferase assay was performed to evaluate the relationship between microRNA-503-5p (miR-503-5p) and serum- and glucocorticoid-inducible kinase-1 (SGK1). Functional experiments were conducted to examine the functional significance of miR-503-5p, histone deacetylase 2 (HDAC2), and SGK1 on the progression of OA by determining proliferation, apoptosis, and expression of apoptosis-associated proteins and inflammatory cytokines. Results HDAC2 could inhibit miR-503-5p expression. SGK1 was the target gene of miR-503-5p. Upregulation of miR-503-5p or silencing of HDAC2 contributed to enhanced proliferation, suppressed apoptosis (reduced expression of Caspase-3 and Bax but elevated expression of Bcl2), and promoted inflammation in chondrocytes of OA rats. Conclusion In conclusion, our study demonstrated that HDAC2 could promote OA through miR-503-5p/SGK1 axis, which might function as a therapeutic target for OA treatment.

show abstract

Bax Targeted by miR-29a Regulates Chondrocyte Apoptosis in Osteoarthritis

Cited by 25 publications

References 54 publications

Potential of miR-25-3p in protection of chondrocytes: emphasis on osteoarthritis

Potential of miR-25-3p in protection of chondrocytes: emphasis on osteoarthritis

Expression and regulation of ccBAX by miR‐124 in the caudal fin cell of C. auratus gibelio upon cyprinid herpesvirus 2 infection

HDAC2 interacts with microRNA-503-5p to regulate SGK1 in osteoarthritis

Contact Info

Product

Resources

About