Reduced apoptosis correlates with enhanced autophagy in synovial tissues of rheumatoid arthritis

Xu, Ke; Xu, Peng; Yao, Jianfeng; Zhang, Yingang; Hou, Weikun; Lu, Shemin

doi:10.1007/s00011-012-0572-1

Cited by 123 publications

(90 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We have observed that the CXCR3-B-mediated signal down-regulates autophagy in breast cancer cells. It has been established that there can be a reverse correlation in the regulation of apoptosis and autophagy (34), which is clearly supportive to our findings. In addition, it has been demonstrated that autophagy can delay apoptotic death in MCF-7 cells (35).…”

Section: Discussionsupporting

confidence: 92%

A Novel CXCR3-B Chemokine Receptor-induced Growth-inhibitory Signal in Cancer Cells Is Mediated through the Regulation of Bach-1 Protein and Nrf2 Protein Nuclear Translocation

Balan

Pal

2014

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background:The chemokine receptor CXCR3-B initiates inhibitory signals. Results: CXCR3-B-mediated signal induced apoptosis and inhibited autophagy of breast cancer cells. It is associated with nuclear translocation of Bach-1, nuclear export of Nrf2, and down-regulation of HO-1. Conclusion: A CXCR3-B-mediated signal promotes apoptosis of breast cancer cells. Significance: Induction of CXCR3-B-mediated signaling can serve as a novel therapeutic approach for the treatment of breast cancer.

show abstract

Section: Discussionsupporting

confidence: 92%

A Novel CXCR3-B Chemokine Receptor-induced Growth-inhibitory Signal in Cancer Cells Is Mediated through the Regulation of Bach-1 Protein and Nrf2 Protein Nuclear Translocation

Balan

Pal

2014

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Ex vivo studies show that the rate of apoptosis in RA FLS has an inverse relationship to the expression of beclin1 and LC3 (REF. 99). Furthermore, inhibition of proteasomal activity in RA FLS increases their LC3II protein levels and prolongs their survival 100 , suggesting that increased autophagy in RA FLS promotes RAassociated synovitis.…”

Section: Autophagy In Rheumatic Diseasesmentioning

confidence: 93%

“…These RA FLS show signs of myofibroblast differentiation (an intermediate cell type between a smooth muscle cell and a fibroblast), such as increased collagen deposition and expression of αsmooth muscle actin, which contribute to syno vial fibrosis 97 . In RA FLS, multiple mechanisms confer resistance to programmed cell death, including increased levels of antiapoptotic factors, downregulation of proap optotic factors 98 and increased autophagy [99][100][101][102] . Ex vivo studies show that the rate of apoptosis in RA FLS has an inverse relationship to the expression of beclin1 and LC3 (REF.…”

Section: Autophagy In Rheumatic Diseasesmentioning

confidence: 99%

Autophagy: controlling cell fate in rheumatic diseases

2016

View full text Add to dashboard Cite

Autophagy, an endogenous process necessary for the turnover of organelles, maintains cellular homeostasis and directs cell fate. Alterations to the regulation of autophagy contribute to the progression of various rheumatic diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), osteoarthritis (OA) and systemic sclerosis (SSc). Implicit in the progression of these diseases are cell-type-specific responses to surrounding factors that alter autophagy: chondrocytes within articular cartilage show decreased autophagy in OA, leading to rapid cell death and cartilage degeneration; fibroblasts from patients with SSc have restricted autophagy, similar to that seen in aged dermal fibroblasts; fibroblast-like synoviocytes from RA joints show altered autophagy, which contributes to synovial hyperplasia; and dysregulation of autophagy in haematopoietic lineage cells alters their function and maturation in SLE. Various upstream mechanisms also contribute to these diseases by regulating autophagy as part of their signalling cascades. In this Review, we discuss the links between autophagy, immune responses, fibrosis and cellular fates as they relate to pathologies associated with rheumatic diseases. Therapies in clinical use, and in preclinical or clinical development, are also discussed in relation to their effects on autophagy in rheumatic diseases.

show abstract

“…Therefore, when RASFs were exposed to ER stress, high level of autophagy is induced and it may contribute to resistance against ER stress-induced cell death [67]. Furthermore, decreased level of miR-30a, which was shown to inhibit Beclin-1 expression, was observed in synovial tissue of RA, and it may contribute to upregulation of autophagy in RASFs [68]. Recently, dual role of autophagy has been investigated in RASFs in response to cellular stress [69].…”

Section: Rheumatoid Arthritis (Ra)mentioning

confidence: 99%

Pathogenic Role of Autophagy in Rheumatic Diseases

Choi

Yoo

2016

J Rheum Dis

View full text Add to dashboard Cite

Autophagy is a principle catabolic process mediated by lysosomes in eukaryotic cells. This is an intracellular homeostatic mechanism crucial for degradation in acidic lysosomal compartments of waste components from the cytoplasm. Autophagy research was initially focused on its degradation mechanism, but focus is now shifting to its effects on immunity. It contributes to detection and removal of pathogens as well as regulation of inflammasomes and neutrophil extracellular traps. Moreover, it is pivotal in antigen presentation and immune cell maturation, survival and homeostasis. The importance of autophagic pathways in normal and dysregulated immunity has become increasingly recognized in the past several years. Dysregulation of the autophagic pathway is implicated in the pathogenesis of several rheumatic diseases. In this review, we summarize the immunological function of autophagy in innate and adaptive immunity, and the functions of autophagy in the pathogenesis of rheumatic diseases. (J Rheum Dis 2016;23:202-211)

show abstract

Reduced apoptosis correlates with enhanced autophagy in synovial tissues of rheumatoid arthritis

Abstract: The impaired apoptosis in RA synovium might result from increased autophagy, which in turn could be due to the deregulation of miRNA-30a.

Cited by 123 publications

References 31 publications

A Novel CXCR3-B Chemokine Receptor-induced Growth-inhibitory Signal in Cancer Cells Is Mediated through the Regulation of Bach-1 Protein and Nrf2 Protein Nuclear Translocation

A Novel CXCR3-B Chemokine Receptor-induced Growth-inhibitory Signal in Cancer Cells Is Mediated through the Regulation of Bach-1 Protein and Nrf2 Protein Nuclear Translocation

Autophagy: controlling cell fate in rheumatic diseases

Pathogenic Role of Autophagy in Rheumatic Diseases

Contact Info

Product

Resources

About