The Role of Decorin in Autoimmune and Inflammatory Diseases

Abstract

Decorin is an extracellular matrix protein that belongs to the family of small leucine-rich proteoglycans. As a matrix protein, the first discovered role of decorin is participating in collagen fibril formation. Many other functions of decorin in various biological processes have been subsequently identified. Decorin is involved in an extensive signaling network and can interact with other extracellular matrix components, growth factors, receptor tyrosine kinases, and various proteases. Decorin has been shown to be involved in wound repair, cell cycle, angiogenesis, tumor metastasis, and autophagy. Recent evidence indicates that it also plays a role in immune regulation and inflammatory diseases. This review summarizes the characteristics of decorin in immune and inflammatory diseases, including inflammatory bowel disease (IBD), Sjögren’s syndrome (SS), chronic obstructive pulmonary disease (COPD), IgA nephropathy, rheumatoid arthritis (RA), spondyloarthritis (SpA), osteoarthritis, multiple sclerosis (MS), idiopathic inflammatory myopathies (IIM), and systemic sclerosis (SSc) and discusses the potential role in these disorders.

AQP4, Astrogenesis, and Hydrocephalus: A New Neurological Perspective

“…Since the inflammatory component plays a fundamental role in reactive astrogliosis, several anti-inflammatory drugs have been proposed to decrease the glial response under hydrocephalic conditions to improve linked cellular alterations. For example, decorin, a proteoglycan that plays a fundamental role in immune regulation and inflammatory diseases [ 79 ], reduces white matter-dependent alterations and cytopathology associated with juvenile hydrocephalus [ 80 , 81 , 82 ].…”

Modic type 2 changes are fibroinflammatory changes with complement system involvement adjacent to degenerated vertebral endplates

“…Also, ECM‐derived proteins can activate the complement system. Cartilage‐derived proteoglycans that we found upregulated in MC2 can activate the complement system 38–40 . For example, FMOD can directly bind to C1Q and consequently activate the classical pathway of the complement system 38 .…”

“…Cartilage‐derived proteoglycans that we found upregulated in MC2 can activate the complement system. 38 , 39 , 40 For example, FMOD can directly bind to C1Q and consequently activate the classical pathway of the complement system. 38 BGN, DCN, and ECM1 are cartilage‐derived proteoglycans that were among the top upregulated proteins in MC2 endplate‐near bone marrow that can also activate the complement system.…”

“…38 BGN, DCN, and ECM1 are cartilage‐derived proteoglycans that were among the top upregulated proteins in MC2 endplate‐near bone marrow that can also activate the complement system. 39 , 40 , 41 , 42 These proteoglycans may have been produced within MC2 bone marrow as part of fibrotic changes, or they may have been expelled from the disc and CEP into the bone marrow as a consequence of degenerative changes. Lost CEP/BEP boundary in MC2 could facilitate their drainage into the bone marrow.…”

“…For example, FMOD can directly bind to C1Q and consequently activate the classical pathway of the complement system 38 . BGN, DCN, and ECM1 are cartilage‐derived proteoglycans that were among the top upregulated proteins in MC2 endplate‐near bone marrow that can also activate the complement system 39–42 . These proteoglycans may have been produced within MC2 bone marrow as part of fibrotic changes, or they may have been expelled from the disc and CEP into the bone marrow as a consequence of degenerative changes.…”