Research progress in the development of osteoarthritis mediated by pericellular matrix

doi:10.3969/j.issn.1674-8115.2021.08.015

Abstract

Abstract:

Osteoarthritis (OA) is one of the most common degenerative diseases in clinic. It causes joint pain and dyskinesia, and seriously affects the quality life of the patients′. However, the pathogenesis of OA has not been fully understood. Pericellular matrix (PCM) is a narrow matrix area around chondrocytes. Numerous evidences have revealed the promotion of PCM in the pathogenesis of osteoarthritis. The degradation of PCM components, the release of growth factor and the alteration of mechanical signal transduction accelerate the occurrence and development of OA. This paper summarizes the structure and functions of PCM, and reviews the latest progresses in the involvement of PCM in OA pathogenesis.

Key words: osteoarthritis (OA), pericellular matrix (PCM), chondron, mechanotransduction

CLC Number:

R684.3

Wen-cheng HU, Hong-yi ZHU, Jun-qing LIN, Xian-you ZHENG. Research progress in the development of osteoarthritis mediated by pericellular matrix[J]. JOURNAL OF SHANGHAI JIAOTONG UNIVERSITY (MEDICAL SCIENCE), 2021, 41(8): 1089-1093.

TrendMD

References 39

1	Zhang ZY, Huang CB, Jiang Q, et al. Guidelines for the diagnosis and treatment of osteoarthritis in China (2019 edition)[J]. Ann Transl Med, 2020, 8(19): 1213.
2	Mantovani V, Maccari F, Volpi N. Chondroitin sulfate and glucosamine as disease modifying anti-osteoarthritis drugs (DMOADs)[J]. Curr Med Chem, 2016, 23(11): 1139-1151.
3	Jeon OH, Kim C, Laberge RM, et al. Local clearance of senescent cells attenuates the development of post-traumatic osteoarthritis and creates a pro-regenerative environment[J]. Nat Med, 2017, 23(6): 775-781.
4	Guilak F, Nims RJ, Dicks A, et al. Osteoarthritis as a disease of the cartilage pericellular matrix[J]. Matrix Biol, 2018, 71-72: 40-50.
5	Poole CA, Flint MH, Beaumont BW. Chondrons in cartilage: ultrastructural analysis of the pericellular microenvironment in adult human articular cartilages[J]. J Orthop Res, 1987, 5(4): 509-522.
6	Lee GM, Paul TA, Slabaugh M, et al. The incidence of enlarged chondrons in normal and osteoarthritic human cartilage and their relative matrix density[J]. Osteoarthritis Cartilage, 2000, 8(1): 44-52.
7	Zhang ZJ. Chondrons and the pericellular matrix of chondrocytes[J]. Tissue Eng Part B Rev, 2015, 21(3): 267-277.
8	Han SK, Federico S, Herzog W. A depth-dependent model of the pericellular microenvironment of chondrocytes in articular cartilage[J]. Comput Methods Biomech Biomed Engin, 2011, 14(7): 657-664.
9	Hofmann UK, Steidle J, Danalache M, et al. Chondrocyte death after mechanically overloading degenerated human intervertebral disk explants is associated with a structurally impaired pericellular matrix[J]. J Tissue Eng Regen Med, 2018, 12(9): 2000-2010.
10	Wilusz RE, Sanchez-Adams J, Guilak F. The structure and function of the pericellular matrix of articular cartilage[J]. Matrix Biol, 2014, 39: 25-32.
11	Di Federico E, Bader DL, Shelton JC. 3D models of chondrocytes within biomimetic scaffolds: effects of cell deformation from loading regimens[J]. Clin Biomech (Bristol, Avon), 2020, 79: 104972.
12	Rodgers KD, Sasaki T, Aszodi A, et al. Reduced perlecan in mice results in chondrodysplasia resembling Schwartz-Jampel syndrome[J]. Hum Mol Genet, 2007, 16(5): 515-528.
13	Wang B, Lai XH, Price C, et al. Perlecan-containing pericellular matrix regulates solute transport and mechanosensing within the osteocyte lacunar-canalicular system[J]. J Bone Miner Res, 2014, 29(4): 878-891.
14	Wilusz RE, Sanchez-Adams J, Guilak F. The structure and function of the pericellular matrix of articular cartilage[J]. Matrix Biol, 2014, 39: 25-32.
15	Peters HC, Otto TJ, Enders JT, et al. The protective role of the pericellular matrix in chondrocyte apoptosis[J]. Tissue Eng Part A, 2011, 17(15-16): 2017-2024.
16	Poole CA, Matsuoka A, Schofield JR. Chondrons from articular cartilage. Ⅲ. Morphologic changes in the cellular microenvironment of chondrons isolated from osteoarthritic cartilage[J]. Arthritis Rheum, 1991, 34(1): 22-35.
17	Lotz MK, Otsuki S, Grogan SP, et al. Cartilage cell clusters[J]. Arthritis Rheum, 2010, 62(8): 2206-2218.
18	Rolauffs B, Williams JM, Aurich M, et al. Proliferative remodeling of the spatial organization of human superficial chondrocytes distant from focal early osteoarthritis[J]. Arthritis Rheum, 2010, 62(2): 489-498.
19	Danalache M, Kleinert R, Schneider J, et al. Changes in stiffness and biochemical composition of the pericellular matrix as a function of spatial chondrocyte organisation in osteoarthritic cartilage[J]. Osteoarthritis Cartilage, 2019, 27(5): 823-832.
20	Danalache M, Erler AL, Wolfgart JM, et al. Biochemical changes of the pericellular matrix and spatial chondrocyte organization: two highly interconnected hallmarks of osteoarthritis[J]. J Orthop Res, 2020, 38(10): 2170-2180.
21	Yuan X, Yang S. Primary cilia and intraflagellar transport proteins in bone and cartilage[J]. J Dent Res, 2016, 95(12): 1341-1349.
22	Ruhlen R, Marberry K. The chondrocyte primary cilium[J]. Osteoarthritis Cartilage, 2014, 22(8): 1071-1076.
23	Zhao ZX, Li YF, Wang MJ, et al. Mechanotransduction pathways in the regulation of cartilage chondrocyte homoeostasis[J]. J Cell Mol Med, 2020, 24(10): 5408-5419.
24	Zelenski NA, Leddy HA, Sanchez-Adams J, et al. Type Ⅵ collagen regulates pericellular matrix properties, chondrocyte swelling, and mechanotransduction in mouse articular cartilage[J]. Arthritis Rheumatol, 2015, 67(5): 1286-1294.
25	Wann AK, Knight MM. Primary cilia elongation in response to interleukin-1 mediates the inflammatory response[J]. Cell Mol Life Sci, 2012, 69(17): 2967-2977.
26	Xiang W, Zhang J, Wang R, et al. Role of IFT88 in icariin‑regulated maintenance of the chondrocyte phenotype[J]. Mol Med Rep, 2018, 17(4): 4999-5006.
27	Chen JQ, Tu XL, Esen E, et al. WNT7B promotes bone formation in part through mTORC1[J]. PLoS Genet, 2014, 10(1): e1004145.
28	Zhang Y, Vasheghani F, Li YH, et al. Cartilage-specific deletion of mTOR upregulates autophagy and protects mice from osteoarthritis[J]. Ann Rheum Dis, 2015, 74(7): 1432-1440.
29	Zhou YC, Wang TY, Hamilton JL, et al. Wnt/β-catenin signaling in osteoarthritis and in other forms of arthritis[J]. Curr Rheumatol Rep, 2017, 19(9): 53.
30	Woods S, Barter MJ, Elliott HR, et al. miR-324-5p is up regulated in end-stage osteoarthritis and regulates Indian Hedgehog signalling by differing mechanisms in human and mouse[J]. Matrix Biol, 2019, 77: 87-100.
31	Rockel JS, Yu CY, Whetstone H, et al. Hedgehog inhibits β-catenin activity in synovial joint development and osteoarthritis[J]. J Clin Invest, 2016, 126(5): 1649-1663.
32	Deng Q, Li P, Che MJ, et al. Activation of hedgehog signaling in mesenchymal stem cells induces cartilage and bone tumor formation via Wnt/β-catenin[J]. Elife, 2019, 8: e50208.
33	van der Kraan PM. The changing role of TGFβ in healthy, ageing and osteoarthritic joints[J]. Nat Rev Rheumatol, 2017, 13(3): 155-163.
34	Zhang XR, Zhu J, Liu F, et al. Reduced EGFR signaling enhances cartilage destruction in a mouse osteoarthritis model[J]. Bone Res, 2014, 2: 14015.
35	Jia H, Ma X, Tong W, et al. EGFR signaling is critical for maintaining the superficial layer of articular cartilage and preventing osteoarthritis initiation[J]. PNAS, 2016, 113(50): 14360-14365.
36	Janssen JN, Batschkus S, Schimmel S, et al. The influence of TGF-β3, EGF, and BGN on SOX9 and RUNX2 expression in human chondrogenic progenitor cells[J]. J Histochem Cytochem, 2019, 67(2): 117-127.
37	Qin L, Beier F. EGFR signaling: friend or foe for cartilage?[J]. JBMR Plus, 2019, 3(2): e10177.
38	Im HJ, Muddasani P, Natarajan V, et al. Basic fibroblast growth factor stimulates matrix metalloproteinase-13 via the molecular cross-talk between the mitogen-activated protein kinases and protein kinase Cδ pathways in human adult articular chondrocytes[J]. J Biol Chem, 2007, 282(15): 11110-11121.
39	Yao XD, Zhang JM, Jing XZ, et al. Fibroblast growth factor 18 exerts anti-osteoarthritic effects through PI3K-AKT signaling and mitochondrial fusion and fission[J]. Pharmacol Res, 2019, 139: 314-324.