Autophagy effects on chondrocyte survival and cartilage damage

doi:10.3969/j.issn.2095-4344.2015.20.023

Abstract

Abstract:

BACKGROUND: Autophagy is the cellular process of lysosomal pathway processing by endogenous substrates, which exists in the body cells and has been considered as type II programmed cell death. Autophagy may be a protective or balancing mechanism of normal chondrocytes.
OBJECTIVE: To discuss the latest research progress in autophagy and cartilage damage aiming to better understanding the role of autophagy in cartilage damage and repair.
METHODS: A computer-based search of CNKI, Wanfang database and PubMed database was performed for articles relevant to autophagy and cartilage damage published in recent 20 years with the key words of “autophagy, cartilage, chondrocytes, beclin1, LC3” in Chinese and English.
RESULTS AND CONCLUSION: Intra-articular chondrocytes can response to the changes in the microenvironment so as to adjust the extracellular matrix metabolism and maintain the biological function of
articular cartilage. Hypoxic environment in which chondrocytes eixt is an important factor to causes autophagy. Autophagy is a normal balance or protection mechanism of chondrocytes. Studies on the correlation of autophagy with cartilage damage have made considerable progress in recent years, but still in its infancy. Atg discovery at the molecular level deepens the understanding of autophagy, but the induction of cartilage autophagy pathway, signal transduction, and their effects on the survival of chondrocytes are not clear yet, which need further studies.

Key words: Autophagy, Cartilage, Chondrocytes

CLC Number:

R318

Zhang Xie-zhuo, Xu Chao, Yilihamu Tuoheti. Autophagy effects on chondrocyte survival and cartilage damage[J]. Chinese Journal of Tissue Engineering Research, 2015, 19(20): 3236-3241.

Figures/Tables 1

References

[1] Reggiori F, Klionsky DJ. Autophagy in the eukaryotic cell. Eukaryot Cell. 2002; 1:11-21.

[2] Shintani T, Klionsky DJ. Autophagy in health and disease: a double-edged sword. Science.2004; 306: 990-995.

[3] Ishida Y, Yamamoto A, Kitamura A, et al. Autophagic elimination of misfolded procollagen aggregates in the endoplasmic reticulum as a means of cell protection. Mol Biol Cell.2009; 20(11):2744-2754.

[4] Pallet N, Bouvier N, Legendre C, et al. Autophagy protects renal tubular cells against cyclosporine toxicity. Autophagy. 2008; 4(6):783-791.

[5] Zhang YB, Li SX, Chen XP, et al. Autophagy is activated and might protect neurons from degeneration after traumatic brain injury. Neurosci Bull.2008; 24(3):143-149.

[6] 刘宁,宋玉文.细胞自噬与退行性骨关节疾病[J].中国骨与关节损伤杂志,2014,29(5):517-518.

[7] 彭红心,徐宏光. 细胞凋亡与软骨终板钙化的关系[J].国际骨科学杂志,2010,31(5):299-301

[8] 李西海,梁文娜,叶蕻芝,等.细胞自噬与骨关节炎软骨退变[J].国际骨科学杂志,2013,34(2):107-108.

[9] 俞云飞,徐宏光,王弘,等.自噬在张力诱导终板软骨细胞退变过程中的变化[J]. 中华骨科杂志, 2014,34(3):317-322.

[10] 张发仁,许丽艳,沈忠英,等.自噬的概述[J]. 汕头大学医学院学报, 2005,18(4):250-253.

[11] Majeski AE, Dice JF. Mechanisms of chaperone-mediated autophagy. Int J Biochem Cell Biol.2004;36(12):2435-2444.

[12] Wang CW, Klionsky DJ. The molecular mechanism of autophagy. Mol Med. 2003;9(3-4):65-76.

[13] 喻琴琴,杨俊,李馨欣.自噬及其抑制剂的研究进展[J]. 实用医学杂志,2013,29(17):2908-2910.

[14] Klionsky DJ, Emr SD.Autophagy as a regulated pathway of cellular degradation. Science.2000;290:1717-1721.

[15] Qin ZH, GU ZL.Huntingtin processing in pathogenesis of Huntington disease. Acta Pharmacol Sin.2004;25(10): 1243-1249.

[16] Bergamini E, Cavallini G, Donati A, et al. The role of macroautophagy in the ageing process, anti-ageing intervention and age-associated diseases. Int J Biochem Cell Biol.2004;36(12):2392-2404.

[17] Lockshin RA, Zakeri Z. Apoptosis, autophagy, and more. Int J Biochem Cell Biol.2004;36(12):2405-2419.

[18] Jacobson MD, Weil M, Raft MC.Role of ced-3/ICE-family proteases in staurosporine-induced programmed cell death. J Cell Biol. 1996;133(5):1041-1051.

[19] Liang XH, Jackson S, Seaman M, et al. Induction of autophagy and inhibition of tumorigenesis by beclin1. Nature. 1999;402,(6762):672-676.

[20] Aita VM, Liang XH, Murty VV, et al. Cloning and genomic organization of beclin1, a candidate tumor suppressor gene on chromosome 17q21. Genomics. 1999;59(1): 59-65.

[21] Scarlatti F, Maffei R, Beau I,et al.Role of non-canonical Beclin1-independent autophagy in cell death induced by resveratrol in human breast cancer cells. Cell Death Differ. 2008;15(8):1318-1329

[22] Edinger A L, Thompson C B. Defective autophagy leads to cancer. Cancer Cell. 2003;4(6):422-424.

[23] 叶挺, 邵增务.Bcl-2/Beclin-1复合体在自噬中的调节作用[J].中国生物化学与分子生物学报,2013,29(6):513-519.

[24] 程加峰,徐宏光.蛋白激酶C对软骨影响的研究进展[J].国际骨科学杂志, 2010,31(5):296-298.

[25] Bhosale AM, Richardson JB.Articular cartilage:structure, injuries and review of management. Br Med Bull.2008;87(1): 77-95.

[26] Taniguchi N, Carames B, Ronfani L, et al. Aging-related loss of the chromatin protein HMGB2 in articular cartilage is linked to reduced cellularity and osteoarthritis. Proc Natl Acad Sci USA.2009;106(4):1181-1186.

[27] Ruiz-Romero C, Calamia V, Mateos J, et al. Mitochondrial dysregulation of osteoarthritic human articular chondrocytes analyzed by proteomics: a decrease in mitochondrial superoxide dismutase points to a redox imbalance. Mol Cell Proteomics.2009;8(1):172-189.

[28] Vellai T. Autophagy genes and ageing. Cell Death Differ. 2009;16(1):94-102.

[29] Aigner T, Haag J, Martin J, et al. Osteoarthritis: aging of matrix and cells: going for a remedy. Curr Drug Targets. 2007; 8(2):325-331.

[30] 宋俊兴,徐宏光,贾瑞平.结缔组织生长因子与软骨修复研究进展[J].国际骨科学杂志, 2011,32(4):241-242.

[31] Mazor M, Lespessailles E, Coursier R, et al. Mesenchymal stem-cell potential in cartilage repair: an update. Cell Mol Med. 2014;18(12) :2340-2350.

[32] Lotz MK, Carames B. Autophagy and cartilage homeostasis mechanisms in joint health, aging and OA. Nat Rev Rheumatol. 2011;7(10):579-587.

[33] Zhang M, Zhang J, Lu L, et al. Enhancement of chondrocyte autophagy is an early response in the degenerative cartilage of the temporomandibular joint to biomechanical dental stimulation. Apoptosis.2013;18:423-434.

[34] Carames B, Hasegawa A, Taniguchi N, et al. Autophagy activation by rapamycin reduces severity of experimental osteoarthritis. Ann Rheum Dis. 2012;71(4):575-581.

[35] Carames B, Taniguchi N, Seino D,et al.Mechanical injury suppresses autophagy regulators and its pharmacological activation results in chondroprotection. Arthritis Rheum. 2012; 64(4):1182-1192.

[36] Srinivas V, Bohensky J, Shapiro IM. Autophagy: a new phase in the maturation of growth plate chondrocytes is regulated by HIF, mTOR and AMP kinase. Cells Tissues Organs.2009; 189(1-4):88-92.

[37] Srinivas V, Shapiro IM. Chondrocytes embedded in the epiphyseal growth plates of long bones undergo autophgay prior to the induction of osteogenesis. Autophagy.2006; 2(3): 215-216.

[38] Bohensky J, Shapiro IM, Leshinsky S, et al. HIF-1 regulation of chondrocyte apoptpsis: induction of the autophagic pathway. Autophagy. 2007;3(3):207-214.

[39] Bohensky J, Terkhorn SP, Freeman TA, et al. Regulation of autophagy in human and murine cartilage: hypoxia-inducible factor 2 suppresses chondrocyte autophagy. Arthritis Rheum. 2009;60(5):1406-1415.

[40] Settembre C, Arteaga-Solis E, McKee MD, et al. Proteoglycan desulfation determines the efficiency of chondrocyte autophagy and the extent of FGF signaling during endochondral ossification. Genes Dev. 2008;22(19): 2645-2650.

[41] Goldring MB, Goldring SR. Osteoarthritis. J Cell Physiol. 2007; 213(3):626-634.

[42] Martin JA, Brown T, Heiner A, et al. Post-traumatic osteoarthritis: the role of accelerated chondrocyte senesoence. Biorheology.2004;41(3-4):479-491.

[43] Brunk UT, Terman A. Lipofuscin: mechanisms of age-related accumulation and influence on cell function. Free Radic Biol Med.2002;33(5):611-619.

[44] Cuervo AM, Bergamini E, Brunk UT, et al. Autophagy and aging: the importance of maintaining“clean”cells. Autophagy. 2005;1(3):131-140.

[45] 张志宇,许珂,王静,等. p53在骨关节炎软骨组织中的表达及与关节软骨细胞自噬的关系研究[J].中国医学创新,2014,11(15): 1-4.

[46] Levine B, Kroemer G.Autophagy in the pathogenesis of disease. Cell. 2008;132(1):27-42.

[47] Carames B, Taniguchi N, Otsuki S, et al. Autophagy is a protective mechanism in normal cartilage, and its aging-related loss is linked with cell death and osteoarthritis. Arthritis Rheum.2010;62(3):791-801.

[48] Kabeya Y, Mizushima N, Ueno T, et al. LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing. EMBO J. 2000;19(21): 5720-5728.

[49] Hiroshi Sasaki , Koji Takayama , Takehiko Matsushita , et al. Autophagy Modulates Osteoarthritis-Related Gene Expression in Human Chondrocytes. Arthritis&Rheumatism. 2012;64(6):1920-1928.

[50] Cuervo AM, Dice JF. Age-related decline in chaperone-mediated autophagy. J Biol Chem.2000; 275(40): 31505-31513.

[51] 章平治,徐宏光,宋俊兴.自噬与软骨及其损伤相关性[J]. 国际骨科学杂志, 2012,32(2):96-98.