Display options
Cite
Yumoto K, Nifuji A, Rittling SR, et al. Osteopontin Deficiency Suppresses Tumor Necrosis Factor-α-Induced Apoptosis in Chondrocytes. Cartilage. 2012;3(1):79-85doi: 10.1177/1947603511421502.
Yumoto, K., Nifuji, A., Rittling, S. R., Tsuchiya, Y., Kon, S., Uede, T., Denhardt, D. T., Hemmi, H., Notomi, T., Hayata, T., Ezura, Y., Nakamoto, T., & Noda, M. (2012). Osteopontin Deficiency Suppresses Tumor Necrosis Factor-α-Induced Apoptosis in Chondrocytes. Cartilage, 3(1), 79-85. https://doi.org/10.1177/1947603511421502
Yumoto, K, et al. "Osteopontin Deficiency Suppresses Tumor Necrosis Factor-α-Induced Apoptosis in Chondrocytes." Cartilage vol. 3,1 (2012): 79-85. doi: https://doi.org/10.1177/1947603511421502
Yumoto K, Nifuji A, Rittling SR, Tsuchiya Y, Kon S, Uede T, Denhardt DT, Hemmi H, Notomi T, Hayata T, Ezura Y, Nakamoto T, Noda M. Osteopontin Deficiency Suppresses Tumor Necrosis Factor-α-Induced Apoptosis in Chondrocytes. Cartilage. 2012 Jan;3(1):79-85. doi: 10.1177/1947603511421502. PMID: 26069621; PMCID: PMC4297182.
Copy Download .nbib Format: NLM
Share it on

Cartilage. 2012 Jan;3(1):79-85. doi: 10.1177/1947603511421502.

Osteopontin Deficiency Suppresses Tumor Necrosis Factor-α-Induced Apoptosis in Chondrocytes.

Cartilage

K Yumoto, A Nifuji, S R Rittling, Y Tsuchiya, S Kon, T Uede, D T Denhardt, H Hemmi, T Notomi, T Hayata, Y Ezura, T Nakamoto, M Noda

Affiliations

  1. Department of Molecular Pharmacology, Tokyo Medical and Dental University, Tokyo, Japan.
  2. Rutgers University, Piscataway, NJ, USA.
  3. Immuno Biological Laboratory (IBL), Maebashi Gumma, Japan.
  4. Hokkaido University, Sapporo, Japan.
  5. Department of Molecular Pharmacology, Tokyo Medical and Dental University, Tokyo, Japan ; Medical Top Track (MTT) Program, Tokyo Medical and Dental University, Tokyo, Japan.
  6. Department of Molecular Pharmacology, Tokyo Medical and Dental University, Tokyo, Japan ; Global Center of Excellence Program, Tokyo Medical and Dental University, Tokyo, Japan ; Core to Core Program, Tokyo Medical and Dental University, Tokyo, Japan ; Hard Tissue Genome Research Center, Tokyo Medical and Dental University, Tokyo, Japan.
  7. Department of Molecular Pharmacology, Tokyo Medical and Dental University, Tokyo, Japan ; Medical Top Track (MTT) Program, Tokyo Medical and Dental University, Tokyo, Japan ; Global Center of Excellence Program, Tokyo Medical and Dental University, Tokyo, Japan ; Core to Core Program, Tokyo Medical and Dental University, Tokyo, Japan ; Hard Tissue Genome Research Center, Tokyo Medical and Dental University, Tokyo, Japan.

PMID: 26069621 PMCID: PMC4297182 DOI: 10.1177/1947603511421502

Abstract

OBJECTIVE: Apoptosis of chondrocytes in articular cartilage has been observed in rheumatoid arthritis patients. However, molecules involved in such chondrocyte apoptosis in arthritic joints have not been fully understood. We previously observed that apoptosis of chondrocytes is enhanced in a murine arthritis model induced by injection with anti-type II collagen antibodies and lipopolysaccharide (mAbs/LPS), and osteopontin (OPN) deficiency suppresses chondrocyte apoptosis in this arthritis model in vivo. To understand how OPN deficiency renders resistance against chondrocyte apoptosis, we examined the cellular basis for this protection.

DESIGN: Chondrocytes were prepared from wild-type and OPN-deficient mouse ribs, and tumor necrosis factor (TNF)-α-induced cell death was examined based on lactate dehydrogenase (LDH) release assay and TUNEL assay.

RESULTS: TNF-α treatment induced LDH release in wild-type chondrocytes, while OPN deficiency suppressed such LDH release in the cultures of these cells. TNF-α-induced increase in the number of TUNEL-positive cells was observed in wild-type chondrocytes, while OPN deficiency in chondrocytes suppressed the TNF-α induction of TUNEL-positive cells. OPN deficiency suppressed TNF-α-induced increase in caspase-3 activity in chondrocytes in culture. Furthermore, OPN overexpression in chondrocytes enhanced TNF-α-induced apoptosis.

CONCLUSION: These results indicated that the presence of OPN in chondrocytes is involved in the susceptibility of these cells to TNF-α-induced apoptosis.

Keywords: animal models < general; biomechanics < general; chondrocytes < cells; chondrogenesis < cells

References

  1. J Cell Physiol. 2004 Jan;198(1):155-67 - PubMed
  2. J Clin Invest. 2003 Jul;112(2):181-8 - PubMed
  3. J Bone Miner Res. 1998 Jul;13(7):1101-11 - PubMed
  4. J Cell Physiol. 2003 Dec;197(3):379-87 - PubMed
  5. J Clin Invest. 2003 Jul;112(2):147-9 - PubMed
  6. Osteoarthritis Cartilage. 2003 Sep;11(9):681-7 - PubMed
  7. J Biol Chem. 2004 Apr 23;279(17 ):16918-26 - PubMed
  8. Z Rheumatol. 2001 Oct;60(5):309-18 - PubMed
  9. Science. 2000 Feb 4;287(5454):860-4 - PubMed
  10. Infect Immun. 2002 Mar;70(3):1372-81 - PubMed
  11. J Orthop Sci. 2000;5(2):150-6 - PubMed
  12. Endocrinology. 2001 Mar;142(3):1325-32 - PubMed
  13. Arthritis Rheum. 1999 Jul;42(7):1528-37 - PubMed
  14. Proc Natl Acad Sci U S A. 2002 Apr 2;99(7):4556-61 - PubMed
  15. J Cell Biochem. 2003 Apr 15;88(6):1077-83 - PubMed
  16. Science. 2001 Nov 23;294(5547):1731-5 - PubMed

Publication Types