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Transduction of Anti–Cell Death Protein FNK Suppresses Graft Degeneration After Autologous Cylindrical Osteochondral Transplantation

Noriki Nakachi, Sadamitsu Asoh, Nobuyoshi Watanabe, Takashi Mori, Takashi Matsushita, Shinro Takai and Shigeo Ohta

Department of Biochemistry and Cell Biology, Institute of Development and Aging Sciences, Graduate School of Medicine, Nippon Medical School, Kanagawa, Japan (NN,SA,SO); Department of Orthopaedic Surgery, Teikyo University School of Medicine, Tokyo, Japan (NN,TMatsushita,ST); Institute of Medical Science, Department of Pathology, Saitama Medical Center/Saitama Medical University, Saitama, Japan (TMori); and Department of Orthopaedic Surgery, Kyoto Kujo Hospital, Kyoto, Japan (NW)

Correspondence to: Prof. Shigeo Ohta, PhD, Department of Biochemistry and Cell Biology, Institute of Development and Aging Sciences, Graduate School of Medicine, Nippon Medical School, 1-396 Kosugi-cho, Nakahara-ku, Kawasaki-city, Kanagawa-pref. 211-8533, Japan. E-mail: ohta{at}nms.ac.jp. Co-corresponding author: Shinro Takai, MD, PhD. E-mail: takai{at}kta.att.ne.jp

This study shows that artificial super antiapoptotic FNK protein fused with a protein transduction domain (PTD-FNK) maintains the quality of osteochondral transplant by preventing chondrocyte death. Cylindrical osteochondral grafts were obtained from enhanced green fluorescent protein (EGFP)-expressing transgenic rats, in which living chondrocytes express green fluorescence, and submerged into medium containing PTD-FNK, followed by transplantation into cartilage defects of wild-type rats by impact insertion simulating autologous transplantation. The tissues were histologically evaluated by hematoxylin–eosin and Safranin-O staining. At 1 week, chondrocyte alignment was normal in the PTD-FNK treatment group, whereas all grafts without PTD-FNK treatment showed mixed cluster cell distribution. At 4 weeks, all grafts with PTD-FNK treatment showed almost normal matrix, whereas two grafts without PTD-FNK treatment showed fibrocartilage. Notably, all grafts with PTD-FNK retained high intensity of Safranin-O staining, but all grafts without PTD-FNK largely lost Safranin-O staining. PTD-FNK significantly suppressed a decrease in the survival rate and the density of EGFP-positive cells at 1 and 2 weeks, and this tendency continued at 4 weeks. The results of terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP)-nick end-labeling staining showed that PTD-FNK inhibited cell death, indicating that PTD-FNK protects chondrocyte death and suppresses graft degeneration. (J Histochem Cytochem 57:197–206, 2009)

Key Words: apoptosis • Bcl-x_L • enhanced green fluorescent protein transgenic rat • mosaicplasty • osteochondral transplantation • protein transduction • Safranin O • TUNEL • articular cartilage

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