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Titolo:
More knee joint osteoarthritis (OA) in mice after inactivation of one allele of type II procollagen gene but less OA after lifelong voluntary wheel running exercise
Autore:
Lapvetelainen, T; Hyttinen, M; Lindblom, J; Langsjo, TK; Sironen, R; Li, SW; Arita, M; Prockop, DJ; Puustjarvi, K; Helminen, HJ;
Indirizzi:
Univ Kuopio, Dept Anat, FIN-70211 Kuopio, Finland Univ Kuopio Kuopio Finland FIN-70211 ept Anat, FIN-70211 Kuopio, Finland Univ Kuopio, Dept Appl Zool & Vet Med, FIN-70211 Kuopio, Finland Univ Kuopio Kuopio Finland FIN-70211 Vet Med, FIN-70211 Kuopio, Finland MCP Hahnemann Univ, Sch Med, Ctr Gene Therapy, Philadelphia, PA USA MCP Hahnemann Univ Philadelphia PA USA ene Therapy, Philadelphia, PA USA Univ Kuopio, Dept Phys Med & Rehabil, FIN-70211 Kuopio, Finland Univ Kuopio Kuopio Finland FIN-70211 Rehabil, FIN-70211 Kuopio, Finland
Titolo Testata:
OSTEOARTHRITIS AND CARTILAGE
fascicolo: 2, volume: 9, anno: 2001,
pagine: 152 - 160
SICI:
1063-4584(200102)9:2<152:MKJO(I>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSGENIC MICE; PHYSICAL-ACTIVITY; COL11A2 GENE; ARTICULAR-CARTILAGE; COLLAGEN MUTATION; SOCCER PLAYERS; KNOCK-OUT; IX; DISEASES; RISK;
Keywords:
inbred C57BL mice; knockout mice; articular cartilage; cartilage diseases; osteoarthritis; aging; running; exercise;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Helminen, HJ Univ Kuopio, Dept Anat, POB 6, FIN-70211 Kuopio, Finland UnivKuopio POB 6 Kuopio Finland FIN-70211 1 Kuopio, Finland
Citazione:
T. Lapvetelainen et al., "More knee joint osteoarthritis (OA) in mice after inactivation of one allele of type II procollagen gene but less OA after lifelong voluntary wheel running exercise", OSTEO CART, 9(2), 2001, pp. 152-160

Abstract

Objective: To investigate the incidence and severity of osteoarthritis (OA) and the effects of voluntary wheel running in normal mice and mice carrying either a targeted inactivation of one allele, heterozygous 'knockout: ofCol2a1 gene or both alleles, homozygous 'knockout', of Col11a2 gene. Methods: Mice lived until 15 months of age in individual cages. Running activity was recorded around the clock. OA changes were evaluated from serialknee joint sections by light microscopy. Results: Heterozygous inactivation of Col2a1 gene coding for type II procollagen made the cartilage more susceptible to OA. At 15 months of age, OA prevalence was 60-90% in knockouts and 20-45% in normal controls (P<0.01-0.001). Unexpectedly, a reduction of OA due to wheel running was observed in both knockout strains (P<0.05-0.01). This effect was most evident in the femoral condyles. Incidence of OA in runners was approximately 50-85% of that in sedentary littermates. OA prevalence was higher in normal control and runner mice with high body weight. Running did not affect OA development in normal mice. Conclusion: Heterozygous knockout of Col2a1 gene increased the OA prevalence in mice. Lifelong voluntary wheel running had a protective effect against OA in both knockout mice lines. The reason for this remains unknown. Reduction of OA may result from the reorganization and strengthening of the articular cartilage collagen network and/or adjacent muscles due to running, or lower body weight. Increased compliance of the articular cartilage and bones of the knockout mice may also contribute to the reduction of OA in exercised animals. (C) 2001 OsteoArthritis Research Society International.

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Documento generato il 05/04/20 alle ore 18:57:40