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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004332naa a2200421 4500
001oai:gup.ub.gu.se/228867
003SwePub
008240528s2015 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:132735838
0247 a https://gup.ub.gu.se/publication/2288672 URI
0247 a https://doi.org/10.1002/jbmr.25752 DOI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1327358382 URI
040 a (SwePub)gud (SwePub)ki
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Vuppalapati, Karuna Ku Karolinska Institutet4 aut
2451 0a Targeted Deletion of Autophagy Genes Atg5 or Atg7 in the Chondrocytes Promotes Caspase-Dependent Cell Death and Leads to Mild Growth Retardation.
264 c 2015-08-07
264 1b Wiley,c 2015
520 a Longitudinal bone growth takes place in epiphyseal growth plates located in the ends of long bones. The growth plate consists of chondrocytes traversing from the undifferentiated (resting zone) to the terminally differentiated (hypertrophic zone) stage. Autophagy is an intracellular catabolic process of lysosome-dependent recycling of intracellular organelles and protein complexes. Autophagy is activated during nutritionally depleted or hypoxic conditions in order to facilitate cell survival. Chondrocytes in the middle of the growth plate are hypoxic and nutritionally depleted owing to the avascular nature of the growth plate. Accordingly, autophagy may facilitate their survival. To explore the role of autophagy in chondrocyte survival and constitutional bone growth, we generated mice with cartilage-specific ablation of either Atg5 (Atg5cKO) or Atg7 (Atg7cKO) by crossing Atg5 or Atg7 floxed mice with cartilage-specific collagen type 2 promoter-driven Cre. Both Atg5cKO and Atg7cKO mice showed growth retardation associated with enhanced chondrocyte cell death and decreased cell proliferation. Similarly, inhibition of autophagy by Bafilomycin A1 (Baf) or 3-methyladenine (3MA) promoted cell death in cultured slices of human growth plate tissue. To delineate the underlying mechanisms we employed ex vivo cultures of mouse metatarsal bones and RCJ3.IC5.18 rat chondrogenic cell line. Baf or 3MA impaired metatarsal bone growth associated with processing of caspase-3 and massive cell death. Similarly, treatment of RCJ3.IC5.18 chondrogenic cells by Baf also showed massive cell death and caspase-3 cleavage. This was associated with activation of caspase-9 and cytochrome C release. Altogether, our data suggest that autophagy is important for chondrocyte survival, and inhibition of this process leads to stunted growth and caspase-dependent death of chondrocytes. © 2015 American Society for Bone and Mineral Research.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Endokrinologi och diabetes0 (SwePub)302052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Endocrinology and Diabetes0 (SwePub)302052 hsv//eng
7001 a Bouderlique, Thibaultu Karolinska Institutet4 aut
7001 a Newton, Phillip Tu Karolinska Institutet4 aut
7001 a Kaminskyy, Vitaliy Ou Karolinska Institutet4 aut
7001 a Wehtje, Henrik4 aut
7001 a Ohlsson, Claes,d 1965u Gothenburg University,Göteborgs universitet,Centre for Bone and Arthritis Research,Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition,Institute of Medicine, Department of Internal Medicine and Clinical Nutrition4 aut0 (Swepub:gu)xohlcl
7001 a Zhivotovsky, Borisu Karolinska Institutet4 aut
7001 a Chagin, Andrei Su Karolinska Institutet4 aut
7102 a Karolinska Institutetb Centre for Bone and Arthritis Research4 org
7730 t Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Researchd : Wileyg 30:12, s. 2249-2261q 30:12<2249-2261x 1523-4681
7730 t Journal of Bone and Mineral Researchd : Wileyg 30:12, s. 2249-2261q 30:12<2249-2261x 0884-0431
8564 u https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/jbmr.2575
8564 8u https://gup.ub.gu.se/publication/228867
8564 8u https://doi.org/10.1002/jbmr.2575
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:132735838

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