Bax deficiency in mice increases cartilage production during fracture repair through a mechanism involving increased chondrocyte proliferation without changes in apoptosis

Bone

Volumn 43, Issue 5, 2008, Pages 880-888

  Rundle, Charles H ^a,b   Wang, Xiaoguang ^a   Sheng, Matilda H C ^a,b   Wergedal, Jon E ^a,b   Lau, K H William ^a,b   Mohan, Subburaman ^a,b  

^a Jerry L Pettis Memorial VA Medical Center   (United States)

^b LOMA LINDA UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Apoptosis; Bax; Cartilage; Chondrocyte proliferation; Fracture

Indexed keywords

COMPLEMENTARY DNA; PROTEIN BAX; RNA;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; BONE MINERAL; C57BL 6 MOUSE; CALLUS; CARTILAGE; CARTILAGE CELL; CELL PROLIFERATION; COMPUTER ASSISTED TOMOGRAPHY; CONTROLLED STUDY; FEMUR FRACTURE; FRACTURE; FRACTURE HEALING; GENE EXPRESSION; HISTOLOGY; IMMUNOHISTOCHEMISTRY; KNOCKOUT MOUSE; MALE; MOUSE; NONHUMAN; NUCLEOTIDE SEQUENCE; PROTEIN DEFICIENCY; REAL TIME POLYMERASE CHAIN REACTION; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; STRAIN DIFFERENCE; X RAY ANALYSIS;

ANIMALS; APOPTOSIS; BCL-2-ASSOCIATED X PROTEIN; BONY CALLUS; CARTILAGE; CELL PROLIFERATION; CHONDROCYTES; FEMALE; FEMUR; FRACTURE HEALING; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT;

EID: 53349162248     PISSN: 87563282     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.bone.2008.07.239     Document Type: Article

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