Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003090 (arthrodesis)
 8,374 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Skeletal muscle atrophy is a serious concern for patients afflicted by limb restriction due to surgery (e.g., arthrodesis), several articular pathologies (e.g., arthralgia), or simply following cast immobilization. To study the molecular events involved in this immobilization-induced debilitating condition, a convenient mouse model for atrophy is lacking. Here we provide a new immobilization procedure exploiting the normal flexion of the mouse hindlimb using a surgical staple to fix the ventral part of the foot to the distal part of the calf. Histological analysis revealed that our approach induced significant skeletal muscle atrophy by reducing the myofiber size of the tibialis anterior (TA) muscle by 36% compared with the untreated contralateral TA within a few days postimmobilization. Two molecular markers for atrophy, atrogin-1/muscle atrophy F-box (atrogin-1/MAFbx) and muscle ring finger 1 (MuRF-1) mRNAs, were significantly upregulated by 1.9- and 5.9-fold, respectively. Interestingly, our model also revealed the presence of an early inflammatory process during atrophy, characterized by the mRNA upregulation of TNF-alpha, IL-1, and IL-6 (1.9-, 2.4-, and 3.4-fold, respectively) simultaneously with the upregulation of the common leukocyte marker CD45 (6.1-fold). Moreover, muscle rapidly recovered on remobilization, an event associated with significantly increased levels of uncoupling protein-3 and peroxisome proliferator-activated receptor gamma coactivator-1alpha mRNA, key components of prooxidative muscle metabolism. This model offers unexpected new insights into the molecular events involved in immobilization atrophy.
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PMID:A novel hindlimb immobilization procedure for studying skeletal muscle atrophy and recovery in mouse. 1934 35

We previously hypothesized that the development of traumatic temporomandibular joint (TMJ) ankylosis was similar to that of hypertrophic non-union. Besides similarities in etiology, hypertrophic bone stumps, and long-term development, the radiolucent zone, frequently located in the ankylosed bone, is another common feature. In this study, we demonstrated that the radiolucent zone also contained multilineage potential cells (RZs, radiolucent-zone-related cells) as the non-union tissues. RZs were characterized and compared with mandibular bone marrow stem cells (BMSCs) by analysis of MSC-related markers, colony-forming-unit assays, multipotential differentiation assays, alkaline phosphatase (ALP) activity assays, and cell transplantation in vivo. Both cell types were positive for CD105, CD166, and Stro-1 expression, negative for CD34 and CD45 expression, and exhibited osteogenic, adipogenic, and chondrogenic differentiation potentials. However, compared with mandibular BMSCs, RZs showed lower colony-forming-unit abilities and proliferation rates. The mineralization and bone-forming ability of RZs was weaker than that of mandibular BMSCs, with Runx2 and ALP mRNA expression and ALP activity significantly lower in RZs. All these results suggest that RZs possess the properties of MSCs but lower proliferation and osteogenic differentiation capacity similar to that of stromal cells in hypertrophic non-union tissues.
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PMID:Decreased osteogenesis in stromal cells from radiolucent zone of human TMJ ankylosis. 2352 32