Flexor pollicis brevis
Ontology highlight
ABSTRACT:
SUBMITTER: 
David Nickerson
PROVIDER: 95c | Physiome Model Repository |
REPOSITORIES: PMR
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Project description: Not available
| S-EPMC5382552 | biostudies-literature
Project description:The various functions of skeletal muscle (movement, respiration, thermogenesis, etc.) require the presence of oxygen (O2). Inadequate O2 bioavailability (i.e., hypoxia) is detrimental to muscle function, and in chronic cases can result in muscle wasting. Current therapeutic interventions have proven largely ineffective to rescue skeletal muscle from hypoxic damage. However, our lab has identified a mammalian skeletal muscle that maintains proper physiological function in an environment depleted of O2. Using mouse models of in vivo hindlimb ischemia and ex vivo anoxia exposure, we observed the preservation of force production in the flexor digitorum brevis (FDB) while in contrast the extensor digitorum longus (EDL) and soleus muscles suffered loss of force output. Unlike other muscles, we found that the FDB phenotype is not dependent on mitochondria, which partially explains the hypoxia resistance. Muscle proteomes were interrogated using a discovery-based approach, which identified significantly greater expression of the transmembrane glucose transporter GLUT1 in the FDB as compared to the EDL and soleus. Through loss-and-gain-of-function approaches, we determined that GLUT1 is necessary for the FDB to survive hypoxia, but overexpression of GLUT1 was insufficient to rescue other skeletal muscles from hypoxic damage. Collectively, the data demonstrate that the FDB is uniquely resistant to hypoxic insults. Defining the mechanisms that explain the phenotype may provide insight towards developing approaches for preventing hypoxia-induced tissue damage.
2024-02-03 | PXD039811 | JPOST Repository
Project description:Abductor pollicis brevis muscle
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Project description:Extensor pollicis brevis muscle
| 955 | Physiome Model Repository
Project description:Background: Niemann-Pick disease type A (NPDA), a disease caused by mutations in acid sphingomyelinase (ASM), involves severe neurodegeneration and early death. Intracellular lipid accumulation and plasma membrane alterations are implicated in the pathology. ASM is also linked to the mechanism of plasma membrane repair, so we investigated the impact of ASM deficiency in skeletal muscle, a tissue that undergoes frequent cycles of injury and repair in vivo. Methods: Utilizing the NPDA/B mouse model ASM−/− and wild type (WT) littermates, we performed excitation- contraction coupling/Ca2+ mobilization and sarcolemma injury/repair assays with isolated flexor digitorum brevis fibers, proteomic analyses with quadriceps femoris, flexor digitorum brevis, and tibialis posterior muscle and in vivo tests of the contractile force (maximal isometric torque) of the quadriceps femoris muscle before and after eccentric contraction-induced muscle injury. Results: ASM−/− flexor digitorum brevis fibers showed impaired excitation-contraction coupling compared to WT, a defect expressed as reduced tetanic [Ca2+]i in response to electrical stimulation and early failure in sustaining [Ca2+]i during repeated tetanic contractions. When injured mechanically by needle passage, ASM−/− flexor digitorum brevis fibers showed susceptibility to injury similar to WT, but a reduced ability to reseal the sarcolemma. Proteomic analyses revealed changes in a small group of skeletal muscle proteins as a consequence of ASM deficiency, with downregulation of calsequestrin occurring in the three different muscles analyzed. In vivo, the loss in maximal isometric torque of WT quadriceps femoris was similar immediately after and 2 min after injury. The loss in ASM−/− mice immediately after injury was similar to WT, but was markedly larger at 2 min after injury. Conclusions: Skeletal muscle fibers from ASM−/− mice have an impairment in intracellular Ca2+ handling that results in reduced Ca2+ mobilization and a more rapid decline in peak Ca2+ transients during repeated contraction-relaxation cycles. Isolated fibers show reduced ability to repair damage to the sarcolemma, and this is associated with an exaggerated deficit in force during recovery from an in vivo eccentric contraction- induced muscle injury. Our findings uncover the possibility that skeletal muscle functional defects may play a role in the pathology of NPDA/B disease.
2023-06-28 | PXD019356 | Pride
Project description: Not available
| S-EPMC5679560 | biostudies-literature
Project description:The presence of anti-microbial phenolic compounds, such as the model compound ferulic acid, in biomass hydrolysates poses significant challenges to the widespread use of biomass in conjunction with whole cell biocatalysis or fermentation. Currently, these inhibitory compounds must be removed through additional downstream processing to create feedstock suitable for most industrially important microbial strains. This study explores the high ferulic acid tolerance in Lactobacillus brevis (L. brevis), a lactic acid bacteria often found in fermentation processes, by global transcriptional response analysis. The transcriptional profile of L. brevis under ferulic acid stress reveals that the presence of ferulic acid primarily triggers the expression of membrane proteins to counteract ferulic acid induced changes in membrane fluidity and ion leakage, in the midst of a generalized stress response. Several promising routes for understanding phenolic acid tolerance have been identified based upon these findings. These insights may be used to guide further engineering of model industrial organisms to better tolerate phenolic compounds in processed biomass.
2011-12-31 | GSE22826 | GEO
Project description:Little is understood about the roles of tendon cells during flexor tendon healing. To better understand tendon cell functions, the Scx-Cre mouse was crossed to the DTR mouse model to facilitate scleraxis lineage cell depletion prior to acute flexor tendon injury and repair. WT (cre-) and experimental (cre+) mice underwent complete transection and repair of the flexor digitorum longus tendon. Repaired tendons were harvested at 14 and 28 days post-repair for bulk RNA-Seq analysis to examine possible mechanisms driving differential healing due to Scx lineage cell depletion.
2021-02-08 | GSE156157 | GEO
Project description:To test the hypothesis that different muscles may express variable amounts of different isoforms of muscle genes, we applied a custom-designed exon microarray containing probes for 57 muscle-specific genes to assay the transcriptional profiles in sets of human adult, lower limb skeletal muscles. Muscle biopsies from 15 individuals were selected for analysis dissected from 21 anatomically different muscles collected from eight men and seven women, ranging from 61 to 91 years The muscle tissue samples collected included samples from 11 different thigh muscles––vastus medialis, vastus lateralis, vastus intermedialis, sartorius, gracilis, semimembranosus, semitendinosus, biceps femoris, adductor magnus, adductor longus, and rectus femoris––and 10 lower leg muscles––flexor digitorum longus, extensor digitorum longus, tibialis posterior, tibialis anterior, peroneus longus/brevis, extensor hallucis longus, gastrocnemius lateralis, gastrocnemius medialis, flexor hallucis longus, and soleus. Approximately five to seven muscle pieces were collected from each individual muscle sampled. The muscle sample pieces obtained for histological analysis measured roughly 10 mm x 5 mm, and the pieces for RNA isolation 5 mm x 5 mm. The samples were obtained directly from the proximal vital parts of the amputated limbs and processed immediately following their removal to avoid tissue degradation.To test the hypothesis that different muscles may express variable amounts of different isoforms of muscle genes, we applied a custom-designed Agilent exon microarray containing probes for 57 muscle-specific genes to assay the transcriptional profiles in sets of human adult, lower limb skeletal muscles
2015-06-17 | E-GEOD-69938 | biostudies-arrayexpress