ScRNAseq data in limb (TA) and craniofacial (Masseter) in conditions of uninjrued and 2 and 4 days after BaCl2 injury
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE298062 | GEO | 2026/05/23
REPOSITORIES: GEO
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Project description:Distinctions between craniofacial and axial muscles exist from the onset of development and throughout adulthood. The masticatory muscles are a specialized group of craniofacial muscles that retain embryonic fiber properties throughout adulthood, suggesting that the developmental origin of these muscles may govern a pattern of expression that differs from limb muscles. To determine the extent of these differences, expression profiling of total RNA isolated from the masseter and tibialis anterior (TA) muscles of adult female mice was performed, which identified transcriptional changes in unanticipated functional classes of genes in addition to those associated with fiber type. In particular, the masseters displayed a reduction of transcripts associated with load-sensing and anabolic processes, and heightened expression of genes associated with stress. Consistent with these observations were a significantly smaller fiber cross-sectional area in masseters, significantly elevated load-sensing signaling (phosphorylated Focal Adhesion Kinase (FAK)), and increased apoptotic index in masseters compared to TA muscles. Based on these results, we hypothesize that masticatory muscles may sense and respond to load differently than limb muscles, where the drive for anabolic processes is reduced, and cell stress mediated processes are enhanced. These results establish a novel classification for the masseter muscle in the spectrum of skeletal muscle allotypes, and may provide insight into the molecular basis for specific muscle-related pathologies associated with masticatory muscles. Keywords: skeletal muscle, developmental origin, craniofacial muscles
2008-05-09 | GSE11114 | GEO
Project description:Distinctions between craniofacial and axial muscles exist from the onset of development and throughout adulthood. The masticatory muscles are a specialized group of craniofacial muscles that retain embryonic fiber properties throughout adulthood, suggesting that the developmental origin of these muscles may govern a pattern of expression that differs from limb muscles. To determine the extent of these differences, expression profiling of total RNA isolated from the masseter and tibialis anterior (TA) muscles of adult female mice was performed, which identified transcriptional changes in unanticipated functional classes of genes in addition to those associated with fiber type. In particular, the masseters displayed a reduction of transcripts associated with load-sensing and anabolic processes, and heightened expression of genes associated with stress. Consistent with these observations were a significantly smaller fiber cross-sectional area in masseters, significantly elevated load-sensing signaling (phosphorylated Focal Adhesion Kinase (FAK)), and increased apoptotic index in masseters compared to TA muscles. Based on these results, we hypothesize that masticatory muscles may sense and respond to load differently than limb muscles, where the drive for anabolic processes is reduced, and cell stress mediated processes are enhanced. These results establish a novel classification for the masseter muscle in the spectrum of skeletal muscle allotypes, and may provide insight into the molecular basis for specific muscle-related pathologies associated with masticatory muscles. Experiment Overall Design: Tissues were isolated from normal adult female mice (C57Bl/6), age 6 months. Paired comparisons between masseter and tibialis anterior muscles were performed on all present genes using "Significance Analysis of Microarrays" (SAM) to identify differentially expressed genes between masticatory and axial muscles.
2008-06-20 | E-GEOD-11114 | biostudies-arrayexpress
Project description:Background: The aim of this study is to improve our understanding of the mechanisms underlying the sparing of masticatory muscles relative to limb muscles in ICU patients with acute quadriplegic myopathy (AQM) by using a unique porcine ICU model, i.e., 5-day longitudinal experiments where animals are sedated, mechanically ventilated and exposed to factors triggering AQM, such as muscle unloading, endotoxin-induced sepsis, and systemic exposure to CS and NMBA. Results: An altered expression was notably observed in heat-shock proteins genes, sarcomeric proteins and myostatin genes were noticed. Hence, modifications in heat-shock proteins, sarcomeric proteins and myostatin genes are in sharp contrast to alterations in the limb muscles and it is postulated that elevated heat-shock proteins and decreased sarcomeric protein and myostatin genes play a protective role in the masticatory muscle relative to limb muscle in ICU patients with AQM. Conclusions: This intervention had no significant effect on masseter muscle fiber size or force-generation capacity. This is in sharp contrast to the dramatic decrease observed in specific force in limb muscle fibers from the same animals. However, significant differences were observed between the craniofacial and the limb muscle with a masseter muscle specific regulation of i) transcriptional and growth factors like RUNX1, FOXO1A, TBX1, PGC1-β and myostatin, ii) several heat shock protein genes like HSP 90, HSP 105/110 and αB-crystallin, iii) a matrix metalloproteinase inhibitor (TIMP2) and iv) oxidative stress responsive elements such as SRXN1 and SOD2. These muscle-type specific differences, the alterations in heat shock protein, sarcomeric protein and myostatin genes are forwarded as important factors underlying the sparing of masticatory muscles compared with limb muscles in critically ill ICU patients with Acute Quadriplegic Myopathy. Keywords: Treatment, immobilization, muscle function.
2010-09-21 | GSE24239 | GEO
Project description:Masseter and Tibialis anterior muscles from adult female control mice to determine expression differences between muscle groups
2007-10-11 | E-MEXP-1288 | biostudies-arrayexpress
Project description:Craniofacial dysmorphisms are among the most common birth defects. Proteasome mutations frequently result in craniofacial dysmorphisms including lower jaw malformations; however, the underlying mechanisms are unknown. Here we use a zebrafish proteasome subunit beta 1 (psmb1) mutant to define the cellular mechanisms underlying proteasome mutation-induced craniofacial dysmorphisms. psmb1 mutants exhibit a flattened ceratohyal and smaller Meckel’s and palatoquadrate cartilages. Ceratohyal flattening is a result of failed chondrocyte convergent extension, accompanied by reduced numbers of chondrocytes in the lower jaw due to defects in chondrocyte differentiation. Morphogenesis of craniofacial muscles and tendons is similarly perturbed. psmb1 mutants lack the hyohyal muscles and craniofacial tendons are shortened and disorganized. We additionally identify a critical period for proteasome function in craniofacial development, specifically during chondrocyte and muscle differentiation. psmb1 overexpression in sox10+ cells of mutant embryos rescued both cartilage and tendon phenotypes but induced only a partial rescue of the muscle phenotype, indicating that psmb1 is required in both tissue-autonomous and non-autonomous fashions during craniofacial development. Overall, our work demonstrates that psmb1 is required for craniofacial cartilage, tendon, and muscle differentiation and morphogenesis.
2024-07-12 | GSE243072 | GEO
Project description:Craniofacial development is a complex developmental process that involves formation of the skeleton, muscle, and tendons. Defects in craniofacial development lead to common hereditary disorders such as orofacial clefting or holoprosencephaly. Among genetic factors regulating craniofacial development, dysregulated hedgehog signaling is commonly associated with craniofacial skeletal defects. Here, we characterize craniofacial phenotypes associated with two hedgehog signaling co-receptors, cdon and boc, in zebrafish. Pedigree analyses have previously linked both CDON and BOC to microform holoprosencephaly skeletal defects, and mutations of Cdon and Boc in mouse result in midline craniofacial phenotypes. However, a detailed analysis of craniofacial phenotypes associated with cdon and boc in zebrafish has not been completed. Our studies show that cdon and boc operate synergistically to promote craniofacial cartilage, tendon, and muscle development in zebrafish. Using RNA-seq and HCR in situ hybridization we show that mutations of cdon and boc result in misregulation of chondrogenesis gene expression including Indian hedgehog ligand, tendon associated thrombospondin genes, and FOX transcription factors. Our data are consistent with a model whereby cdon and boc together modify hedgehog activity in the head, and establishes a foundation for using zebrafish to further understand the role of cdon and boc in craniofacial hereditary disorders such as holoprosencephaly.
2026-01-10 | GSE313297 | GEO
Project description:Non-syndromic facial asymmetry is commonly found in dentofacial deformity populations with skeletal malocclusions. Asymmetry of this type may result from imbalanced growth and function of both the jaw and associated muscles. Among the multiple genes that interact to affect the craniofacial musculoskeletal complex during pre and postnatal growth and development, NODAL signaling pathwy (NSP) genes are active in adult skeletal muscle and may be key factors in development, growth and maintenance of facial asymmetry. It is of interest to determine whether expression of NODAL pathway genes might differ in masseter muscles between individuals with malocclusion that have facial asymmetry and normal symmetry. Human Transcriptome 2.0 GeneChips (HTA2.0) were used to examine global gene expression in masster muscles between malocclusion subjects with posterior facial asymmetry and with normal facial symmetry. Eleven patients undergoing orthoganthic surgery were selected for comparison of masseter muscle gene expression on microarrays. Two subjects had posterior facial asymmetry (one with class II open bite and one with class III open bite malocclusion) and nine subjects had normal facial symmetry (three with class II open bite, two with class III open bite and four with class II deep bite malocclusion). RNA representative of total gene expression in masseter muscles of the malocclusion subjects with and without posterior facial asymmetry was prepared for labeling and hybridization on HTA2.0 chips. The two subjects with facial asymmetry clustered separately from eight other malocclusion subjects by a principle component analysis (PCA), even though one had a class II and the other a class III malocclusion. Sample 4L_Open_II is from a subject who has sleep apnea. Data from 4L_Open_II clustered independent of the asymmetry group and the eight other subjects of the symmetry group by PCA and was not included in analysis of differential expression with facial symmetry. Masseter muscles are paired jaw muscles (i.e. right and left masseter). In some cases, there was not sufficient quantity/quality of RNA from one side, thus the other side was used. Please note that the following information is provided in the 'source name' field of each sample record; subject ID number; either left or right masseter; J CRANIOFAC SURG_ID# corresponding to the data presented in the manuscript
2014-05-20 | E-GEOD-57775 | biostudies-arrayexpress
Project description:Background: Musculoskeletal injuries comprise a growing source of disability worldwide, and the recovery of muscle strength following injury is a critical determinant of patient reported outcomes. Females experience exacerbated muscle atrophy, poorer outcomes, and higher re-injury rates, necessitating a comprehensive interrogation of sex-specific skeletal muscle differences. Our purpose in the current study was to perform an unbiased transcriptomic profiling of muscle samples to identify putative sex-specific molecular targets to enhance recovery in patients who underwent anterior cruciate ligament reconstruction (ACLR). Methods: We performed cellular phenotyping, bulk and single nucleus RNA-sequencing on muscle biopsy samples obtained from thirty-six participants (18M, 18F). Muscle samples were obtained from the ACLR and contralateral limb with follow-up tissue collection of the injured limb also occurring at seven days and four months post-ACLR. Transcriptomic analyses illuminated putative molecular mechanisms through which sex influences muscle recovery following acute injury. Results: Females exhibited greater muscle atrophy relative to males at 4 months post-ACLR compared to the uninjured limb. Bulk and single nucleus paired-limb transcriptomic analyses revealed the emergence of sex-specific myonuclear signaling cascades that demonstrate impaired reactive oxygen species scavenging in females. Females exhibited attenuated SOD2 expression that was associated with increased indices of oxidative stress and protein damage. Within females, angiogenesis signaling was also impaired and associated with capillary rarefaction after reconstructive surgery. Conclusions: These findings reveal inherent sex-based differences in muscle pathology that likely necessitate unique clinical treatments following musculoskeletal injury.
2026-05-15 | GSE324033 | GEO
Project description:Specific genes for treated masseter muscle are identified
2024-01-02 | GSE190183 | GEO
Project description:Aberrations in tissue-specific enhancers underlie many developmental defects. Disrupting a distal noncoding region of the human SOX9 gene causes the Pierre Robin sequence (PRS) characterized by the undersized lower jaw. Such a craniofacial-specific defect has been previously linked to enhancers transiently active in cranial neural crest cells (CNCCs). We demonstrate the PRS region also strongly regulates Sox9 in CNCC-derived Meckel's cartilage (MC), but not in limb cartilages. The MC-specific regulatory function of the PRS region cannot be attributed to the CNCC enhancers that have been inactivated in cartilages, but correlates with its MC-specific interactions with the Sox9 gene. By integrating the enhancer signatures and chromatin topology, we uncovered ~20,000 enhancers that function differentially between MC and limb cartilages and demonstrated their association with human diseases. Our findings highlight the importance of lineage-dependent chromatin topology in instructing enhancer usage and provide critical insights for interpreting the genetic basis of craniofacial pathologies.
2023-01-04 | GSE185255 | GEO