scholarly journals Mechanotransduction-The relationship between gravity, cells and tensile loading in extracellular matrix

BIOCELL ◽  
2022 ◽  
Vol 46 (2) ◽  
pp. 297-299
Author(s):  
FREDERICK H. SILVER
Author(s):  
Takuya Ishimoto ◽  
Keita Kawahara ◽  
Aira Matsugaki ◽  
Hiroshi Kamioka ◽  
Takayoshi Nakano

AbstractOsteocytes are believed to play a crucial role in mechanosensation and mechanotransduction which are important for maintenance of mechanical integrity of bone. Recent investigations have revealed that the preferential orientation of bone extracellular matrix (ECM) mainly composed of collagen fibers and apatite crystallites is one of the important determinants of bone mechanical integrity. However, the relationship between osteocytes and ECM orientation remains unclear. In this study, the association between ECM orientation and anisotropy in the osteocyte lacuno-canalicular system, which is thought to be optimized along with the mechanical stimuli, was investigated using male rat femur. The degree of ECM orientation along the femur longitudinal axis was significantly and positively correlated with the anisotropic features of the osteocyte lacunae and canaliculi. At the femur middiaphysis, there are the osteocytes with lacunae that highly aligned along the bone long axis (principal stress direction) and canaliculi that preferentially extended perpendicular to the bone long axis, and the highest degree of apatite c-axis orientation along the bone long axis was shown. Based on these data, we propose a model in which osteocytes can change their lacuno-canalicular architecture depending on the mechanical environment so that they can become more susceptible to mechanical stimuli via fluid flow in the canalicular channel.


2004 ◽  
Vol 204 (5) ◽  
pp. 605-612 ◽  
Author(s):  
Hitoshi Hirata ◽  
Takeshi Nagakura ◽  
Masaya Tsujii ◽  
Akimasa Morita ◽  
Kohzo Fujisawa ◽  
...  

ORL ◽  
2008 ◽  
Vol 70 (6) ◽  
pp. 352-358 ◽  
Author(s):  
Zhao Han ◽  
Guo-Jing Lin ◽  
Fang-Lu Chi ◽  
Shu-Yi Wang ◽  
Jian-Min Huang ◽  
...  

2022 ◽  
Author(s):  
Shani Stern ◽  
Shong Lau ◽  
Andreea Manole ◽  
Idan Rosh ◽  
Menahem Percia ◽  
...  

Several mutations that cause Parkinson's disease (PD) have been identified over the past decade. These account for 15-25% of PD cases; the rest of the cases are considered sporadic. Currently, it is accepted that PD is not a single monolithic disease but rather a constellation of diseases with some common phenotypes. While rodent models exist for some of the PD-causing mutations, research on the sporadic forms of PD is lagging due to a lack of cellular models. In our study, we differentiated PD patient-derived dopaminergic (DA) neurons from induced pluripotent stem cells (iPSCs) of several PD-causing mutations as well as from sporadic PD patients. Strikingly, we observed a common neurophysiological phenotype: Neurons derived from PD patients had a severe reduction in the rate of synaptic currents compared to those derived from healthy controls. While the relationship between mutations in genes such as the SNCA and LRRK2 and a reduction in synaptic transmission has been investigated before, here we show evidence that the pathogenesis of the synapses in neurons is a general phenotype in PD. Analysis of RNA sequencing results displayed changes in gene expression in different synaptic mechanisms as well as other affected pathways such as extracellular matrix-related pathways. Some of these dysregulated pathways are common to all PD patients (monogenic or idiopathic). Our data, therefore, shows pathways and mechanisms that are central and convergent to PD and suggests a strong involvement of the tetra-partite synapse in PD pathology.


2021 ◽  
Vol 11 ◽  
Author(s):  
Heming Ge ◽  
Mengxiang Tian ◽  
Qian Pei ◽  
Fengbo Tan ◽  
Haiping Pei

In recent years, in-depth studies have shown that extracellular matrix stiffness plays an important role in cell growth, proliferation, migration, immunity, malignant transformation, and apoptosis. Most of these processes entail metabolic reprogramming of cells. However, the exact mechanism through which extracellular matrix stiffness leads to metabolic reprogramming remains unclear. Insights regarding the relationship between extracellular matrix stiffness and metabolism could help unravel novel therapeutic targets and guide development of clinical approaches against a myriad of diseases. This review provides an overview of different pathways of extracellular matrix stiffness involved in regulating glucose, lipid and amino acid metabolism.


Author(s):  
Kyle P. Quinn ◽  
Jason F. Luck ◽  
Roger W. Nightingale ◽  
Beth A. Winkelstein

Motor vehicle crashes are the leading cause of injury to the pediatric spine, and the mortality rate of pediatric spinal trauma victims has been approximated at 25–32% [1]. In addition, non-fatal painful traumatic injuries resulting from motor vehicle crashes or sports-related activities contribute to an estimated prevalence of neck pain of 21–41% in children and adolescents [2]. It has been hypothesized that the anatomy of the pediatric neck, combined with a relatively large head mass, presents an increased risk for traumatic inertial loading in that population, particularly during early development. However, the relationship between mechanical metrics related to pain and age remains undefined, limiting the development of meaningful estimates of tolerance to painful injury in this population.


2020 ◽  
Vol 78 (2) ◽  
Author(s):  
Elinor Hortle ◽  
Stefan H Oehlers

ABSTRACT Mycobacteria have co-evolved with their hosts resulting in pathogens adept at intracellular survival. Pathogenic mycobacteria actively manipulate infected macrophages to drive granuloma formation while subverting host cell processes to create a permissive niche. Granuloma residency confers phenotypic antimicrobial resistance by physically excluding or neutralising antibiotics. Host-directed therapies (HDTs) combat infection by restoring protective immunity and reducing immunopathology independent of pathogen antimicrobial resistance status. This review covers innovative research that has discovered ‘secondary’ symptoms of infection in the granuloma stroma are actually primary drivers of infection and that relieving these stromal pathologies with HDTs benefits the host. Advances in our understanding of the relationship between tuberculosis and the host vasculature, haemostatic system and extracellular matrix reorganisation are discussed. Preclinical and clinical use of HDTs against these stromal targets are summarised.


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