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Effect of cyclic strain in neurons isolated from dorsal root ganglia

ABSTRACT: Organs and cells in our body are continuously exposed to mechanical forces. Neurons, in particular, encounter mechanical stimuli during neurodevelopment, aging, pathological conditions, and routine functions such as homeostatic processes and movement. How do cells, which endure mechanical stress on a daily basis, withstand these forces and remain functional throughout our long lifespans? To maintain their functionality, cells must have evolved self-repair mechanisms that allow them to tolerate stress and repair damage up to a manageable threshold. This study aims to explore the relationship between damage and repair mechanisms that are crucial for preserving the structural and functional integrity of axons over time. Dorsal Root Ganglia neurons are used as a model system, as they are particularly relevant due to their exposure to daily mechanical movements. An experimental setup has been developed to apply repeated cycles of compression to neurons grown on an elastic substrate. Understanding how neurons respond to mechanical strain and sustain homeostasis will not only deepen our knowledge of the effects of mechanical stress on neurons but also provide valuable insights into restoring cellular functions.

ORGANISM(S): Mus musculus

PROVIDER: GSE286272 | GEO | 2025/01/31

REPOSITORIES: GEO

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Project description:Adhesion formation after flexor tendon repair remains a clinical problem. Early postoperative motion after tendon repair has been demonstrated to reduce adhesion formation while increasing tendon strength. It is hypothesized that during mobilization, tendon cells experience mechanical shear forces that alter their biology in a fashion that reduces scar formation but also activates key genes involved in tendon healing. To test this hypothesis, primary intrinsic tenocyte cultures were established from flexor tendons of 20 Sprague-Dawley rats and sheared at 50 rpm (0.41 Pa) using a cone viscometer for 6 and 12 hours. Total RNA was harvested and compared with time-matched unsheared controls using cDNA microarrays and Northern blot analysis. Microarray analysis demonstrated that mechanical shear stress induced an overall "antifibrotic" expression pattern with decreased transcription of collagen type I and collagen type III. Shear stress down-regulated profibrotic molecules in the platelet-derived growth factor, insulin-like growth factor, and fibroblast growth factor signaling pathways. In addition, shear stress induced an overall decrease in transforming growth factor (TGF)-beta signaling pathway molecules with down-regulation of TGF-beta2, TGF-beta3, TGF-RI, and TGF-RII expression. Moreover, sheared tendon cells increased expression of matrix metalloproteinases and decreased expression of tissue inhibitors of metalloproteinase, an expression pattern consistent with an antifibrotic increase in extracellular matrix degradation. However, up-regulation of genes implicated in tendon healing, specifically, vascular endothelial growth factor-A and several bone morphogenetic proteins. Interestingly, the known mechanoresponsive gene, TGF-beta1, also implicated in tendon healing, was differentially up-regulated by shear stress. Northern blot validation of our results for TGF-beta1, TGF-beta2, TGF-beta3, and collagen type I demonstrated direct correlation with microarray data.

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Effect of cyclic strain in neurons isolated from dorsal root ganglia

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