Mechanotransduction, the conversion of mechanical stimuli into intracellular biochemical signals, plays fundamental functions in the regulation of development, immunity, inflammation, neurodegeneration, wound healing, fibrogenesis, pain transmission, and oncogenesis. Changes in matrix tension, stiffness, compression, and shear as well as cellular contact with neighboring cells and foreign bodies produce intracellular signals by acting on specialized membrane receptors and channels (‘mechanotransducers’) to affect a wide range of physiological or pathological outcomes. Emerging data support a role for substrate tension, compression, stiffness (or rigidity) of the extracellular and intracellular matrix in numerous cellular processes including gene expression, cell migration, cell proliferation, and differentiation. Soluble modulators such as cytokines, chemokines, growth factors, lipopolysaccharides, and osmotic stress may alter tissue stiffness and cell elasticity, although the mechanisms by which mechanical and soluble signals are integrated to drive biological functions remain elusive. However, the mechanisms by which mechanical and soluble signals are integrated to drive biological functions remain elusive and continue to be investigated.
All immune cells including T-cells, B-cells, macrophages/monocytes, neutrophils, and glial cells of peripheral and central nervous systems are subjected to biochemical and mechanical cues when in systemic circulation and in tissues. Mechanical cues from surrounding cellular environments such as the vascular bed or dermal/epidermal layers can significantly influence these cues via shear and stretch. In contrast to the intense focus on cytokines and chemokines as regulators of immune cell function, the physical microenvironment has traditionally received considerably less attention. However, the function of immune cells that continuously patrol the body and navigate vascular (blood-brain, blood-retina) barriers is contingent upon their ability to rapidly detect and respond to mechanical and biochemical stimuli. To understand immune signaling and inflammation it is critical to define the mechanisms by which these specific mechanotransduction processes occur, and how these functional responses are influenced by the local and systemic biochemical milieu. Specific examples of systems and diseases associated with mechanotransduction and matrix stiffness changes include development, wound healing, atherosclerosis, asthma, IPF, COPD, solid tumors, obesity, virus infection, glaucoma, retinal remodeling, bacterial phagocytosis, foreign body response, autoimmune disease, hypertrophic scarring, fibrosis, and scleroderma.
This Research Topic calls for Original Research articles, Reviews, Clinical Trials, and Methods focusing on, but not limited to, the following subtopics in “mechanotransduction by immune cells in physiological and pathological conditions”:
1. Mechanisms of mechanosensing in T cells, B-cells, macrophages/monocytes, NK cells, neutrophils, microglia, endothelial cells, and astrocytes.
2. Role of transient receptor potential (TRP) and Piezo families and other mechanosensitive ion channels
3. Mechanosensing roles of TLRs, and Scavenger Receptors.
4. Mechanosensing roles of Small RhoGTPases, cytoskeletal, and focal adhesion proteins (e.g., integrins).
5. Extracellular matrix remodeling, and intracellular force generation.
We welcome manuscripts that focus on the role of mechanotransduction in physiological and pathophysiological conditions including development, immunity, inflammation, pain transmission, wound healing, foreign body response, fibrogenesis, atherosclerosis, oncogenesis, vascular disease (hypertension, barrier dysfunction), and neurodegeneration. In addition, the contributions of genetics, autoimmunity, metabolic disorders, and infection are of interest.
Mechanotransduction, the conversion of mechanical stimuli into intracellular biochemical signals, plays fundamental functions in the regulation of development, immunity, inflammation, neurodegeneration, wound healing, fibrogenesis, pain transmission, and oncogenesis. Changes in matrix tension, stiffness, compression, and shear as well as cellular contact with neighboring cells and foreign bodies produce intracellular signals by acting on specialized membrane receptors and channels (‘mechanotransducers’) to affect a wide range of physiological or pathological outcomes. Emerging data support a role for substrate tension, compression, stiffness (or rigidity) of the extracellular and intracellular matrix in numerous cellular processes including gene expression, cell migration, cell proliferation, and differentiation. Soluble modulators such as cytokines, chemokines, growth factors, lipopolysaccharides, and osmotic stress may alter tissue stiffness and cell elasticity, although the mechanisms by which mechanical and soluble signals are integrated to drive biological functions remain elusive. However, the mechanisms by which mechanical and soluble signals are integrated to drive biological functions remain elusive and continue to be investigated.
All immune cells including T-cells, B-cells, macrophages/monocytes, neutrophils, and glial cells of peripheral and central nervous systems are subjected to biochemical and mechanical cues when in systemic circulation and in tissues. Mechanical cues from surrounding cellular environments such as the vascular bed or dermal/epidermal layers can significantly influence these cues via shear and stretch. In contrast to the intense focus on cytokines and chemokines as regulators of immune cell function, the physical microenvironment has traditionally received considerably less attention. However, the function of immune cells that continuously patrol the body and navigate vascular (blood-brain, blood-retina) barriers is contingent upon their ability to rapidly detect and respond to mechanical and biochemical stimuli. To understand immune signaling and inflammation it is critical to define the mechanisms by which these specific mechanotransduction processes occur, and how these functional responses are influenced by the local and systemic biochemical milieu. Specific examples of systems and diseases associated with mechanotransduction and matrix stiffness changes include development, wound healing, atherosclerosis, asthma, IPF, COPD, solid tumors, obesity, virus infection, glaucoma, retinal remodeling, bacterial phagocytosis, foreign body response, autoimmune disease, hypertrophic scarring, fibrosis, and scleroderma.
This Research Topic calls for Original Research articles, Reviews, Clinical Trials, and Methods focusing on, but not limited to, the following subtopics in “mechanotransduction by immune cells in physiological and pathological conditions”:
1. Mechanisms of mechanosensing in T cells, B-cells, macrophages/monocytes, NK cells, neutrophils, microglia, endothelial cells, and astrocytes.
2. Role of transient receptor potential (TRP) and Piezo families and other mechanosensitive ion channels
3. Mechanosensing roles of TLRs, and Scavenger Receptors.
4. Mechanosensing roles of Small RhoGTPases, cytoskeletal, and focal adhesion proteins (e.g., integrins).
5. Extracellular matrix remodeling, and intracellular force generation.
We welcome manuscripts that focus on the role of mechanotransduction in physiological and pathophysiological conditions including development, immunity, inflammation, pain transmission, wound healing, foreign body response, fibrogenesis, atherosclerosis, oncogenesis, vascular disease (hypertension, barrier dysfunction), and neurodegeneration. In addition, the contributions of genetics, autoimmunity, metabolic disorders, and infection are of interest.