TRPV4 Plays a Role in Matrix Stiffness-Induced Macrophage Polarization

Dutta, Bidisha; Goswami, Rishov; Rahaman, Shaik O.

doi:10.3389/fimmu.2020.570195

Cited by 68 publications

(55 citation statements)

References 68 publications

(168 reference statements)

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“…Additionally, it has been shown that cultivation of THP-1 derived macrophages on stiff surfaces increases the expression of M2-markers compared to culture on softer surfaces (130). However, other studies have shown that macrophages can also upregulate the expression of M1-markers when cultured on stiff surfaces (131)(132)(133). The opposing results could be due to the different range of stiffness, type of coating, cell types, and stimulation used.…”

Section: Collagen-mediated Regulation Of the Immune Suppressive Activity Of Macrophagesmentioning

confidence: 99%

“…They found that pulmonary macrophages isolated from patients with idiopathic pulmonary fibrosis acquired a more M2-like phenotype when cultured on various types of collagen compared to pulmonary macrophages isolated from healthy donors ( 134 ). The mechanosensing ability of macrophages has been suggested to involve the ion channel transient receptor potential cation channel subfamily V member 4 (TRPV4) ( 128 , 132 ) and the transcriptional coactivator YAP ( 135 ).…”

Section: Collagen Can Affect the Immune Environment In Tumorsmentioning

confidence: 99%

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Immune Modulatory Properties of Collagen in Cancer

2021

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During tumor growth the extracellular matrix (ECM) undergoes dramatic remodeling. The normal ECM is degraded and substituted with a tumor-specific ECM, which is often of higher collagen density and increased stiffness. The structure and collagen density of the tumor-specific ECM has been associated with poor prognosis in several types of cancer. However, the reason for this association is still largely unknown. Collagen can promote cancer cell growth and migration, but recent studies have shown that collagens can also affect the function and phenotype of various types of tumor-infiltrating immune cells such as tumor-associated macrophages (TAMs) and T cells. This suggests that tumor-associated collagen could have important immune modulatory functions within the tumor microenvironment, affecting cancer progression as well as the efficacy of cancer immunotherapy. The effects of tumor-associated collagen on immune cells could help explain why a high collagen density in tumors is often correlated with a poor prognosis. Knowledge about immune modulatory functions of collagen could potentially identify targets for improving current cancer therapies or for development of new treatments. In this review, the current knowledge about the ability of collagen to influence T cell activity will be summarized. This includes direct interactions with T cells as well as induction of immune suppressive activity in other immune cells such as macrophages. Additionally, the potential effects of collagen on the efficacy of cancer immunotherapy will be discussed.

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Section: Collagen-mediated Regulation Of the Immune Suppressive Activity Of Macrophagesmentioning

confidence: 99%

Section: Collagen Can Affect the Immune Environment In Tumorsmentioning

confidence: 99%

Immune Modulatory Properties of Collagen in Cancer

2021

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“…Consequently, modulating receptor engagement by modulating implant surfaces affects the ability of macrophages to attach and spread on surfaces [ 144 ] and to fuse into FBGCs [ 138 , 139 , 145 ]. In addition to integrins and RhoA/ROCK signaling [ 146 ], transient receptor potential vanilloid 4 (TRPV4) channels appear to be critical in mediating macrophage responses and polarization on differently stiff substrates [ 147 ] and macrophage fusion in a Rac1-dependent manner [ 148 ].…”

Section: Implant Surfaces From the Perspective Of A Macrophagementioning

confidence: 99%

Implant Fibrosis and the Underappreciated Role of Myofibroblasts in the Foreign Body Reaction

Noskovičová

Hinz

Pakshir

2021

Cells

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Body implants and implantable medical devices have dramatically improved and prolonged the life of countless patients. However, our body repair mechanisms have evolved to isolate, reject, or destroy any object that is recognized as foreign to the organism and inevitably mounts a foreign body reaction (FBR). Depending on its severity and chronicity, the FBR can impair implant performance or create severe clinical complications that will require surgical removal and/or replacement of the faulty device. The number of review articles discussing the FBR seems to be proportional to the number of different implant materials and clinical applications and one wonders, what else is there to tell? We will here take the position of a fibrosis researcher (which, coincidentally, we are) to elaborate similarities and differences between the FBR, normal wound healing, and chronic healing conditions that result in the development of peri-implant fibrosis. After giving credit to macrophages in the inflammatory phase of the FBR, we will mainly focus on the activation of fibroblastic cells into matrix-producing and highly contractile myofibroblasts. While fibrosis has been discussed to be a consequence of the disturbed and chronic inflammatory milieu in the FBR, direct activation of myofibroblasts at the implant surface is less commonly considered. Thus, we will provide a perspective how physical properties of the implant surface control myofibroblast actions and accumulation of stiff scar tissue. Because formation of scar tissue at the surface and around implant materials is a major reason for device failure and extraction surgeries, providing implant surfaces with myofibroblast-suppressing features is a first step to enhance implant acceptance and functional lifetime. Alternative therapeutic targets are elements of the myofibroblast mechanotransduction and contractile machinery and we will end with a brief overview on such targets that are considered for the treatment of other organ fibroses.

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“…TRPV4 activation is associated with phenotypic switch by macrophages ( 12 , 13 , 17 , 51 , 94 ). Current understanding of macrophage polarization is based largely on the use of biochemical cues such as cytokines or LPS to alter cellular phenotype.…”

Section: Trpv4 Activity Influences Macrophage Polarization and Metabolismmentioning

confidence: 99%

Diverse Roles of TRPV4 in Macrophages: A Need for Unbiased Profiling

et al. 2022

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Transient receptor potential vanilloid 4 (TRPV4) is a non-selective mechanosensitive ion channel expressed by various macrophage populations. Recent reports have characterized the role of TRPV4 in shaping the activity and phenotype of macrophages to influence the innate immune response to pathogen exposure and inflammation. TRPV4 has been studied extensively in the context of inflammation and inflammatory pain. Although TRPV4 activity has been generally described as pro-inflammatory, emerging evidence suggests a more complex role where this channel may also contribute to anti-inflammatory activities. However, detailed understanding of how TRPV4 may influence the initiation, maintenance, and resolution of inflammatory disease remains limited. This review highlights recent insights into the cellular processes through which TRPV4 contributes to pathological conditions and immune processes, with a focus on macrophage biology. The potential use of high-throughput and omics methods as an unbiased approach for studying the functional outcomes of TRPV4 activation is also discussed.

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TRPV4 Plays a Role in Matrix Stiffness-Induced Macrophage Polarization

Cited by 68 publications

References 68 publications

Immune Modulatory Properties of Collagen in Cancer

Immune Modulatory Properties of Collagen in Cancer

Implant Fibrosis and the Underappreciated Role of Myofibroblasts in the Foreign Body Reaction

Diverse Roles of TRPV4 in Macrophages: A Need for Unbiased Profiling

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