Transcription factor activation and protein phosphorylation patterns are distinct for CD28 and ICAM-1 co-stimulatory molecules

Bhatta, Anuja; Chan, Marcia A.; Benedict, Stephen H.

doi:10.1016/j.imbio.2021.152067

Cited by 2 publications

(2 citation statements)

References 29 publications

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“…ICAM-1 could enhance myonuclear transcription, as well as downstream processes of muscle regeneration by regulating multiple processes. In cultured cells (e.g., endothelial cells and leukocytes) [13,14], ligation of membrane ICAM-1 activates transcription factors (e.g., AP-1 and FAST-1) [30,31], membrane receptors (e.g., IGF-1R and HGFR) [31], nonreceptor kinases (e.g., Src family) [32], signaling molecules (e.g., MAPK, Akt, and Rho GTPases) [33][34][35][36], and cytoskeletal-associated proteins (e.g., focal adhesion kinase and paxillin) [34]. Ligation of membrane ICAM-1 also increases expression of early response genes (e.g., c-fos) [37], cytokines (e.g., IL-1ß and MIP-1α) [30,38,39], and adhesion molecules (e.g., VCAM-1 and ICAM-1) [40,41].…”

Section: Discussionmentioning

confidence: 99%

Intercellular Adhesion Molecule-1 Enhances Myonuclear Transcription during Injury-Induced Muscle Regeneration

Buckley

Nestor-Kalinoski

Pizza

2022

IJMS

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The local inflammatory environment of injured skeletal muscle contributes to the resolution of the injury by promoting the proliferation of muscle precursor cells during the initial stage of muscle regeneration. However, little is known about the extent to which the inflammatory response influences the later stages of regeneration when newly formed (regenerating myofibers) are accumulating myonuclei and undergoing hypertrophy. Our prior work indicated that the inflammatory molecule ICAM-1 facilitates regenerating myofiber hypertrophy through a process involving myonuclear positioning and/or transcription. The present study tested the hypothesis that ICAM-1 enhances global transcription within regenerating myofibers by augmenting the transcriptional activity of myonuclei positioned in linear arrays (nuclear chains). We found that transcription in regenerating myofibers was ~2-fold higher in wild type compared with ICAM-1-/- mice at 14 and 28 days post-injury. This occurred because the transcriptional activity of individual myonuclei in nuclei chains, nuclear clusters, and a peripheral location were ~2-fold higher in wild type compared with ICAM-1-/- mice during regeneration. ICAM-1’s enhancement of transcription in nuclear chains appears to be an important driver of myofiber hypertrophy as it was statistically associated with an increase in myofiber size during regeneration. Taken together, our findings indicate that ICAM-1 facilitates myofiber hypertrophy after injury by enhancing myonuclear transcription.

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Section: Discussionmentioning

confidence: 99%

Intercellular Adhesion Molecule-1 Enhances Myonuclear Transcription during Injury-Induced Muscle Regeneration

Buckley

Nestor-Kalinoski

Pizza

2022

IJMS

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“…In B cells, clustering of ICAM-1 upregulated MHC-II molecules and activated ERK1/2 and the Src kinase Lyn [161], whereas in naïve CD4 + T cells, the combination of anti-CD3 plus anti-ICAM-1 or anti-ICAM-3 Abs caused prolonged proliferation in a manner similar to costimulation by LFA-1 [162][163][164][165]. However, costimulation with ICAM-1 provided greater protection against apoptosis and memory T-cell fate, as did CD28 through the activation of different downstream factors since CD28 activated Dtk and FGFR1 receptor tyrosine kinases, whereas ICAM-1 rather activated IGF-1R and HGFR [166,167]. This function of ICAM-1 and ICAM-3 may be complemented by their involvement in the clearance of apoptotic cells, the former on phagocytic macrophages and the latter on apoptotic leukocytes and leukocyte-derived microparticles that stimulate the chemotaxis of phagocytes towards apoptotic immune cells and tissues during the resolution of inflammatory processes [168][169][170].…”

Section: Reciprocal Signalling By Icamsmentioning

confidence: 95%

ICAMs in Immunity, Intercellular Adhesion and Communication

Guerra-Espinosa,

Jiménez-Fernández,

Sánchez-Madrid

et al. 2024

Cells

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Interactions among leukocytes and leukocytes with immune-associated auxiliary cells represent an essential feature of the immune response that requires the involvement of cell adhesion molecules (CAMs). In the immune system, CAMs include a wide range of members pertaining to different structural and functional families involved in cell development, activation, differentiation and migration. Among them, β2 integrins (LFA-1, Mac-1, p150,95 and αDβ2) are predominantly involved in homotypic and heterotypic leukocyte adhesion. β2 integrins bind to intercellular (I)CAMs, actin cytoskeleton-linked receptors belonging to immunoglobulin superfamily (IgSF)-CAMs expressed by leukocytes and vascular endothelial cells, enabling leukocyte activation and transendothelial migration. β2 integrins have long been viewed as the most important ICAMs partners, propagating intracellular signalling from β2 integrin-ICAM adhesion receptor interaction. In this review, we present previous evidence from pioneering studies and more recent findings supporting an important role for ICAMs in signal transduction. We also discuss the contribution of immune ICAMs (ICAM-1, -2, and -3) to reciprocal cell signalling and function in processes in which β2 integrins supposedly take the lead, paying particular attention to T cell activation, differentiation and migration.

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Transcription factor activation and protein phosphorylation patterns are distinct for CD28 and ICAM-1 co-stimulatory molecules

Cited by 2 publications

References 29 publications

Intercellular Adhesion Molecule-1 Enhances Myonuclear Transcription during Injury-Induced Muscle Regeneration

Intercellular Adhesion Molecule-1 Enhances Myonuclear Transcription during Injury-Induced Muscle Regeneration

ICAMs in Immunity, Intercellular Adhesion and Communication

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