Pannexin Channel Regulation of Cell Migration: Focus on Immune Cells

Harcha, Paloma A.; López-López, Tamara; Palacios, Adrián; Sáez, Pablo J.

doi:10.3389/fimmu.2021.750480

Cited by 15 publications

(10 citation statements)

References 152 publications

(255 reference statements)

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“…In this sense, Zhao et al reported that betacellulin, a member of the EGF family, induces Cx43 expression through the activation of the MEK-ERK signaling pathway promoting ovarian cancer cell migration, and this effect is likely gap junction-independent [37]. In addition, we cannot discard the participation of Cx43 or other membrane channel proteins, such as Pannexins, that contribute to ERK signaling during migration through the release or uptake of ATP [44,45].…”

Section: Plos Onementioning

confidence: 82%

StarD7 deficiency hinders cell motility through p-ERK1/2/Cx43 reduction

et al. 2022

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StarD7 belongs to START protein family involved in lipid traffic, metabolism, and signaling events. Its precursor, StarD7.I which is important for mitochondrial homeostasis, is processed to the StarD7.II isoform that lacks the mitochondrial targeting sequence and is mainly released to the cytosol. StarD7 knockdown interferes with cell migration by an unknown mechanism. Here, we demonstrate that StarD7 silencing decreased connexin 43 (Cx43), integrin β1, and p-ERK1/2 expression in the non-tumoral migratory HTR-8/SVneo cells. StarD7-deficient cells exhibited Golgi disruption and reduced competence to reorient the microtubule-organizing center. The migratory capacity of StarD7-silenced cells was reestablished when Cx43 level was resettled, while p-ERK1/2 expression remained low. Importantly, ectopic expression of the StarD7.II isoform not only restored cell migration but also ERK1/2, Cx43, and integrin β1 expression. Thus, StarD7 is implicated in cell migration through an ERK1/2/Cx43 dependent mechanism but independent of the StarD7.I function in the mitochondria.

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Section: Plos Onementioning

confidence: 82%

StarD7 deficiency hinders cell motility through p-ERK1/2/Cx43 reduction

et al. 2022

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“…In previous studies, OPRPN was associated with better survival in oral squamous carcinoma and as a pain-relieving agent in the eye [ 45 , 46 ]. PANX3, on the other hand, represents a channel in cell-to-cell communication and migration that affects the cytoskeleton [ 47 ]. Additionally, PANX3 has a role in the recruitment of CD4+ T cells, neutrophils, and macrophages in mice [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Differentiation of Phenotypes in Chronic Rhinosinusitis and Its Implications for Understanding the Underlying Mechanisms

Urbančič

Soklič

Luzar

et al. 2023

IJMS

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Chronic rhinosinusitis (CRS) is a multifaceted disease with variable clinical courses and outcomes. We aimed to determine CRS-associated nasal-tissue transcriptome in clinically well-characterized and phenotyped individuals, to gain a novel insight into the biological pathways of the disease. RNA-sequencing of tissue samples of patients with CRS with polyps (CRSwNP), without polyps (CRSsNP), and controls were performed. Characterization of differently expressed genes (DEGs) and functional and pathway analysis was undertaken. We identified 782 common CRS-associated nasal-tissue DEGs, while 375 and 328 DEGs were CRSwNP- and CRSsNP-specific, respectively. Common key DEGs were found to be involved in dendritic cell maturation, the neuroinflammation pathway, and the inhibition of the matrix metalloproteinases. Distinct CRSwNP-specific DEGs were involved in NF-kβ canonical pathways, Toll-like receptor signaling, HIF1α regulation, and the Th2 pathway. CRSsNP involved the NFAT pathway and changes in the calcium pathway. Our findings offer new insights into the common and distinct molecular mechanisms underlying CRSwNP and CRSsNP, providing further understanding of the complex pathophysiology of the CRS, with future research directions for novel treatment strategies.

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“…Upon exposure to an inflammatory stimulus, monocytes have been found to rapidly upregulate the transcription of genes for oxidative phosphorylation. It has been suggested that this occurs to increase ATP production in order to mobilize monocytes toward the site of inflammation (Harcha et al, 2021; Purvis et al, 2021). Overall, we are seeing that monocyte reprogramming through metabolic changes alters their activity (Purvis et al, 2021).…”

Section: The Main Playersmentioning

confidence: 99%

From infection to repair: Understanding the workings of our innate immune cells

Mawhinney

Kulle

Thanabalasuriar

2022

WIREs Mechanisms of Disease

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In a world filled with microbes, some posing a threat to our body, our immune system is key to living a healthy life. The innate immune system is made of various cell types that act to guard our bodies. Unlike the adaptive immune system that has a specific response, our innate immune system encompasses cells that elicit unspecific immune responses, triggered whenever the right signals are detected. Our understanding of immunity started with the concept of our immune system only responding to "nonself" like the pathogens that invade our body. However, over the past few decades, we have learned that the immune system is more than an on/off switch that recognizes nonself. The innate immune system regularly patrols our bodies for pathogens and tissue damage. Our innate immune system not only seeks to resolve infection but also repair tissue injury, through phagocytosing debris and initiating the release of growth factors. Recently, we are starting to see that it is not just recognizing danger, our innate immune system plays a crucial role in repair.Innate immune cells phenotypically change during repair. In the context of severe injury or trauma, our innate immune system is modified quite drastically to help repair, resulting in reduced infection control. Moreover, these changes in immune cell function can be modified by sex as a biological variable. From past to present, in this overview, we provide a summary of the innate immune cells and pathways in infection and tissue repair. This article is categorized under:Immune System Diseases > Molecular and Cellular Physiologyimmunology, innate immune cells, sterile injury | INTRODUCTIONEvery minute of every hour of every day, our body's immune cells are in a silent battle with tiny microbes in the environment around us. These microbes consist of bacteria, fungi, viruses, and parasites found in the air, water, soil, and on surfaces. In tropical climates, the range of pathogens differ from subarctic climates, but we are all faced with similar challenges daily. Immunodeficiencies, or the absence of immune cells, result in regular microbial attacks on our bodies and disease development. The concept of immunology emerged with Elias Metchnikoff's (1845-1916) identification of phagocytic cells, which engulf and destroy invading pathogens (Kaufmann, 2019). This laid the basis for innate immunity.

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Pannexin Channel Regulation of Cell Migration: Focus on Immune Cells

Cited by 15 publications

References 152 publications

StarD7 deficiency hinders cell motility through p-ERK1/2/Cx43 reduction

StarD7 deficiency hinders cell motility through p-ERK1/2/Cx43 reduction

Transcriptomic Differentiation of Phenotypes in Chronic Rhinosinusitis and Its Implications for Understanding the Underlying Mechanisms

From infection to repair: Understanding the workings of our innate immune cells

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