The Role of MicroRNAs in Epidermal Barrier

MicroRNAs (miRNAs), which mostly cause target gene silencing via transcriptional repression and degradation of target mRNAs, regulate a plethora of cellular activities, such as cell growth, differentiation, development, and apoptosis. In the case of skin keratinocytes, the role of miRNA in epidermal barrier integrity has been identified. Based on the impact of key genetic and environmental factors on the integrity and maintenance of skin barrier, the association of miRNAs within epidermal cell differentiation and proliferation, cell–cell adhesion, and skin lipids is reviewed. The critical role of miRNAs in the epidermal barrier extends the use of miRNAs for control of relevant skin diseases such as atopic dermatitis, ichthyoses, and psoriasis via miRNA-based technologies. Most of the relevant miRNAs have been associated with keratinocyte differentiation and proliferation. Few studies have investigated the association of miRNAs with structural proteins of corneocytes and cornified envelopes, cell–cell adhesion, and skin lipids. Further studies investigating the association between regulatory and structural components of epidermal barrier and miRNAs are needed to elucidate the role of miRNAs in epidermal barrier integrity and their clinical implications.

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Regulation of Herpes Simplex Virus Glycoprotein-Induced Cascade of Events Governing Cell-Cell Fusion

Journal of Virology ◽

10.1128/jvi.01501-16 ◽

2016 ◽

Vol 90 (23) ◽

pp. 10535-10544 ◽

Cited By ~ 14

Author(s):

Doina Atanasiu ◽

Wan Ting Saw ◽

Roselyn J. Eisenberg ◽

Gary H. Cohen

Keyword(s):

Herpes Simplex Virus ◽

Herpes Simplex ◽

Cell Fusion ◽

Critical Role ◽

Fusion Process ◽

Simplex Virus ◽

The Impact ◽

Hsv 1 ◽

Cell Cell

ABSTRACTReceptor-dependent herpes simplex virus (HSV)-induced cell-cell fusion requires glycoproteins gD, gH/gL, and gB. Our current model posits that during fusion, receptor-activated conformational changes in gD activate gH/gL, which subsequently triggers the transformation of the prefusion form of gB into a fusogenic state. To examine the role of each glycoprotein in receptor-dependent cell-cell fusion, we took advantage of our discovery that fusion by wild-type herpes simplex virus 2 (HSV-2) glycoproteins occurs twice as fast as that achieved by HSV-1 glycoproteins. By sequentially swapping each glycoprotein between the two serotypes, we established that fusion speed was governed by gH/gL, with gH being the main contributor. While the mutant forms of gB fuse at distinct rates that are dictated by their molecular structure, these restrictions can be overcome by gH/gL of HSV-2 (gH2/gL2), thereby enhancing their activity. We also found that deregulated forms of gD of HSV-1 (gD1) and gH2/gL2can alter the fusogenic potential of gB, promoting cell fusion in the absence of a cellular receptor, and that deregulated forms of gB can drive the fusion machinery to even higher levels. Low pH enhanced fusion by affecting the structure of both gB and gH/gL mutants. Together, our data highlight the complexity of the fusion machinery, the impact of the activation state of each glycoprotein on the fusion process, and the critical role of gH/gL in regulating HSV-induced fusion.IMPORTANCECell-cell fusion mediated by HSV glycoproteins requires gD, gH/gL, gB, and a gD receptor. Here, we show that fusion by wild-type HSV-2 glycoproteins occurs twice as fast as that achieved by HSV-1 glycoproteins. By sequentially swapping each glycoprotein between the two serotypes, we found that the fusion process was controlled by gH/gL. Restrictions imposed on the gB structure by mutations could be overcome by gH2/gL2, enhancing the activity of the mutants. Under low-pH conditions or when using deregulated forms of gD1and gH2/gL2, the fusogenic potential of gB could only be increased in the absence of receptor, underlining the exquisite regulation that occurs in the presence of receptor. Our data highlight the complexity of the fusion machinery, the impact of the activation state of each glycoprotein on the fusion process, and the critical role of gH/gL in regulating HSV-induced fusion.

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NLRP7 Promotes Choriocarcinoma Growth and Progression through the Establishment of an Immunosuppressive Microenvironment

Cancers ◽

10.3390/cancers13122999 ◽

2021 ◽

Vol 13 (12) ◽

pp. 2999

Author(s):

Deborah Reynaud ◽

Roland Abi Nahed ◽

Nicolas Lemaitre ◽

Pierre-Adrien Bolze ◽

Wael Traboulsi ◽

...

Keyword(s):

Immune Response ◽

Tumor Cells ◽

Major Gene ◽

Critical Role ◽

Orthotopic Model ◽

Independent Manner ◽

Maternal Immune Response ◽

The Impact

The inflammatory gene NLRP7 is the major gene responsible for recurrent complete hydatidiform moles (CHM), an abnormal pregnancy that can develop into gestational choriocarcinoma (CC). However, the role of NLRP7 in the development and immune tolerance of CC has not been investigated. Three approaches were employed to define the role of NLRP7 in CC development: (i) a clinical study that analyzed human placenta and sera collected from women with normal pregnancies, CHM or CC; (ii) an in vitro study that investigated the impact of NLRP7 knockdown on tumor growth and organization; and (iii) an in vivo study that used two CC mouse models, including an orthotopic model. NLRP7 and circulating inflammatory cytokines were upregulated in tumor cells and in CHM and CC. In tumor cells, NLRP7 functions in an inflammasome-independent manner and promoted their proliferation and 3D organization. Gravid mice placentas injected with CC cells invalidated for NLRP7, exhibited higher maternal immune response, developed smaller tumors, and displayed less metastases. Our data characterized the critical role of NLRP7 in CC and provided evidence of its contribution to the development of an immunosuppressive maternal microenvironment that not only downregulates the maternal immune response but also fosters the growth and progression of CC.

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Specialized Pro-Resolving Lipid Mediators in Neonatal Cardiovascular Physiology and Diseases

Antioxidants ◽

10.3390/antiox10060933 ◽

2021 ◽

Vol 10 (6) ◽

pp. 933

Author(s):

Andrea Gila-Diaz ◽

Gloria Herranz Carrillo ◽

Pratibha Singh ◽

David Ramiro-Cortijo

Keyword(s):

Tissue Repair ◽

Cardiovascular Health ◽

Critical Role ◽

Potential Effect ◽

Lipid Mediators ◽

Physiological Effects ◽

Therapeutic Approaches ◽

The Impact ◽

Long Chain

Cardiovascular disease remains a leading cause of mortality worldwide. Unresolved inflammation plays a critical role in cardiovascular diseases development. Specialized Pro-Resolving Mediators (SPMs), derived from long chain polyunsaturated fatty acids (LCPUFAs), enhances the host defense, by resolving the inflammation and tissue repair. In addition, SPMs also have anti-inflammatory properties. These physiological effects depend on the availability of LCPUFAs precursors and cellular metabolic balance. Most of the studies have focused on the impact of SPMs in adult cardiovascular health and diseases. In this review, we discuss LCPUFAs metabolism, SPMs, and their potential effect on cardiovascular health and diseases primarily focusing in neonates. A better understanding of the role of these SPMs in cardiovascular health and diseases in neonates could lead to the development of novel therapeutic approaches in cardiovascular dysfunction.

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Critical role of fractalkine (CX3CL1) in cigarette smoke-induced mononuclear cell adhesion to the arterial endothelium

Thorax ◽

10.1136/thoraxjnl-2012-202212 ◽

2012 ◽

Vol 68 (2) ◽

pp. 177-186 ◽

Cited By ~ 25

Author(s):

Cristina Rius ◽

Chantal Company ◽

Laura Piqueras ◽

Jose Miguel Cerdá-Nicolás ◽

Cruz González ◽

...

Keyword(s):

Cell Adhesion ◽

Cigarette Smoke ◽

Mononuclear Cell ◽

Critical Role ◽

Arterial Endothelium

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The Role of Cell-Cell Adhesion in Epithelial Tissue Mechanics and Morphogenesis

10.1115/1.0004742v ◽

2021 ◽

Author(s):

Xun Wang ◽

Christian Cupo ◽

Karen Kasza

Keyword(s):

Cell Adhesion ◽

Tissue Mechanics ◽

Epithelial Tissue ◽

Cell Cell

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Novel role of nectin: implication in the co-localization of JAM-A and claudin-1 at the same cell-cell adhesion membrane domain

Genes to Cells ◽

10.1111/j.1365-2443.2008.01206.x ◽

2008 ◽

Vol 13 (8) ◽

pp. 797-805 ◽

Cited By ~ 10

Author(s):

Kaori Kuramitsu ◽

Wataru Ikeda ◽

Naoya Inoue ◽

Yoshiyuki Tamaru ◽

Yoshimi Takai

Keyword(s):

Cell Adhesion ◽

Membrane Domain ◽

Cell Cell

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Combining experiments and in silico modeling to infer the role of adhesion and proliferation on the collective dynamics of cells

10.1101/2021.03.29.437400 ◽

2021 ◽

Author(s):

Hygor P. M. Melo ◽

F. Raquel Maia ◽

André S. Nunes ◽

Rui L. Reis ◽

Joaquim M. Oliveira ◽

...

Keyword(s):

Tissue Engineering ◽

Cell Adhesion ◽

Glioblastoma Multiforme ◽

In Silico ◽

Relative Importance ◽

Collective Dynamics ◽

Surfaces And Interfaces ◽

In Silico Modeling ◽

Cell Cell

ABSTRACTThe collective dynamics of cells on surfaces and interfaces poses technological and theoretical challenges in the study of morphogenesis, tissue engineering, and cancer. Different mechanisms are at play, including, cell-cell adhesion, cell motility, and proliferation. However, the relative importance of each one is elusive. Here, experiments with a culture of glioblastoma multiforme cells on a substrate are combined with in silico modeling to infer the rate of each mechanism. By parametrizing these rates, the time-dependence of the spatial correlation observed experimentally is reproduced. The obtained results suggest a reduction in cell-cell adhesion with the density of cells. The reason for such reduction and possible implications for the collective dynamics of cancer cells are discussed.

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COVID-19 as an “Infodemic” in Public Health: Critical Role of the Social Media

Frontiers in Public Health ◽

10.3389/fpubh.2021.610623 ◽

2021 ◽

Vol 9 ◽

Author(s):

Debanjan Banerjee ◽

K. S. Meena

Keyword(s):

Public Health ◽

Social Media ◽

Critical Role ◽

Global Public Health ◽

Sources Of Information ◽

Multiple Sources ◽

Health Crisis ◽

Digital Platforms ◽

The Impact

The Coronavirus disease 2019 (COVID-19) pandemic has emerged as a significant and global public health crisis. Besides the rising number of cases and fatalities, the outbreak has also affected economies, employment and policies alike. As billions are being isolated at their homes to contain the infection, the uncertainty gives rise to mass hysteria and panic. Amidst this, there has been a hidden epidemic of “information” that makes COVID-19 stand out as a “digital infodemic” from the earlier outbreaks. Repeated and detailed content about the virus, geographical statistics, and multiple sources of information can all lead to chronic stress and confusion at times of crisis. Added to this is the plethora of misinformation, rumor and conspiracy theories circulating every day. With increased digitalization, media penetration has increased with a more significant number of people aiding in the “information pollution.” In this article, we glance at the unique evolution of COVID-19 as an “infodemic” in the hands of social media and the impact it had on its spread and public reaction. We then look at the ways forward in which the role of social media (as well as other digital platforms) can be integrated into social and public health, for a better symbiosis, “digital balance” and pandemic preparedness for the ongoing crisis and the future.

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Paracrine interactions between epithelial cells promote colon cancer growth

10.1101/2020.12.16.423051 ◽

2020 ◽

Author(s):

Guillaume Jacquemin ◽

Annabelle Wurmser ◽

Mathilde Huyghe ◽

Wenjie Sun ◽

Meghan Perkins ◽

...

Keyword(s):

Epithelial Cells ◽

Cancer Cells ◽

Stromal Cells ◽

Critical Role ◽

Essential Factor ◽

Transcriptional Responses ◽

Tumour Formation ◽

Different Types ◽

The Impact

AbstractTumours are complex ecosystems composed of different types of cells that communicate and influence each other. While the critical role of stromal cells in affecting tumour growth is well established, the impact of mutant cancer cells on healthy surrounding tissues remains poorly defined. Here, we uncovered a paracrine mechanism by which intestinal cancer cells reactivate foetal and regenerative Yap-associated transcriptional programs in neighbouring wildtype epithelial cells, rendering them adapted to thrive in the tumour context. We identified the glycoprotein Thrombospondin-1 (Thbs1) as the essential factor that mediates non-cell autonomous morphological and transcriptional responses. Importantly, Thbs1 is associated with bad prognosis in several human cancers. This study reveals the Thbs1-YAP axis as the mechanistic link mediating paracrine interactions between epithelial cells, promoting tumour formation and progression.

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