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Notch Signaling in Health and Disease

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 31012

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Dr. Paola Maura Ticarico

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Institute for Maternal and Child Health - IRCCS “Burlo Garofolo”, Via dell’Istria 65/1, 34137 Trieste, Italy
Interests: cell biology; apoptosis; keratinocytes; keratinocytes differentiation; keratinocytes proliferation; notch signaling; dermatology diseases
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Prof. Dr. Sergio Crovella

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1. Institute for Maternal and Child Health—IRCCS “Burlo Garofolo”, 34137 Trieste, Italy
2. Department of Biological and Environmental Sciences, College of Arts and Sciences, Qatar University, Doha, Qatar
Interests: immunology; clinical pathology; molecular genetics; molecular biology; OMICs; bioinformatics
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Dear Colleagues,

Notch signaling plays a crucial role in various cellular processes, such as proliferation, differentiation, migration, cellular fate, and death, during both normal development and pathological conditions.

Notch signaling controls the induction of keratinocyte growth, promotes the activation of the differentiation program, and is also involved in the regulation of inflammatory responses. Alterations and hyper- or hypo-activation in Notch signaling molecules and in their target genes can induce failure in the regulation of keratinocyte functions, which, in turn, produces skin diseases.

The pathogenetic role of the Notch pathway in skin diseases is not currently fully understood. In recent years, attention has been focused on the correlation between Notch signaling and skin diseases; Notch signaling alterations have recently been reported for the following five human skin diseases, suggesting the involvement of Notch in their pathogenesis: hidradenitis suppurativa, Dowling-Degos disease, Adams–Oliver syndrome, psoriasis, and atopic dermatitis.

This Special Issue is dedicated to the role of Notch signaling in health and skin diseases. Areas of particular interest include but are not limited to defects in keratinocytes and skin health and diseases, autoinflammatory keratinization diseases, and Notch signaling regulation in health and skin diseases.

Dr. Paola Maura Ticarico
Prof. Dr. Sergio Crovella
Guest Editors

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Keywords

dermatological diseases
notch signaling
keratinocytes
inflammation
autoinflammation
differentiation
keratinization
proliferation

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Related Special Issue

Notch Signaling in Health and Disease 2.0 in International Journal of Molecular Sciences (3 articles)

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Editorial

Jump to: Research, Review

3 pages, 182 KiB

Open AccessEditorial

Notch Signaling in Health and Disease

by Paola Maura Tricarico and Sergio Crovella

Int. J. Mol. Sci. 2023, 24(22), 16113; https://doi.org/10.3390/ijms242216113 - 9 Nov 2023

Cited by 1 | Viewed by 1016

Abstract

The Notch signaling pathway, a vital and evolutionarily conserved regulator of cellular processes, intricately shapes both health and disease [...] Full article

(This article belongs to the Special Issue Notch Signaling in Health and Disease)

Research

Jump to: Editorial, Review

13 pages, 3366 KiB

Open AccessArticle

CD109 Promotes Drug Resistance in A2780 Ovarian Cancer Cells by Regulating the STAT3-NOTCH1 Signaling Axis

by Jun Se Kim, Min Joo Shin, Seo Yul Lee, Dae Kyoung Kim, Kyung-Un Choi, Dong-Soo Suh, Dayea Kim and Jae Ho Kim

Int. J. Mol. Sci. 2023, 24(12), 10306; https://doi.org/10.3390/ijms241210306 - 18 Jun 2023

Cited by 4 | Viewed by 2279

Abstract

Epithelial ovarian cancer (EOC) is the most lethal gynecological malignancy owing to relapse caused by resistance to chemotherapy. We previously reported that cluster of differentiation 109 (CD109) expression is positively correlated with poor prognosis and chemoresistance in patients with EOC. To further explore the role of CD109 in EOC, we explored the signaling mechanism of CD109-induced drug resistance. We found that CD109 expression was upregulated in doxorubicin-resistant EOC cells (A2780-R) compared with that in their parental cells. In EOC cells (A2780 and A2780-R), the expression level of CD109 was positively correlated with the expression level of ATP-binding cassette (ABC) transporters, such as ABCB1 and ABCG2, and paclitaxel (PTX) resistance. Using a xenograft mouse model, it was confirmed that PTX administration in xenografts of CD109-silenced A2780-R cells significantly attenuated in vivo tumor growth. The treatment of CD109-overexpressed A2780 cells with cryptotanshinone (CPT), a signal transducer and activator of transcription 3 (STAT3) inhibitor, inhibited the CD109 overexpression-induced activation of STAT3 and neurogenic locus notch homolog protein 1 (NOTCH1), suggesting a STAT3-NOTCH1 signaling axis. The combined treatment of CD109-overexpressed A2780 cells with CPT and N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester (DAPT), a NOTCH inhibitor, markedly abrogated PTX resistance. These results suggest that CD109 plays a key role in the acquisition of drug resistance by activating the STAT3-NOTCH1 signaling axis in patients with EOC. Full article

(This article belongs to the Special Issue Notch Signaling in Health and Disease)

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17 pages, 6457 KiB

Open AccessArticle

Cdk4 Regulates Glioblastoma Cell Invasion and Stemness and Is Target of a Notch Inhibitor Plus Resveratrol Combined Treatment

by Francesca Giordano, Maria D’Amico, Francesca Ida Montalto, Rocco Malivindi, Adele Chimento, Francesca Luisa Conforti, Vincenzo Pezzi, Maria Luisa Panno, Sebastiano Andò and Francesca De Amicis

Int. J. Mol. Sci. 2023, 24(12), 10094; https://doi.org/10.3390/ijms241210094 - 13 Jun 2023

Cited by 6 | Viewed by 2093

Abstract

Glioblastoma multiforme (GBM) is one of the most aggressive types of cancer characterized by poor patient outcomes. To date, it is believed that the major cause of its recurrence and chemoresistance is represented by the enrichment of GBM stem cells (GSCs) sustained by the abnormal activation of a number of signaling pathways. In this study, we found that in GBM cells, treatment with low toxicity doses of the γ-secretase inhibitor RO4929097 (GSI), blocking the Notch pathway activity, in combination with resveratrol (RSV) was able to reverse the basal mesenchymal phenotype to an epithelial-like phenotype, affecting invasion and stemness interplay. The mechanism was dependent on cyclin D1 and cyclin-dependent kinase (CDK4), leading to a reduction of paxillin (Pxn) phosphorylation. Consequently, we discovered the reduced interaction of Pxn with vinculin (Vcl), which, during cell migration, transmits the intracellular forces to the extracellular matrix. The exogenous expression of a constitutively active Cdk4 mutant prevented the RSV + GSI inhibitory effects in GBM cell motility/invasion and augmented the expression of stemness-specific markers, as well as the neurosphere sizes/forming abilities in untreated cells. In conclusion, we propose that Cdk4 is an important regulator of GBM stem-like phenotypes and invasive capacity, highlighting how the combined treatment of Notch inhibitors and RSV could be prospectively implemented in the novel therapeutic strategies to target Cdk4 for these aggressive brain tumors. Full article

(This article belongs to the Special Issue Notch Signaling in Health and Disease)

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17 pages, 8967 KiB

Open AccessArticle

The Clinical Application of Immunohistochemical Expression of Notch4 Protein in Patients with Colon Adenocarcinoma

by Marlena Brzozowa-Zasada, Adam Piecuch, Marek Michalski, Natalia Matysiak, Marek Kucharzewski and Marek J. Łos

Int. J. Mol. Sci. 2023, 24(8), 7502; https://doi.org/10.3390/ijms24087502 - 19 Apr 2023

Cited by 4 | Viewed by 1484

Abstract

The Notch signalling pathway is one of the most conserved and well-characterised pathways involved in cell fate decisions and the development of many diseases, including cancer. Among them, it is worth noting the Notch4 receptor and its clinical application, which may have prognostic value in patients with colon adenocarcinoma. The study was performed on 129 colon adenocarcinomas. Immunohistochemical and fluorescence expression of Notch4 was performed using the Notch4 antibody. The associations between the IHC expression of Notch4 and clinical parameters were analysed using the Chi² test or Chi²_Yatesa test. The Kaplan–Meier analysis and the log-rank test were used to verify the relationship between the intensity of Notch4 expression and the 5-year survival rate of patients. Intracellular localisation of Notch4 was detected by the use of the immunogold labelling method and TEM. 101 (78.29%) samples had strong Notch4 protein expression, and 28 (21.71%) samples were characterised by low expression. The high expression of Notch4 was clearly correlated with the histological grade of the tumour (p < 0.001), PCNA immunohistochemical expression (p < 0.001), depth of invasion (p < 0.001) and angioinvasion (p < 0.001). We can conclude that high expression of Notch4 is correlated with poor prognosis of colon adenocarcinoma patients (log-rank, p < 0.001). Full article

(This article belongs to the Special Issue Notch Signaling in Health and Disease)

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14 pages, 557 KiB

Open AccessArticle

ARID1A, NOTCH and WNT Signature in Gynaecological Tumours

by Ieva Vaicekauskaitė, Daiva Dabkevičienė, Julija Šimienė, Diana Žilovič, Rūta Čiurlienė, Sonata Jarmalaitė and Rasa Sabaliauskaitė

Int. J. Mol. Sci. 2023, 24(6), 5854; https://doi.org/10.3390/ijms24065854 - 19 Mar 2023

Cited by 2 | Viewed by 2017

Abstract

Ovarian cancer (OC) is among the deadliest gynaecologic malignancies in the world. The majority of OC patients are diagnosed at an advanced stage, with high-grade serous OC (HGSOC). The lack of specific symptoms and suitable screening strategies lead to short progression-free survival times in HGSOC patients. The chromatin-remodelling, WNT and NOTCH pathways are some of the most dysregulated in OC; thus their gene mutations and expression profile could serve as diagnostic or prognostic OC biomarkers. Our pilot study investigated mRNA expression of the SWI/SNF chromatin-remodelling complex gene ARID1A, NOTCH receptors, WNT pathway genes CTNNB1 and FBXW7 mRNA expression in two OC cell cultures as well as 51 gynaecologic tumour tissues. A four-gene panel consisting of ARID1A, CTNNB1, FBXW7 and PPP2R1A was used to investigate mutations in gynaecologic tumour tissue. All seven analysed genes were found to be significantly downregulated in OC when compared with non-malignant gynaecologic tumour tissues. NOTCH3 was also downregulated in SKOV3 cells when compared to A2780. Fifteen mutations were found in 25.5% (13/51) of the tissue samples. ARID1A predicted mutations were the most prevalent with alterations detected in 19% (6/32) HGSOC and 67% (6/9) of other OC cases. Thus, ARID1A and NOTCH/WNT-pathway-related changes could be useful diagnostic biomarkers in OC. Full article

(This article belongs to the Special Issue Notch Signaling in Health and Disease)

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15 pages, 1923 KiB

Open AccessArticle

Deletion of Notch3 Impairs Contractility of Renal Resistance Vessels Due to Deficient Ca²⁺ Entry

by Frank Helle, Michael Hultström, Panagiotis Kavvadas, Bjarne Iversen, Christos E. Chadjichristos and Christos Chatziantoniou

Int. J. Mol. Sci. 2022, 23(24), 16068; https://doi.org/10.3390/ijms232416068 - 16 Dec 2022

Cited by 1 | Viewed by 1935

Abstract

Notch3 plays an important role in the differentiation and development of vascular smooth muscle cells. Mice lacking Notch3 show deficient renal autoregulation. The aim of the study was to investigate the mechanisms involved in the Notch3-mediated control of renal vascular response. To this end, renal resistance vessels (afferent arterioles) were isolated from Notch3^−/− and wild-type littermates (WT) and stimulated with angiotensin II (ANG II). Contractions and intracellular Ca²⁺ concentrations were blunted in Notch3^−/− vessels. ANG II responses in precapillary muscle arterioles were similar between the WT and Notch3^−/− mice, suggesting a focal action of Notch3 in renal vasculature. Abolishing stored Ca²⁺ with thapsigargin reduced Ca²⁺ responses in the renal vessels of the two strains, signifying intact intracellular Ca²⁺ mobilization in Notch3^−/−. EGTA (Ca²⁺ chelating agent), nifedipine (L-type channel-blocker), or mibefradil (T-type channel-blocker) strongly reduced contraction and Ca²⁺ responses in WT mice but had no effect in Notch3^−/− mice, indicating defective Ca²⁺ entry. Notch3^−/− vessels responded normally to KCl-induced depolarization, which activates L-type channels directly. Differential transcriptomic analysis showed a major down-regulation of Cacna1h gene expression, coding for the α_1H subunit of the T-type Ca²⁺ channel, in Notch3^−/− vessels. In conclusion, renal resistance vessels from Notch3^−/− mice display altered vascular reactivity to ANG II due to deficient Ca²⁺-entry. Consequently, Notch3 is essential for proper excitation–contraction coupling and vascular-tone regulation in the kidney. Full article

(This article belongs to the Special Issue Notch Signaling in Health and Disease)

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29 pages, 9958 KiB

Open AccessArticle

Indirect Immobilised Jagged-1 Enhances Matrisome Proteins Associated with Osteogenic Differentiation of Human Dental Pulp Stem Cells: A Proteomic Study

by Ajjima Chansaenroj, Chatvadee Kornsuthisopon, Sittiruk Roytrakul, Suphalak Phothichailert, Sunisa Rochanavibhata, Benjamin P. J. Fournier, Supreda Suphanantachat Srithanyarat, Nunthawan Nowwarote and Thanaphum Osathanon

Int. J. Mol. Sci. 2022, 23(22), 13897; https://doi.org/10.3390/ijms232213897 - 11 Nov 2022

Cited by 6 | Viewed by 2073

Abstract

The indirect immobilisation of Jagged-1 (Jagged-1) promoted osteogenic differentiation of human dental pulp cells (hDPs). Furthermore, the analysis of the Reactome pathway of RNA sequencing data indicates the upregulated genes involved with the extracellular matrix (ECM). Hence, our objective was to investigate the effects of Jagged-1 on proteomic profiles of human dental pulp stem cells (hDPSC). hDPSCs were cultured on the surface coated with human IgG Fc fragment (hFc) and the surface coated with rhJagged1/Fc recombinant protein-coated surface. Cells were differentiated to the osteogenic lineage using an osteogenic differentiation medium (OM) for 14 days, and cells cultured in a growth medium were used as a control. The protein component of the cultured cells was extracted into the cytosol, membrane, nucleus, and cytoskeletal compartment. Subsequently, the proteomic analysis was performed using liquid chromatography–tandem mass spectrometry (LC-MS). Metascape gene list analysis reported that Jagged-1 stimulated the expression of the membrane trafficking protein (DOP1B), which can indirectly improve osteogenic differentiation. hDPSCs cultured on Jagged-1 surface under OM condition expressed COL27A1, MXRA5, COL7A1, and MMP16, which played an important role in osteogenic differentiation. Furthermore, common matrisome proteins of all cellular components were related to osteogenesis/osteogenic differentiation. Additionally, the gene ontology categorised by the biological process of cytosol, membrane, and cytoskeleton compartments was associated with the biomineralisation process. The gene ontology of different culture conditions in each cellular component showed several unique gene ontologies. Remarkably, the Jagged-1_OM culture condition showed the biological process related to odontogenesis in the membrane compartment. In conclusion, the Jagged-1 induces osteogenic differentiation could, mainly through the regulation of protein in the membrane compartment. Full article

(This article belongs to the Special Issue Notch Signaling in Health and Disease)

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20 pages, 3926 KiB

Open AccessArticle

The Binding of CSL Proteins to Either Co-Activators or Co-Repressors Protects from Proteasomal Degradation Induced by MAPK-Dependent Phosphorylation

by Johannes Fechner, Manuela Ketelhut, Dieter Maier, Anette Preiss and Anja C. Nagel

Int. J. Mol. Sci. 2022, 23(20), 12336; https://doi.org/10.3390/ijms232012336 - 15 Oct 2022

Cited by 4 | Viewed by 3477

Abstract

The primary role of Notch is to specify cellular identities, whereby the cells respond to amazingly small changes in Notch signalling activity. Hence, dosage of Notch components is crucial to regulation. Central to Notch signal transduction are CSL proteins: together with respective cofactors, they mediate the activation or the silencing of Notch target genes. CSL proteins are extremely similar amongst species regarding sequence and structure. We noticed that the fly homologue suppressor of hairless (Su(H)) is stabilised in transcription complexes. Using specific transgenic fly lines and HeLa RBPJ^KO cells we provide evidence that Su(H) is subjected to proteasomal degradation with a half-life of about two hours if not protected by binding to co-repressor hairless or co-activator Notch. Moreover, Su(H) stability is controlled by MAPK-dependent phosphorylation, matching earlier data for RBPJ in human cells. The homologous murine and human RBPJ proteins, however, are largely resistant to degradation in our system. Mutating presumptive protein contact sites, however, sensitised RBPJ for proteolysis. Overall, our data highlight the similarities in the regulation of CSL protein stability across species and imply that turnover of CSL proteins may be a conserved means of regulating Notch signalling output directly at the level of transcription. Full article

(This article belongs to the Special Issue Notch Signaling in Health and Disease)

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10 pages, 1463 KiB

Open AccessArticle

Determination of Blood NOTCH3 Extracellular Domain and Jagged-1 Levels in Healthy Subjects

by Hyesung Kim, Bogun Jang, Yang-Ji Kim and Jay Chol Choi

Int. J. Mol. Sci. 2022, 23(18), 10547; https://doi.org/10.3390/ijms231810547 - 11 Sep 2022

Viewed by 1886

Abstract

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most common genetic disorder among those responsible for hereditary strokes, and it is caused by a mutation in the NOTCH3 gene on chromosome 19. Blood biomarkers related to the Notch signaling pathway have not been investigated extensively in CADASIL. In this study, we measured the serum and plasma levels of NOTCH3 extracellular domain (N3ECD) and its ligand, Jagged-1, in 279 healthy subjects. The levels of N3ECD and Jagged-1 showed significant correlations in both serum (p < 0.0001, r = 0.2681) and plasma (p < 0.0001, r = 0.4065). The N3ECD levels were significantly higher in the serum than in plasma and tend to increase with age. In contrast, there was no significant difference between the serum and plasma levels of Jagged-1 levels. To summarize, we were able to measure N3ECD and Jagged-1 protein levels in healthy human serum and plasma. Taken together, our findings provide the basis for further studies investigating the clinical use of blood N3ECD and Jagged-1 levels for CADASIL and other Notch signaling-related diseases. Full article

(This article belongs to the Special Issue Notch Signaling in Health and Disease)

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16 pages, 4209 KiB

Open AccessArticle

A γ-Secretase Inhibitor Attenuates Cell Cycle Progression and Invasion in Human Oral Squamous Cell Carcinoma: An In Vitro Study

by Sarai Pongjantarasatian, Nunthawan Nowwarote, Varumporn Rotchanakitamnuai, Watcharee Srirodjanakul, Ritmongkol Saehun, Kajohnkiart Janebodin, Jeeranan Manokawinchoke, Benjamin P. J. Fournier and Thanaphum Osathanon

Int. J. Mol. Sci. 2022, 23(16), 8869; https://doi.org/10.3390/ijms23168869 - 9 Aug 2022

Cited by 5 | Viewed by 2071

Abstract

Notch signaling is associated with many human malignancies, including oral squamous cell carcinoma (OSCC). However, the exact function of Notch signaling in OSCC remains unclear. Here, we investigated the effect of Notch signaling inhibition using a γ-secretase inhibitor (DAPT) on OSCC behaviours in vitro. Bioinformatic analysis of public-available gene expression profiles revealed the dysregulation of the Notch signaling pathway in OSCC compared with normal tissues, indicating the role of Notch signaling in OSCC regulation. RNA sequencing analysis of DAPT-treated human OSCC cells revealed the dysregulation of genes related to cell cycle-related pathways. Blocking Notch signaling significantly inhibited cell proliferation. DAPT-induced G0/G1 cell cycle arrest induced cell apoptosis. Furthermore, cell migration and invasion were also reduced in DAPT-treated cells. These findings indicate that Notch signaling activation participates in OSCC regulation by promoting cell growth, cell cycle progression, cell migration, and invasion. These mechanisms could facilitate OSCC progression. These results imply the potential use of Notch signaling inhibitors as a candidate adjuvant treatment in OSCC patients. Full article

(This article belongs to the Special Issue Notch Signaling in Health and Disease)

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Review

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26 pages, 1091 KiB

Open AccessReview

Notch Signaling in Acute Inflammation and Sepsis

by Nadia Gallenstein, Lucas Tichy, Markus Alexander Weigand and Judith Schenz

Int. J. Mol. Sci. 2023, 24(4), 3458; https://doi.org/10.3390/ijms24043458 - 9 Feb 2023

Cited by 16 | Viewed by 6000

Abstract

Notch signaling, a highly conserved pathway in mammals, is crucial for differentiation and homeostasis of immune cells. Besides, this pathway is also directly involved in the transmission of immune signals. Notch signaling per se does not have a clear pro- or anti-inflammatory effect, but rather its impact is highly dependent on the immune cell type and the cellular environment, modulating several inflammatory conditions including sepsis, and therefore significantly impacts the course of disease. In this review, we will discuss the contribution of Notch signaling on the clinical picture of systemic inflammatory diseases, especially sepsis. Specifically, we will review its role during immune cell development and its contribution to the modulation of organ-specific immune responses. Finally, we will evaluate to what extent manipulation of the Notch signaling pathway could be a future therapeutic strategy. Full article

(This article belongs to the Special Issue Notch Signaling in Health and Disease)

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12 pages, 2983 KiB

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The Role of the Notch Signaling Pathway in Recovery of Cardiac Function after Myocardial Infarction

by Olga Kachanova, Arseniy Lobov and Anna Malashicheva

Int. J. Mol. Sci. 2022, 23(20), 12509; https://doi.org/10.3390/ijms232012509 - 19 Oct 2022

Cited by 21 | Viewed by 3429

Abstract

Myocardial infarction (MI) is a pathological process, evidencing as massive death of cardiomyocytes associated with hypoxic and oxidative stress. The formation of areas of fibrosis ultimately leads to heart failure. There are some mechanisms that contribute to the functional repair of the heart. In most mammals, including humans, the Notch signaling pathway has cardioprotective effects. It is involved in the formation of the heart in embryogenesis and in the restoration of cardiac function after MI due to: (1) reducing oxidative stress; (2) prevention of apoptosis; (3) regulation of inflammation; (4) containment of fibrosis and hypertrophy of cardiomyocytes; (5) tissue revascularization; and (6) regulation of proliferation and differentiation of cardiomyocytes. In addition, the Notch signaling pathway interacts with other signaling cascades involved in the pathogenesis of MI and subsequent cardiac repair. In this review, we consider the Notch signaling pathway as a potential target for therapeutic approaches aimed at improving cardiac recovery after MI. Full article

(This article belongs to the Special Issue Notch Signaling in Health and Disease)

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