Clobetasol Modulates Adult Neural Stem Cell Growth via Canonical Hedgehog Pathway Activation

Vicario, Nunzio; Bernstock, Joshua D.; Spitale, Federica Maria; Giallongo, Cesarina; Giunta, Maria A.S.; Volti, Giovanni Li; Leanza, Giampiero; Tibullo, Daniele; Parenti, Rosalba; Gulino, Rosario

doi:10.3390/ijms20081991

Cited by 28 publications

(19 citation statements)

References 47 publications

(76 reference statements)

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“…The rate of cell growth (R.C.G.) was calculated as previously described [ 11 ]. Briefly, cells were seeded on six multiwell plates at a final density of 2 × 10 4 cells/cm 2 .…”

Section: Methodsmentioning

confidence: 99%

“…Sonic Hedgehog (SHH) represents one of the most relevant signalling pathways mediating both cell fate and differentiation [ 8 , 9 , 10 ]. The activation of 7-transmembrane protein Smoothened (SMO) determines the GLI-Kruppel family member 1 (GLI1) nuclear translocation promoting proliferation, stem cell renewal and survival [ 10 , 11 , 12 ]. SHH dysregulation has been reported in brain tumors, including GBM [ 13 , 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

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Connexin 43 and Sonic Hedgehog Pathway Interplay in Glioblastoma Cell Proliferation and Migration

Torrisi

Alberghina

Furno

et al. 2021

Biology

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Glioblastoma (GBM) represents the most common primary brain tumor within the adult population. Current therapeutic options are still limited by high rate of recurrences and signalling axes that promote GBM aggressiveness. The contribution of gap junctions (GJs) to tumor growth and progression has been proven by experimental evidence. Concomitantly, tumor microenvironment has received increasing interest as a critical process in dysregulation and homeostatic escape, finding a close link between molecular mechanisms involved in connexin 43 (CX43)-based intercellular communication and tumorigenesis. Moreover, evidence has come to suggest a crucial role of sonic hedgehog (SHH) signalling pathway in GBM proliferation, cell fate and differentiation. Herein, we used two human GBM cell lines, modulating SHH signalling and CX43-based intercellular communication in in vitro models using proliferation and migration assays. Our evidence suggests that modulation of the SHH effector smoothened (SMO), by using a known agonist (i.e., purmorphamine) and a known antagonist (i.e., cyclopamine), affects the CX43 expression levels and therefore the related functions. Moreover, SMO activation also increased cell proliferation and migration. Importantly, inhibition of CX43 channels was able to prevent SMO-induced effects. SHH pathway and CX43 interplay acts inducing tumorigenic program and supporting cell migration, likely representing druggable targets to develop new therapeutic strategies for GBM.

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“…The rate of cell growth (R.C.G.) was calculated as previously described [ 11 ]. Briefly, cells were seeded on six multiwell plates at a final density of 2 × 10 4 cells/cm 2 .…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Connexin 43 and Sonic Hedgehog Pathway Interplay in Glioblastoma Cell Proliferation and Migration

Torrisi

Alberghina

Furno

et al. 2021

Biology

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“…The efficiency of each biomarker was assessed by the receiver operating characteristic (ROC) curve analyses [ 86 , 87 ]. Nonparametric ROC curves analyzed AD vs. NDHC.…”

Section: Methodsmentioning

confidence: 99%

Brain CHID1 Expression Correlates with NRGN and CALB1 in Healthy Subjects and AD Patients

Castrogiovanni

Sanfilippo

Imbesi

et al. 2021

Cells

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Alzheimer’s disease is a progressive, devastating, and irreversible brain disorder that, day by day, destroys memory skills and social behavior. Despite this, the number of known genes suitable for discriminating between AD patients is insufficient. Among the genes potentially involved in the development of AD, there are the chitinase-like proteins (CLPs) CHI3L1, CHI3L2, and CHID1. The genes of the first two have been extensively investigated while, on the contrary, little information is available on CHID1. In this manuscript, we conducted transcriptome meta-analysis on an extensive sample of brains of healthy control subjects (n = 1849) (NDHC) and brains of AD patients (n = 1170) in order to demonstrate CHID1 involvement. Our analysis revealed an inverse correlation between the brain CHID1 expression levels and the age of NDHC subjects. Significant differences were highlighted comparing CHID1 expression of NDHC subjects and AD patients. Exclusive in AD patients, the CHID1 expression levels were correlated positively to calcium-binding adapter molecule 1 (IBA1) levels. Furthermore, both in NDHC and in AD patient’s brains, the CHID1 expression levels were directly correlated with calbindin 1 (CALB1) and neurogranin (NRGN). According to brain regions, correlation differences were shown between the expression levels of CHID1 in prefrontal, frontal, occipital, cerebellum, temporal, and limbic system. Sex-related differences were only highlighted in NDHC. CHID1 represents a new chitinase potentially involved in the principal processes underlying Alzheimer’s disease.

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“…All these pathways promote bone remodeling, inducing MSC differentiation into mature OBs. Several works have demonstrated that WNT/β-catenin signaling is involved in microenvironmental transformation in PMF [ 125 ]. Moreover, the SHH pathway has been found to be upregulated in PMF, suggesting a potential interplay with WNT/β-catenin in mediating osteosclerotic mechanisms [ 126 ].…”

Section: The Biochemical Network Of Osteosclerosis In Pmfmentioning

confidence: 99%

Focus on Osteosclerotic Progression in Primary Myelofibrosis

et al. 2021

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Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by hematopoietic stem-cell-derived clonal proliferation, leading to bone marrow (BM) fibrosis. Hematopoiesis alterations are closely associated with modifications of the BM microenvironment, characterized by defective interactions between vascular and endosteal niches. As such, neoangiogenesis, megakaryocytes hyperplasia and extensive bone marrow fibrosis, followed by osteosclerosis and bone damage, are the most relevant consequences of PMF. Moreover, bone tissue deposition, together with progressive fibrosis, represents crucial mechanisms of disabilities in patients. Although the underlying mechanisms of bone damage observed in PMF are still unclear, the involvement of cytokines, growth factors and bone marrow microenvironment resident cells have been linked to disease progression. Herein, we focused on the role of megakaryocytes and their alterations, associated with cytokines and chemokines release, in modulating functions of most of the bone marrow cell populations and in creating a complex network where impaired signaling strongly contributes to progression and disabilities.

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Clobetasol Modulates Adult Neural Stem Cell Growth via Canonical Hedgehog Pathway Activation

Cited by 28 publications

References 47 publications

Connexin 43 and Sonic Hedgehog Pathway Interplay in Glioblastoma Cell Proliferation and Migration

Connexin 43 and Sonic Hedgehog Pathway Interplay in Glioblastoma Cell Proliferation and Migration

Brain CHID1 Expression Correlates with NRGN and CALB1 in Healthy Subjects and AD Patients

Focus on Osteosclerotic Progression in Primary Myelofibrosis

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