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Cells
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Molecular and Cellular Regulation of the Skeletal System in Healthy...
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Molecular and Cellular Regulation of the Skeletal System in Healthy and Pathological Conditions

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 May 2021) | Viewed by 6936

Special Issue Editors

Dr. Maria Teresa Valenti

E-Mail Website
Guest Editor
Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37128 Verona, Italy
Interests: bone degenerative diseases; cancer; transcription factors
Special Issues, Collections and Topics in MDPI journals
Prof. Monica Mottes

E-Mail Website
Guest Editor
Department of Neurosciences, Biomedicine and Movement Sciences, Biology and Genetics Section, University of Verona, Verona, Italy
Interests: bone; molecular genetics; heritable connective tissues disorders; mesenchymal stem cells; differentiation

Special Issue Information

Dear Colleagues,

Molecular pathways and cellular processes regulating the skeletal system play a central role in maintaining lifelong physiological conditions. However, alterations in molecular and cellular processes regulating osteogenic or chondrogenic differentiation impair the skeletal system. In this context, the transcription factors involved in mesenchymal stem cells’ commitment towards osteogenic or chondrogenic lineages can be considered as leading agents of cell signaling regulation. The aging process, as well as metabolic and degenerative diseases, may affect bone and cartilage. Mutations affecting the expression of genes involved in the regulation of skeletal development cause several disorders as well.

This Special Issue provides a collection of original research and review articles related to the physiological regulation of the skeletal system and its impairment caused by molecular and cellular disruption as well as by mutations of key genes involved in osteogenesis or chondrogenesis.

Dr. Maria Teresa Valenti
Prof. Monica Mottes
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • bone
  • cartilage
  • mesenchymal stem cells
  • transcription factors
  • cell signaling
  • gene mutations

Related Special Issue

Published Papers (2 papers)

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Research

26 pages, 4966 KiB  
Article
Intracellular Signaling Responses Induced by Radiation within an In Vitro Bone Metastasis Model after Pre-Treatment with an Estrone Analogue
by Jolene Helena, Anna Joubert, Peace Mabeta, Magdalena Coetzee, Roy Lakier and Anne Mercier
Cells 2021, 10(8), 2105; https://doi.org/10.3390/cells10082105 - 17 Aug 2021
Cited by 2 | Viewed by 2820
Abstract
2-Ethyl-3-O-sulfamoyl-estra-1,3,5(10)16-tetraene (ESE-16) is an in silico-designed estradiol analogue which has improved the parent compound’s efficacy in anti-cancer studies. In this proof-of-concept study, the potential radiosensitizing effects of ESE-16 were investigated in an in vitro deconstructed bone metastasis model. Prostate (DU 145) and breast [...] Read more.
2-Ethyl-3-O-sulfamoyl-estra-1,3,5(10)16-tetraene (ESE-16) is an in silico-designed estradiol analogue which has improved the parent compound’s efficacy in anti-cancer studies. In this proof-of-concept study, the potential radiosensitizing effects of ESE-16 were investigated in an in vitro deconstructed bone metastasis model. Prostate (DU 145) and breast (MDA-MB-231) tumor cells, osteoblastic (MC3T3-E1) and osteoclastic (RAW 264.7) bone cells and human umbilical vein endothelial cells (HUVECs) were representative components of such a lesion. Cells were exposed to a low-dose ESE-16 for 24 hours prior to radiation at non-lethal doses to determine early signaling and molecular responses of this combination treatment. Tartrate-resistant acid phosphatase activity and actin ring formation were investigated in osteoclasts, while cell cycle progression, reactive oxygen species generation and angiogenic protein expression were investigated in HUVECs. Increased cytotoxicity was evident in tumor and endothelial cells while bone cells appeared to be spared. Increased mitotic indices were calculated, and evidence of increased deoxyribonucleic acid damage with retarded repair, together with reduced metastatic signaling was observed in tumor cells. RAW 264.7 macrophages retained their ability to differentiate into osteoclasts. Anti-angiogenic effects were observed in HUVECs, and expression of hypoxia-inducible factor 1-α was decreased. Through preferentially inducing tumor cell death and potentially inhibiting neovascularization whilst preserving bone physiology, this low-dose combination regimen warrants further investigation for its promising therapeutic application in bone metastases management, with the additional potential of limited treatment side effects. Full article
(This article belongs to the Special Issue Molecular and Cellular Regulation of the Skeletal System in Healthy and Pathological Conditions)
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13 pages, 1359 KiB  
Article
Irisin Recovers Osteoarthritic Chondrocytes In Vitro
by Gianluca Vadalà, Giuseppina Di Giacomo, Luca Ambrosio, Francesca Cannata, Claudia Cicione, Rocco Papalia and Vincenzo Denaro
Cells 2020, 9(6), 1478; https://doi.org/10.3390/cells9061478 - 17 Jun 2020
Cited by 29 | Viewed by 3539
Abstract
Physical exercise favors weight loss and ameliorates articular pain and function in patients suffering from osteoarthritis. Irisin, a myokine released upon muscle contraction, has demonstrated to yield anabolic effects on different cell types. This study aimed to investigate the effect of irisin on [...] Read more.
Physical exercise favors weight loss and ameliorates articular pain and function in patients suffering from osteoarthritis. Irisin, a myokine released upon muscle contraction, has demonstrated to yield anabolic effects on different cell types. This study aimed to investigate the effect of irisin on human osteoarthritic chondrocytes (hOAC) in vitro. Our hypothesis was that irisin would improve hOAC metabolism and proliferation. Cells were cultured in growing media and then exposed to either phosphate-buffered saline (control group) or human recombinant irisin (experimental group). Cell proliferation, glycosaminoglycan content, type II/X collagen gene expression and protein quantification as well as p38/extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase (MAPK), protein kinase B (Akt), c-Jun N-terminal kinase (JNK), and nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) involvement were evaluated. Furthermore, gene expression of interleukin (IL)-1 and -6, matrix metalloproteinase (MMP)-1 and -13, inducible nitric oxide synthase (iNOS), and tissue inhibitor of matrix metalloproteinases (TIMP)-1 and -3 were investigated following irisin exposure. Irisin increased hOAC cell content and both type II collagen gene expression and protein levels, while decreased type X collagen gene expression and protein levels. Moreover, irisin decreased IL-1, IL-6, MMP-1, MMP-13 and iNOS gene expression, while increased TIMP-1 and TIMP-3 levels. These effects seemed to be mediated by inhibition of p38, Akt, JNK and NFκB signaling pathways. The present study suggested that irisin may stimulate hOAC proliferation and anabolism inhibiting catabolism through p38, Akt, JNK, and NFκB inactivation in vitro, demonstrating the existence of a cross-talk between muscle and cartilage. Full article
(This article belongs to the Special Issue Molecular and Cellular Regulation of the Skeletal System in Healthy and Pathological Conditions)
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