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Cells
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Wnt Signaling in Health and Diseases 2022
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Wnt Signaling in Health and Diseases 2022

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

Deadline for manuscript submissions: closed (1 June 2022) | Viewed by 2619

Special Issue Editor

Dr. Masaru Katoh

E-Mail Website1 Website2
Guest Editor
National Cancer Center, Tokyo, Japan
Interests: precision medicine; human genetics; FGF signaling; Hedgehog signaling; WNT signaling; tumor microenvironment; angiogenesis; immuno-oncology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

WNT signals are transduced through frizzled receptors and co-receptors to the WNT/β-catenin, WNT/planar cell polarity, WNT/G protein, and WNT/tyrosine kinase signaling cascades. WNT signaling cascades cross-talk with the FGF, Notch, Hedgehog, and TGFβ/BMP signaling cascades to regulate embryogenesis, fetal development, and tissue homeostasis.

Dysregulation of the WNT signaling network gives rise to human diseases, such as bone diseases, cancers, cardiovascular diseases, neurological diseases, and ophthalmic diseases. Germline alterations in WNT signaling molecules cause hereditary colorectal cancer, bone diseases, exudative vitreoretinopathy, intellectual disability syndrome, and PCP-related diseases. Somatic alterations in WNT signaling components, such as APC, AXIN2, CTNNB1, RSPO2, RSPO3, and RNF43, occur in colorectal cancer and other types of human cancers. Microenvironmental reprogramming of the WNT signaling network also play key roles in human pathologies.

This Special Issue is calling for original articles and review articles on the WNT signaling network in cancers as well as con-cancerous diseases, with strong emphases on complete genome sequencing, microenvironmental reprogramming and single-cell analysis.

Dr. Masaru Katoh
Guest Editor

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

  • angiogenesis
  • breast cancer
  • cancer-associated fibroblast
  • cardiovascular disease
  • colorectal cancer
  • diabetes mellitus
  • gastric cancer
  • immune evasion
  • lung cancer
  • neurodegenerative disease

Published Papers (1 paper)

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Research

21 pages, 7795 KiB  
Article
Possible Underlying Mechanisms for the Renoprotective Effect of Retinoic Acid-Pretreated Wharton’s Jelly Mesenchymal Stem Cells against Renal Ischemia/Reperfusion Injury
by Mai Barakat, Abdelaziz M. Hussein, Mohamed F. Salama, Amira Awadalla, Nashwa Barakat, Mohamed Serria, Mohamed El-Shafey, Mohamed El-Sherbiny and Mohamed A. El Adl
Cells 2022, 11(13), 1997; https://doi.org/10.3390/cells11131997 - 22 Jun 2022
Cited by 5 | Viewed by 2194
Abstract
Objectives: The current work investigated the effect of Wharton jelly mesenchymal stem cells (WJ-MSCs) pretreated with all-trans-retinoic acid (ATRA) on renal ischemia in rats and the possible role of oxidative stress, apoptotic and Wnt/β-Catenin signaling pathways, and inflammatory cytokines in their effects. Methods: [...] Read more.
Objectives: The current work investigated the effect of Wharton jelly mesenchymal stem cells (WJ-MSCs) pretreated with all-trans-retinoic acid (ATRA) on renal ischemia in rats and the possible role of oxidative stress, apoptotic and Wnt/β-Catenin signaling pathways, and inflammatory cytokines in their effects. Methods: The study included 90 male Sprague Dawley rats that were allocated to five groups (n = 18 rats): (I) Sham-operated group (right nephrectomy was performed); (II) Ischemia/reperfusion injury (IRI) group, a sham group with 45-min renal ischemia on the left kidney; (III) ATRA group, an ischemic group with an intravenous (i.v.) administration of ATRA 10 µM, 10 min post-surgery); (IV) WJ-MSCs group, an IRI group with an i.v. administration of 150 µL containing 7 × 106 WJ-MSCs, 10 min post-surgery; (V) WJ-MSCs + ATRA group, an IRI group with an i.v. administration of 150 µL of 7 × 106 WJ-MSCs pretreated with 10 µM ATRA. At the end of the experiments, serum creatinine, BUN micro-albuminuria (MAU), urinary protein, markers of redox state in the left kidney (MDA, CAT, SOD, and GSH), and the expression of Bax, IL-6, HIF-1α, Wnt7B, and β-catenin genes at the level of mRNA as well as for immunohistochemistry for NFkB and β-Catenin markers were analyzed. Results: The current study found that 45-min of renal ischemia resulted in significant impairment of kidney function (evidenced by the increase in serum creatinine, BUN, and urinary proteins) and deterioration of the kidney morphology, which was associated with a significant increase in redox state (evidenced by an increase in MDA and a decrease in GSH, SOD, and CAT), and a significant increase in inflammatory and apoptotic processes (evidenced by an increase in Bax and IL-6, NFkB, Wnt7B, β-catenin and HIF-1α) in kidney tissues (p < 0.05). On the other hand, treatment with ATRA, WJ-MSCs, or a combination of both, caused significant improvement in kidney function and morphology, which was associated with significant attenuation of oxidative stress, apoptotic markers, and inflammatory cytokines (IL6 and NFkB) with the upregulation of HIF-1α and β-catenin in kidney tissues (p < 0.05). Moreover, the renoprotective effect of WJ-MSCs pretreated with ATRA was more potent than WJ-MSCs alone. Conclusions: It is concluded that preconditioning of WJ-MSCs with ATRA may enhance their renoprotective effect. This effect could be due to the upregulation of the beta-catenin/Wnt pathway and attenuation of apoptosis, inflammation, and oxidative stress. Full article
(This article belongs to the Special Issue Wnt Signaling in Health and Diseases 2022)
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