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3.9
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Biomedicines
Special Issues
Stem Cell Signaling
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Stem Cell Signaling

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Gene and Cell Therapy".

Deadline for manuscript submissions: closed (30 September 2020) | Viewed by 14968

Special Issue Editor

Dr. Hyuk-Jin Cha

E-Mail Website
Guest Editor
College of Pharmacy, Seoul National University, Seoul, Korea
Interests: pluripotency; signaling; gene editing; disease modeling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

While stem cell research has been mainly focused on preclinical studies aimed at the development of stem cell-based cell therapy, many fundamental questions regarding the cellular and molecular features of stem cells remain. Thanks to technical advances in culture and differentiation of a number of different stem cells, the self-renewal and differentiation potential—which define the properties of stem cells—have been explored through their epigenetic regulation, transcriptional networks, and signaling pathways. Furthermore, recent advances in various interesting stem cell models, such as cellular reprogramming, naïve pluripotent stem cells, and organoids, have extended understanding of the underlying mechanisms behind how stem cells maintain stemness and commit fate determination.

This Special Issue of Biomedicines focuses on recent advances in understanding the underlying mechanisms of pluripotency, self-renewal, lineage differentiation, cellular reprogramming, regeneration, and related diseases. The goal is to promote the fundamental knowledge in this exciting field in order to provide the inclusive basic knowledge necessary for regenerative medicine.

We encourage authors to submit original research and review articles that focus on the various biological features and underlying mechanisms of both pluripotent stem cells and somatic stem cells. Potential topics include, but are not limited to:

  • The mechanism of pluripotency maintenance;
  • The mechanism of cellular reprogramming or cellular plasticity;
  • The mechanism of lineage determination or differentiation;
  • The mechanism of stemness (or self-renewal) maintenance or regeneration;
  • The mechanism of stem cell aging;
  • The mechanism of embryo development;
  • Conversion between naïve and primed pluripotency.

Dr. Hyuk-Jin Cha
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • stem cells
  • signaling
  • development
  • reprogramming
  • differentiation
  • self-renewal
  • regeneration
  • cellular plasticity

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Published Papers (4 papers)

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Research

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15 pages, 4577 KiB  
Article
Luteolin Induces Selective Cell Death of Human Pluripotent Stem Cells
by Young-Hyun Go, Jumee Kim, Ho-Chang Jeong, Seong-Min Kim, Yun-Jeong Kim, Soon-Jung Park, Sung-Hwan Moon and Hyuk-Jin Cha
Biomedicines 2020, 8(11), 453; https://doi.org/10.3390/biomedicines8110453 - 27 Oct 2020
Cited by 3 | Viewed by 2871
Abstract
Despite recent advances in clinical stem cell therapy applications based on human pluripotent stem cells (hPSCs), potential teratoma formation due to the presence of residual undifferentiated hPSCs remains a serious risk factor that challenges widespread clinical application. To overcome this risk, a variety [...] Read more.
Despite recent advances in clinical stem cell therapy applications based on human pluripotent stem cells (hPSCs), potential teratoma formation due to the presence of residual undifferentiated hPSCs remains a serious risk factor that challenges widespread clinical application. To overcome this risk, a variety of approaches have been developed to eliminate the remaining undifferentiated hPSCs via selective cell death induction. Our study seeks to identify natural flavonoids that are more potent than quercetin (QC), to selectively induce hPSC death. Upon screening in-house flavonoids, luteolin (LUT) is found to be more potent than QC to eliminate hPSCs in a p53-dependent manner, but not hPSC-derived smooth muscle cells or perivascular progenitor cells. Particularly, treating human embryonic stem cell (hESC)-derived cardiomyocytes with LUT efficiently eliminates the residual hESCs and only results in marginal effects on cardiomyocyte (CM) functions, as determined by calcium influx. Considering the technical limitations of isolating CMs due to a lack of exclusive surface markers at the end of differentiation, LUT treatment is a promising approach to minimize teratoma formation risk. Full article
(This article belongs to the Special Issue Stem Cell Signaling)
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17 pages, 4586 KiB  
Article
Babam2 Regulates Cell Cycle Progression and Pluripotency in Mouse Embryonic Stem Cells as Revealed by Induced DNA Damage
by Cheuk Yiu Tenny Chung, Paulisally Hau Yi Lo and Kenneth Ka Ho Lee
Biomedicines 2020, 8(10), 397; https://doi.org/10.3390/biomedicines8100397 - 10 Oct 2020
Cited by 3 | Viewed by 3273
Abstract
BRISC and BRCA1-A complex member 2 (Babam2) plays an essential role in promoting cell cycle progression and preventing cellular senescence. Babam2-deficient fibroblasts show proliferation defect and premature senescence compared with their wild-type (WT) counterpart. Pluripotent mouse embryonic stem cells (mESCs) [...] Read more.
BRISC and BRCA1-A complex member 2 (Babam2) plays an essential role in promoting cell cycle progression and preventing cellular senescence. Babam2-deficient fibroblasts show proliferation defect and premature senescence compared with their wild-type (WT) counterpart. Pluripotent mouse embryonic stem cells (mESCs) are known to have unlimited cell proliferation and self-renewal capability without entering cellular senescence. Therefore, studying the role of Babam2 in ESCs would enable us to understand the mechanism of Babam2 in cellular aging, cell cycle regulation, and pluripotency in ESCs. For this study, we generated Babam2 knockout (Babam2−/−) mESCs to investigate the function of Babam2 in mESCs. We demonstrated that the loss of Babam2 in mESCs leads to abnormal G1 phase retention in response to DNA damage induced by gamma irradiation or doxorubicin treatments. Key cell cycle regulators, CDC25A and CDK2, were found to be degraded in Babam2−/− mESCs following gamma irradiation. In addition, Babam2−/− mESCs expressed p53 strongly and significantly longer than in control mESCs, where p53 inhibited Nanog expression and G1/S cell cycle progression. The combined effects significantly reduced developmental pluripotency in Babam2−/− mESCs. In summary, Babam2 maintains cell cycle regulation and pluripotency in mESCs in response to induced DNA damage. Full article
(This article belongs to the Special Issue Stem Cell Signaling)
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13 pages, 2276 KiB  
Article
Regulation of JAM2 Expression in the Lungs of Streptozotocin-Induced Diabetic Mice and Human Pluripotent Stem Cell-Derived Alveolar Organoids
by Roya Rasaei, Eunbi Kim, Ji-Young Kim, Sunghun Na, Jung-Hyun Kim, Jinbeom Heo, Dong-Myung Shin, Sun Shim Choi and Seok-Ho Hong
Biomedicines 2020, 8(9), 346; https://doi.org/10.3390/biomedicines8090346 - 11 Sep 2020
Cited by 5 | Viewed by 3459
Abstract
Hyperglycemia is a causative factor in the pathogenesis of respiratory diseases, known to induce fibrosis and inflammation in the lung. However, little attention has been paid to genes related to hyperglycemic-induced lung alterations and stem cell applications for therapeutic use. In this study, [...] Read more.
Hyperglycemia is a causative factor in the pathogenesis of respiratory diseases, known to induce fibrosis and inflammation in the lung. However, little attention has been paid to genes related to hyperglycemic-induced lung alterations and stem cell applications for therapeutic use. In this study, our microarray data revealed significantly increased levels of junctional adhesion molecule 2 (JAM2) in the high glucose (HG)-induced transcriptional profile in human perivascular cells (hPVCs). The elevated level of JAM2 in HG-treated hPVCs was transcriptionally and epigenetically reversible when HG treatment was removed. We further investigated the expression of JAM2 using in vivo and in vitro hyperglycemic models. Our results showed significant upregulation of JAM2 in the lungs of streptozotocin (STZ)-induced diabetic mice, which was greatly suppressed by the administration of conditioned medium obtained from human mesenchymal stem cell cultures. Furthermore, JAM2 was found to be significantly upregulated in human pluripotent stem cell-derived multicellular alveolar organoids by exposure to HG. Our results suggest that JAM2 may play an important role in STZ-induced lung alterations and could be a potential indicator for predicting the therapeutic effects of stem cells and drugs in diabetic lung complications. Full article
(This article belongs to the Special Issue Stem Cell Signaling)
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Review

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20 pages, 1204 KiB  
Review
The Hippo–YAP Signaling as Guardian in the Pool of Intestinal Stem Cells
by Yoojin Seo, So-Yeon Park, Hyung-Sik Kim and Jeong-Seok Nam
Biomedicines 2020, 8(12), 560; https://doi.org/10.3390/biomedicines8120560 - 1 Dec 2020
Cited by 13 | Viewed by 4732
Abstract
Despite endogenous insults such as mechanical stress and danger signals derived from the microbiome, the intestine can maintain its homeostatic condition through continuous self-renewal of the crypt–villus axis. This extraordinarily rapid turnover of intestinal epithelium, known to be 3 to 5 days, can [...] Read more.
Despite endogenous insults such as mechanical stress and danger signals derived from the microbiome, the intestine can maintain its homeostatic condition through continuous self-renewal of the crypt–villus axis. This extraordinarily rapid turnover of intestinal epithelium, known to be 3 to 5 days, can be achieved by dynamic regulation of intestinal stem cells (ISCs). The crypt base-located leucine-rich repeat-containing G-protein-coupled receptor 5-positive (Lgr5+) ISCs maintain intestinal integrity in the steady state. Under severe damage leading to the loss of conventional ISCs, quiescent stem cells and even differentiated cells can be reactivated into stem-cell-like cells with multi-potency and contribute to the reconstruction of the intestinal epithelium. This process requires fine-tuning of the various signaling pathways, including the Hippo–YAP system. In this review, we summarize recent advances in understanding the correlation between Hippo–YAP signaling and intestinal homeostasis, repair, and tumorigenesis, focusing specifically on ISC regulation. Full article
(This article belongs to the Special Issue Stem Cell Signaling)
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